Journal articles on the topic 'Neuron counts'
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1
West, Christian Alexander, Andrew McKay Hart, Giorgio Terenghi, and Mikael Wiberg. "Sensory Neurons of the Human Brachial Plexus." Neurosurgery 70, no. 5 (October 27, 2011): 1183–94. http://dx.doi.org/10.1227/neu.0b013e318241ace1.
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Abstract BACKGROUND: Extensive neuron death following peripheral nerve trauma is implicated in poor sensory recovery. Translational research for experimentally proven neuroprotective drugs requires knowledge of the numbers and distribution of sensory neurons in the human upper limb and a novel noninvasive clinical measure of neuron loss. OBJECTIVE: To compare optical fractionation and volumetric magnetic resonance imaging (MRI) of dorsal root ganglia (DRG) in histological quantification and objective clinical assessment of human brachial plexus sensory neurons. METHODS: Bilateral C5-T1 DRG were harvested from 5 human cadavers for stereological volume measurement and sensory neuron counts (optical fractionator). MRI scans were obtained from 14 healthy volunteers for volumetric analysis of C5-T1 DRG. RESULTS: The brachial plexus is innervated by 425 409 (standard deviation 15 596) sensory neurons with a significant difference in neuron counts and DRG volume between segmental levels (P < .001), with C7 ganglion containing the most. DRG volume correlated with neuron counts (r = 0.75, P < .001). Vertebral artery pulsation hindered C5 and 6 imaging, yet high-resolution MRI of C7, C8, and T1 DRG permitted unbiased volume measurement. In accord with histological analysis, MRI confirmed a significant difference between C7, C8, and T1 DRG volume (P < .001), interindividual variability (CV = 15.3%), and sex differences (P = .04). Slight right-left sided disparity in neuron counts (2.5%, P = .04) was possibly related to hand dominance, but no significant volume disparity existed. CONCLUSION: Neuron counts for the human brachial plexus are presented. These correlate with histological DRG volumes and concur with volumetric MRI results in human volunteers. Volumetric MRI of C7-T1 DRG is a legitimate noninvasive proxy measure of sensory neurons for clinical study.
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Christov, Florian, Erik G. Nelson, and Michael B. Gluth. "Human Superior Olivary Nucleus Neuron Populations in Subjects With Normal Hearing and Presbycusis." Annals of Otology, Rhinology & Laryngology 127, no. 8 (June 4, 2018): 527–35. http://dx.doi.org/10.1177/0003489418779405.
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Introduction: Normative data on superior olivary nucleus neuron counts derived from human specimens are sparse, and little is known about their coherence with structure and function of the cochlea. The purpose of this study was to quantify the neuron populations of the divisions of the superior olivary nucleus in human subjects with normal hearing and presbycusis and investigate potential relationships between these findings and histopathology in the cochlea and hearing phenotype Methods: Histopathologic examination of temporal bone and brainstem specimens from 13 subjects having normal hearing or presbycusis was undertaken. The following was determined for each: number and density of superior olivary nucleus and cochlear nucleus neurons, inner and outer hair cell counts, spiral ganglion cell counts, and pure tone audiometry. Results: The results demonstrate a significant relationship between cells within structures of the cochlear nucleus and the number of neurons of the medial superior olivary nucleus. No relationship between superior olivary nucleus neuron counts/density and cochlear histopathology or hearing phenotype was encountered. Conclusion: Normative data for superior olivary nucleus neuron populations are further established in the data presented in this study that includes subjects with normal hearing and also presbycusis.
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Barnes, Christopher L., Daniel Bonnéry, and Albert Cardona. "Synaptic counts approximate synaptic contact area in Drosophila." PLOS ONE 17, no. 4 (April 4, 2022): e0266064. http://dx.doi.org/10.1371/journal.pone.0266064.
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The pattern of synaptic connections among neurons defines the circuit structure, which constrains the computations that a circuit can perform. The strength of synaptic connections is costly to measure yet important for accurate circuit modeling. Synaptic surface area has been shown to correlate with synaptic strength, yet in the emerging field of connectomics, most studies rely instead on the counts of synaptic contacts between two neurons. Here we quantified the relationship between synaptic count and synaptic area as measured from volume electron microscopy of the larval Drosophila central nervous system. We found that the total synaptic surface area, summed across all synaptic contacts from one presynaptic neuron to a postsynaptic one, can be accurately predicted solely from the number of synaptic contacts, for a variety of neurotransmitters. Our findings support the use of synaptic counts for approximating synaptic strength when modeling neural circuits.
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Gooler, D. M., and A. S. Feng. "Temporal coding in the frog auditory midbrain: the influence of duration and rise-fall time on the processing of complex amplitude-modulated stimuli." Journal of Neurophysiology 67, no. 1 (January 1, 1992): 1–22. http://dx.doi.org/10.1152/jn.1992.67.1.1.
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1. Single-unit recordings were made in the auditory midbrain, the torus semicircularis (TS) of the northern leopard frog, to independently characterize the processing of different temporal attributes (signal duration, rise-fall time, and rate of amplitude modulation) of natural sounds and to investigate how these temporal variables interact to produce the observed responses to complex amplitude-modulated (AM) signals. Response functions, on the basis of mean spike count, were derived and categorized to describe the unit's temporal response characteristics to each of the variables. 2. To characterize the duration response functions, tone bursts of different durations (stimuli repeated at a constant repetition rate) at the unit's characteristic frequency (CF) and 10 dB above minimum threshold at CF (MT) were presented monaurally to the contralateral ear. The duration response function of a TS neuron was often related to the temporal discharge characteristics of the neuron. Increases in stimulus duration elicited an increase in spike counts (therefore, long-pass response function) from most neurons (74%) in the TS; 91% of these neurons showed tonic discharge patterns. Phasic-burst (PB) cells that were rapidly adapting showed long-pass duration response functions that were highly nonlinear, having peaks and notches embedded within the functions. On the other hand, one-third of phasic neurons tended to be insensitive to stimulus duration, giving similar spike counts in response to stimuli of greatly different durations (i.e., all pass). In the TS, some neurons (9%) only responded to a limited range of durations (i.e., band-duration pass), and still others showed a preference for shorter durations (9%; i.e., short pass); these were exhibited primarily by phasic and PB neurons. 3. To characterize the rise-fall time response functions, tone bursts having different rise-fall times were presented. The rise-fall time response functions of TS neurons had two distinct characteristics. The majority of tonic cells (91%), as well as some PB (38%) and phasic (29%) neurons, gave essentially invariant spike counts for all stimulus rise-fall times (i.e., all pass; 73% of neurons). Despite the relatively stable spike counts of neurons showing all-pass functions, the peristimulus time histograms (PSTHs) deriving from responses to slower rise-fall time stimuli exhibited a longer and somewhat more variable onset latency. About one-fourth (27%) of TS neurons, mostly phasic and PB neurons, showed higher spike counts for signals with rapid rise-fall times.(ABSTRACT TRUNCATED AT 400 WORDS)
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Saari, Laura, Katri Kivinen, Maria Gardberg, Juho Joutsa, Tommi Noponen, and Valtteri Kaasinen. "Dopamine transporter imaging does not predict the number of nigral neurons in Parkinson disease." Neurology 88, no. 15 (March 10, 2017): 1461–67. http://dx.doi.org/10.1212/wnl.0000000000003810.
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Objective:To examine possible associations between in vivo brain dopamine transporter SPECT imaging and substantia nigra pars compacta (SNc) neuronal survival in Parkinson disease (PD).Methods:Nigral neuron numbers were calculated for 18 patients (11 patients with neuropathologically confirmed PD) who had been examined with dopamine transporter (DAT) SPECT before death. Correlation analyses between SNc tyrosine hydroxylase (TH)–positive and neuromelanin-containing neuron counts and DAT striatal specific binding ratios (SBRs) were performed with semiquantitative region of interest–based and voxel-based analyses.Results:Mean putamen SBR did not correlate with the number of substantia nigra TH-positive (r = −0.11, p = 0.66) or neuromelanin-containing (r = −0.07, p = 0.78) neurons. Correlations remained clearly nonsignificant when the time interval between SPECT and death was used as a covariate, when the voxel-based analysis was used, and when only patients with PD were included.Conclusions:This cohort study demonstrates that postmortem SNc neuron counts are not associated with striatal DAT binding in PD. These results fit with the theory that there is no correlation between the number of substantia nigra neurons and striatal dopamine after a certain level of damage has occurred. Striatal DAT binding in PD may reflect axonal dysfunction or DAT expression rather than the number of viable neurons.
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Gütig, Robert, Ad Aertsen, and Stefan Rotter. "Statistical Significance of Coincident Spikes: Count-Based Versus Rate-Based Statistics." Neural Computation 14, no. 1 (January 1, 2002): 121–53. http://dx.doi.org/10.1162/089976602753284473.
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Inspired by different conceptualizations of temporal neural coding schemes, there has been recent interest in the search for signs of precisely synchronized neural activity in the cortex. One method developed for this task is unitary-event analysis. This method tests multiple single-neuron recordings for short epochs with significantly more coincident spikes than expected from independent neurons. We reformulated the statistical test underlying this method using a coincidence count distribution based on empirical spike counts rather than on estimated spike probabilities. In the case of two neurons, the requirement of stationary firing rates, originally imposed on both neurons, can be relaxed; only the rate of one neuron needs to be stationary, while the other may follow an arbitrary time course. By analytical calculations of the test power curves of the original and the revised method, we demonstrate that the test power can be increased by a factor of two or more in physiologically realistic regimes. In addition, we analyze the effective significance levels of both methods for neural firing rates ranging between 0.2 Hz and 30 Hz.
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Förstl, H., R. Levy, A. Burns, P. Luthert, and N. Cairns. "Pathways and Patterns of Cell Loss in Verified Alzheimer’s Disease: A Factor and Cluster Analysis of Clinico-Pathological Subgroups." Behavioural Neurology 7, no. 3-4 (1994): 175–80. http://dx.doi.org/10.1155/1994/325374.
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Thirty-seven patients with neuropathologically verified Alzheimer's disease (AD) have been studied prospectively. A principal components analysis of neuron numbers in cortical and subcortical areas revealed two variables: Variable I with high loadings for the hippocampo-parahippocampo-parietal neuron counts and Variable II with high loadings for coeruleo-frontal cell numbers. Both may reflect functional neuroanatomical connections which may act as pathways of neurodegeneration in AD. A cluster analysis based on these neuron numbers yielded three groups of patients: Cluster A with low hippocampo-parahippocampo-parietal cell counts, Cluster B with well-preserved neuron numbers, and Cluster C with low coeruleo-frontal neuron numbers. Differences in clinical features between these patient groups indicated the potential clinical relevance of these clusters.
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Collins, Christine E., Emily C. Turner, Eva Kille Sawyer, Jamie L. Reed, Nicole A. Young, David K. Flaherty, and Jon H. Kaas. "Cortical cell and neuron density estimates in one chimpanzee hemisphere." Proceedings of the National Academy of Sciences 113, no. 3 (January 4, 2016): 740–45. http://dx.doi.org/10.1073/pnas.1524208113.
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The density of cells and neurons in the neocortex of many mammals varies across cortical areas and regions. This variability is, perhaps, most pronounced in primates. Nonuniformity in the composition of cortex suggests regions of the cortex have different specializations. Specifically, regions with densely packed neurons contain smaller neurons that are activated by relatively few inputs, thereby preserving information, whereas regions that are less densely packed have larger neurons that have more integrative functions. Here we present the numbers of cells and neurons for 742 discrete locations across the neocortex in a chimpanzee. Using isotropic fractionation and flow fractionation methods for cell and neuron counts, we estimate that neocortex of one hemisphere contains 9.5 billion cells and 3.7 billion neurons. Primary visual cortex occupies 35 cm2 of surface, 10% of the total, and contains 737 million densely packed neurons, 20% of the total neurons contained within the hemisphere. Other areas of high neuron packing include secondary visual areas, somatosensory cortex, and prefrontal granular cortex. Areas of low levels of neuron packing density include motor and premotor cortex. These values reflect those obtained from more limited samples of cortex in humans and other primates.
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Walters, Karen M., Magalie Boucher, Germaine G. Boucher, Alan C. Opsahl, Peter R. Mouton, Chang-Ning Liu, Casey R. Ritenour, Thomas T. Kawabe, Hayley N. Pryski, and Christopher J. Somps. "No Evidence of Neurogenesis in Adult Rat Sympathetic Ganglia Following Guanethidine-Induced Neuronal Loss." Toxicologic Pathology 48, no. 1 (April 15, 2019): 228–37. http://dx.doi.org/10.1177/0192623319843052.
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The potential for neurogenesis in the cranial (superior) cervical ganglia (SCG) of the sympathetic nervous system was evaluated. Eleven consecutive daily doses of guanethidine (100 mg/kg/d) were administered intraperitoneally to rats in order to destroy postganglionic sympathetic neurons in SCG. Following the last dose, animals were allowed to recover 1, 3, or 6 months. Right and left SCG from guanethidine-treated and age-matched, vehicle-treated control rats were harvested for histopathologic, morphometric, and stereologic evaluations. Both morphometric and stereologic evaluations confirmed neuron loss following guanethidine treatment. Morphometric analysis revealed a 50% to 60% lower number of tyrosine hydroxylase (TH)-positive neurons per unit area of SCG at both 3 and 6 months of recovery, compared to ganglia of age-matched controls, with no evidence of restoration of neuron density between 3 and 6 months. Reductions in TH-positive neurons following guanethidine treatment were corroborated by unbiased stereology of total hematoxylin and eosin-stained neuron numbers in SCG. Stereologic analyses revealed that total neuron counts were lower by 37% at 3 months of recovery when compared to age-matched vehicle controls, again with no obvious restoration between 3 and 6 months. Thus, no evidence was found that postganglionic neurons of the sympathetic nervous system in the adult rat have a neurogenic capacity.
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Settanni, Gianni, and Alessandro Treves. "Analytical Model for the Effects of Learning on Spike Count Distributions." Neural Computation 12, no. 8 (August 1, 2000): 1773–87. http://dx.doi.org/10.1162/089976600300015132.
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The spike count distribution observed when recording from a variety of neurons in many different conditions has a fairly stereotypical shape, with a single mode at zero or close to a low average count, and a long, quasi-exponential tail to high counts. Such a distribution has been suggested to be the direct result of three simple facts: the firing frequency of a typical cortical neuron is close to linear in the summed input current entering the soma, above a threshold; the input current varies on several timescales, both faster and slower than the window used to count spikes; and the input distribution at any timescale can be taken to be approximately normal. The third assumption is violated by associative learning, which generates correlations between the synaptic weight vector on the dendritic tree of a neuron, and the input activity vectors it is repeatedly subject to. We show analytically that for a simple feed-forward model, the normal distribution of the slow components of the input current becomes the sum of two quasi-normal terms. The term important below threshold shifts with learning, while the term important above threshold does not shift but grows in width. These deviations from the standard distribution may be observable in appropriate recording experiments.
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Olkowicz, Seweryn, Martin Kocourek, Radek K. Lučan, Michal Porteš, W. Tecumseh Fitch, Suzana Herculano-Houzel, and Pavel Němec. "Birds have primate-like numbers of neurons in the forebrain." Proceedings of the National Academy of Sciences 113, no. 26 (June 13, 2016): 7255–60. http://dx.doi.org/10.1073/pnas.1517131113.
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Some birds achieve primate-like levels of cognition, even though their brains tend to be much smaller in absolute size. This poses a fundamental problem in comparative and computational neuroscience, because small brains are expected to have a lower information-processing capacity. Using the isotropic fractionator to determine numbers of neurons in specific brain regions, here we show that the brains of parrots and songbirds contain on average twice as many neurons as primate brains of the same mass, indicating that avian brains have higher neuron packing densities than mammalian brains. Additionally, corvids and parrots have much higher proportions of brain neurons located in the pallial telencephalon compared with primates or other mammals and birds. Thus, large-brained parrots and corvids have forebrain neuron counts equal to or greater than primates with much larger brains. We suggest that the large numbers of neurons concentrated in high densities in the telencephalon substantially contribute to the neural basis of avian intelligence.
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Moore, David R., Nina J. Rogers, and Stephen J. O'Leary. "Loss of Cochlear Nucleus Neurons following Aminoglycoside Antibiotics or Cochlear Removal." Annals of Otology, Rhinology & Laryngology 107, no. 4 (April 1998): 337–43. http://dx.doi.org/10.1177/000348949810700413.
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This study compared the effects of aminoglycoside ototoxicity and surgical ablation of the cochlea in infancy on the survival of neurons in the rat cochlear nucleus (CN). Ototoxicity was induced by a single, systemic dose of gentamicin sulfate and furosemide on postnatal day 6 (P6), P7, or P10, and assessed by the elevation of auditory brain stem response thresholds, as described in a companion paper. Unilateral cochlear removals were performed under Saffan anesthesia on P6, P9, and P12. Rats were painlessly sacrificed in adulthood, and the formalin-perfused brains and cochleas were embedded in wax, sectioned, and stained. Ototoxic treatment at P6 through P10 did not reduce neuron counts in the CN. Cochlear removal at P6 resulted in a 40% loss of CN neurons, but removal at P12 did not result in CN neuron loss. These data suggest that the critical period for the dependence of CN neurons on afferent input from the cochlea ends at the same time that susceptibility to aminoglycoside ototoxicity begins.
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Förstl, Hans, Alistair Burns, Philip Luthert, Nigel Cairns, Peter Lantos, and Raymond Levy. "Clinical and neuropathological correlates of depression in Alzheimer's disease." Psychological Medicine 22, no. 4 (November 1992): 877–84. http://dx.doi.org/10.1017/s0033291700038459.
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SynopsisDepressive symptoms have been reported in patients with mild to moderate Alzheimer's disease (AD). Recent evidence suggests that a noradrenergic deficit originating from neuronal degeneration in brainstem nuclei may represent an organic correlate of these disturbances. We examined the neuropathological changes in the locus coeruleus (LC), substantia nigra (SN), basal nucleus of Meynert and cortex of 52 patients (12 male, 40 female, mean age 83·2 ± 6·4 years) with pathologically verified AD. Fourteen patients (1 male, 13 female) showed signs of depression. The majority of these patients suffered from severe physical disability or sensory impairment and developed persistent delusions, but had less cognitive impairment. Neuronal counts in the LC were significantly lower than in the 38 patients without depression (36·9 ± 14 ·0; 51·4 ± 28·0 neuromelaninpigmented cells per section per nucleus;F= 3·4, df = 1, 50,P= 0·04). Neuron counts were higher in the basal nucleus of Meynert in depressed AD patients and there were no differences of the neuron numbers in the SN. Depression (main effect;F= 4·5,P= 0·04) contributed significantly to the variance of neuronal counts in the LC, even when covarying for gender, age of onset, cognitive impairment and cortical Alzheimer pathology. The observed disproportionate loss of noradrenergic and cholinergic neurons in the LC and basal nucleus of Meynert may represent an important organic substrate of depression in AD.
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Chuenkova, Marina V., and Miercio A. Pereira. "A Trypanosomal Protein Synergizes with the Cytokines Ciliary Neurotrophic Factor and Leukemia Inhibitory Factor to Prevent Apoptosis of Neuronal Cells." Molecular Biology of the Cell 11, no. 4 (April 2000): 1487–98. http://dx.doi.org/10.1091/mbc.11.4.1487.
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Despite the neuronal degeneration in the chronic stage of Chagas' disease, neuron counts actually increase in the preceding, asymptomatic stage, in contrast to the age-related decrease in neuron counts in age-matched normal individuals. Relevant to this observation, we found that the trans-sialidase (TS) of Trypanosoma cruzi, the etiologic agent of Chagas' disease, induces neurite outgrowth and rescues PC12 cells from apoptotic death caused by growth factor deprivation. These properties, novel for a parasite protein, were independent of catalytic activity and were mapped to the C terminus of the catalytic domain of TS. TS activated protein kinase Akt in a phosphoinositide-3 kinase-inhibitable manner, suggesting a molecular mechanism for the TS-induced neuroprotection. TS also triggered bcl-2 gene expression in growth factor-deprived cells, an effect consistent with TS protecting against apoptosis. Ciliary neurotrophic factor and leukemia inhibitory factor, two cytokines critical to the repair of injured motor neurons, specifically potentiated the TS action. The results suggest that TS acts in synergy with host ciliary neurotrophic factor or leukemia inhibitory factor to promote neuronal survival in T. cruzi-infected individuals.
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Crema, Eduardo, Lara Beatriz Prata Ribeiro, Sheila Jorge Adad, Renata Margarida Ectchebehere, Aiodair Martins Júnior, and Alex Augusto Silva. "Gallbladder neuron count in cholelithiasis patients with and without Chagas disease." Revista da Sociedade Brasileira de Medicina Tropical 40, no. 1 (February 2007): 15–17. http://dx.doi.org/10.1590/s0037-86822007000100003.
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Various investigators agree that the incidence of cholelithiasis is greater in patients with Chagas disease. The most plausible explanation for this is based on the parasympathetic denervation that occurs over the whole digestive tract due to Chagas disease. In order to analyze the occurrence of this alteration, gallbladder neuron counts were performed on cholelithiasis patients with and without Chagas disease who were being treated at the Department of Digestive Surgery, Universidade Federal do Triângulo Mineiro, Uberaba, Brazil. In the present study, a notable reduction in the number of neurons in the gallbladder wall was observed in Chagas patients, in comparison with non-Chagas subjects.
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Brewer, Gregory J., Jose A. Espinosa, and Robert G. Struble. "Effect of Neuregen nutrient medium on survival of cortical neurons after aspiration lesion in rats." Journal of Neurosurgery 98, no. 6 (June 2003): 1291–98. http://dx.doi.org/10.3171/jns.2003.98.6.1291.
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Object. During brain surgery, it would be beneficial to irrigate the surgical cavity with a solution that promotes neuronal growth and survival. The authors find that incubation of cultured neurons with normal saline, also known as buffered salts, which are often used in brain surgery in humans, does not support neuron survival. Neuregen is an optimized serum-free culture medium that promotes regeneration of adult rat and human central nervous system neurons in vitro. It includes balanced salts, glucose, amino acids, vitamins, essential fatty acids, hormones, antioxidants, and other ingredients. The authors hypothesize that brain lesions irrigated and soaked in Neuregen nutrients will have better neuron survival rates in deafferented regions than lesions irrigated with saline. Methods. Lesioning of the rat fimbria—fornix area was achieved by aspiration through the cortex; animals were killed 4 weeks later. Brain sections were stained with cresyl violet for neuron counts in the medial septum and cortex. Treatment of the lesion cavity with Neuregen resulted in a 55% increase in neuron density in the septum compared with saline treatment (p = 0.02). Cortical lesions treated with Neuregen showed a 27% increase in neuron density compared with saline-treated lesions (p = 0.015); the neuron density in Neuregen-treated rat brains was equivalent to that seen with sham treatment. Efficacy of Neuregen with basic fibroblast growth factor (bFGF) was significantly better than with Dulbecco modified Eagle medium bFGF, but not better than Neuregen alone. Neuregen produced a coincidental fourfold reduction in glial fibrillary acidic protein immunoreactivity at 4 weeks compared with saline (p = 0.002), to levels equivalent to those found in sham lesions. Conclusions. These results indicate that a highly optimized nutrient medium promotes neuron survival after brain surgery.
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BLASCO, BEATRIZ, CARLOS AVENDAÑO, and CARMEN CAVADA. "A stereological analysis of the lateral geniculate nucleus in adult Macaca nemestrina monkeys." Visual Neuroscience 16, no. 5 (September 1999): 933–41. http://dx.doi.org/10.1017/s0952523899165131.
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The Cavalieri method and the optical fractionator were employed to estimate the volume and neuron numbers, respectively, of the dorsal lateral geniculate nucleus (dLGN) in seven adult male pigtail monkeys (Macaca nemestrina). Unbiased estimates were selectively obtained for the parvocellular (P), magnocellular (M), and interlaminar plus superficial (I + S) layers of the nucleus. The dLGN had a mean volume of 56.5 mm3, and contained on average 1.79 million neurons. The P layers contributed 64% of the volume and 83% of the neurons in the dLGN; the corresponding proportions for the other layers were 13% and 9% (M), and 23% and 8% (I + S). Interindividual variability was large for neuron counts, which varied within a two-fold range, and lower for volume estimates. Since no published data are available for the pigtail dLGN, the present results are compared with quantitative studies of the dLGN in other macaque species, placing special emphasis in the discussion of the methodologies used.
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Liu, Wenshu, J. Franklin Bailey, Visaka Limwongse, and Mark DeSantis. "Scanning Electron Microscopy of neuronal cell bodies isolated from the adult mammalian central nervous system." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 426–27. http://dx.doi.org/10.1017/s0424820100159679.
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Action potentials generated in a motor neuron reflect the summation of synaptic inputs it receives from other neurons. Those synapses occur at points of contiguity between the presynaptic boutons and the surface of the motor neuron. Evidence that the density of axosomalic boutons on motor neurons varies directly with the size of the motor neuronal soma is indirect. Counts of the number of boutons per unit area at the surface of the motor neuron’s cell body using scanning electron microscopy (SEM) would allow an independent, direct assessment of that inference. We describe here procedures for consistently isolating the somas of CNS neurons, specifically those associated with the adult rat’s trigeminal nerve, so that axosomatic boutons can be seen by SEM (Figures 1 and 2).Adult male and female rats were anesthetized and then perfused with saline followed by 4% paraformaldehyde. The brain stem was removed and sectioned at 200 um thickness on a vibratome. Sections containing the trigeminal motor and mesencephalic nuclei were pinned to Sylgard-lined dishes containing phosphate buffer (0.1 M, pH 7.2).
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Huang, Xin, and Stephen G. Lisberger. "Noise Correlations in Cortical Area MT and Their Potential Impact on Trial-by-Trial Variation in the Direction and Speed of Smooth-Pursuit Eye Movements." Journal of Neurophysiology 101, no. 6 (June 2009): 3012–30. http://dx.doi.org/10.1152/jn.00010.2009.
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Smooth-pursuit eye movements are variable, even when the same tracking target motion is repeated many times. We asked whether variation in pursuit could arise from noise in the response of visual motion neurons in the middle temporal visual area (MT). In physiological experiments, we evaluated the mean, variance, and trial-by-trial correlation in the spike counts of pairs of simultaneously recorded MT neurons. The correlations between responses of pairs of MT neurons are highly significant and are stronger when the two neurons in a pair have similar preferred speeds, directions, or receptive field locations. Spike count correlation persists when the same exact stimulus form is repeatedly presented. Spike count correlations increase as the analysis window increases because of correlations in the responses of individual neurons across time. Spike count correlations are highest at speeds below the preferred speeds of the neuron pair and increase as the contrast of a square-wave grating is decreased. In computational analyses, we evaluated whether the correlations and variation across the population response in MT could drive the observed behavioral variation in pursuit direction and speed. We created model population responses that mimicked the mean and variance of MT neural responses as well as the observed structure and amplitude of noise correlations between pairs of neurons. A vector-averaging decoding computation revealed that the observed variation in pursuit could arise from the MT population response, without postulating other sources of motor variation.
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Desky, Fitria, Hermanto Tri Joewono, and Widjiati Widjiati. "FR 50% in pregnancy results in different neuron and glial cell count (astrocytes, olygodendrocytes, and microglia) in the cerebrum and cerebellum of newborn Rattus norvegicus." Majalah Obstetri & Ginekologi 27, no. 2 (September 19, 2019): 56. http://dx.doi.org/10.20473/mog.v27i22019.56-65.
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Objectives: To analyze the difference neuronal and glial (astrocytes, oligodendrocyte, microglia) cell count in cerebrum and cerebellum of Rattus norvegicus newborns with 50% food restriction and control group.Materials and Methods: This was an analytical experimental study with single blind randomized post test only control group design using animals subjects Rattus norvegicus. This study was conducted at Animal laboratory, Veterinary Faculty, Universitas Airlangga. Animal subjects were divided into FR50% group and control. Neuron and glial (astrocytes, oligodendrocytes, microglia) counts were analyzed using comparison test, with CI 95%.Results: There was a significant difference in cerebrum and cerebellum neuron cell count between intervention and control group (9.88+3.59 vs 16.88+2.553; p=0.000 and 7.5+1.789 vs 11.44+4.56; p=0.02). There was no difference in cerebrum and cerebellum glial cell count. There was a significant difference in cerebellum astrocyte between intervention and control group (80.94+24.255 vs 59.69+18.77; p=0.02) but no difference in cerebrum. There was a significant difference in cerebrum and cerebellum oligodendrocyte between intervention and control group (14.06+12.195 vs 25.13+8.609; p<0.000 and 13.63+6.712 vs 24.00+8.862; p=0.001), and there were significant difference in cerebrum and cerebellum microglia cell between intervention and control group (5.25+3.435 vs 4.94+3.838; p=0.620 and 8.81+4.119 vs 5.25+1.483; p=0.004).Conclusion: Food Restriction 50% (FR50%) in Rattus norvegicus decreased cerebrum and cerebellum neuron cell and oligodendrocyte count and increased cerebrum and cerebellum microglial count.
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Förstl, H., A. Burns, N. Cairns, P. Luthert, and R. Levy. "Basal Ganglia Mineralization in Alzheimer’s Disease: A Comparative Study of Clinical, Neuroradiological and Neuropathological Findings." Behavioural Neurology 5, no. 1 (1992): 53–57. http://dx.doi.org/10.1155/1992/947260.
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Fifty patients from a longitudinal study on 178 cases of Alzheimer's disease were examined at postmortem. The clinical features, CT-scans and neuropathological findings of five patients, with verified Alzheimer's disease, who had bilateral basal ganglia mineralization (BGM; 2 male, 3 female; age 78–91 years) were compared with the data of five age- and sex-matched Alzheimer patients without BGM and of five control subjects. Persecutory and other delusions (4 patients), persistent depression (2), parkinsonism (4), myoclonus (1) and epileptic seizures (1) were observed more frequently in the patients with BGM than was expected. The BGM-group had significantly lower counts of large neurons in the pallidum internum than the demented patients without BGM or the control group. We did not find other differences between the dementia groups regarding the CT-scans, or plaque, tangle and neuron counts in neocortex and brainstem. We suggest that the combined effects of Alzheimer pathology and BGM might lead to an increased manifestation of psychotic and motor disturbances.
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Thajeb, P., Z. D. Ling, E. D. Potter, and P. M. Carvey. "The Effects of Storage Conditions and Trophic Supplementation on the Survival of Fetal mesencephalic cells." Cell Transplantation 6, no. 3 (May 1997): 297–307. http://dx.doi.org/10.1177/096368979700600312.
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It is estimated that only 5-10% of dopamine (DA) neurons implanted into the striatum of patients undergoing fetal-nigral transplantation as a treatment for Parkinson's Disease survive. Because it is often necessary to store fetal tissue prior to transplantation, we evaluated various storage parameters that could influence DA neuron viability in rostral mesencephalic tegmentum (RMT) cultures using tyrosine hydroxylase immunoreactive (THir) cell counts as an index of DA neuron survival. A high K+ hibernation media (HM) was used in all studies. We found that RMT cell viability and THir cell counts decreased as storage duration increased (up to 120 h). Storage at 37°C in HM killed all cells, while storage at 10°C yielded higher survival rates than 4° C. In comparison to trypsinization, mechanical dissociation of tissue increased cell viability. Neutral pH and a storage density of at least 1 × 106 cells/mL were found to be optimal, while striatal coculture of RMT cells with striatal feeder layers increased THir viability up to 16-fold in comparison to monocultures. The nurturing effect of striatal coculture may be explained by the release of autotrophic factors, and we tested this hypothesis by supplementing the HM with human placental cord serum (HPCS, 8%), glial-derived neurotrophic factor (GDNF; 10 μg/mL), and brain-derived neurotrophic factor (BDNF; 10 μg/mL). GDNF and HPCS supplements increased RMT cell viability by 10-15%, while GDNF, BDNF, and HPCS increased viability of THir cells by approximately 40% at all time points studied. As Klenow enzyme labeling technique indicated that 33% of stored RMT cells were undergoing apoptosis, we found that GDNF, BDNF, and HPCS reduced apoptosis by 50%. DNA laddering and DAPI nuclear stain confirmed the presence of apoptosis in hibernated RMT cells, leading us to postulate that the high viability counts seen with trypan blue exclusion are misleading.
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Joris, Philip X. "Measuring ongoing delay with reverse noise." Journal of the Acoustical Society of America 151, no. 4 (April 2022): A257. http://dx.doi.org/10.1121/10.0011249.
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Counts of spike coincidences provide a powerful means to compare responses to different stimuli or of different neurons, particularly regarding temporal factors. A drawback is that these methods do not provide an absolute measure of latency, i.e., the temporal interval between stimulus and response. It is desirable to obtain such a measurement within the same analysis framework of coincidence counting. Single neuron responses were obtained from several fiber tracts (nerve, trapezoid body, lateral lemniscus) in two species to a broadband noise and its polarity-inverted version. The spike trains in response to these stimuli are the “forward noise” responses. The same stimuli were also played time-reversed. The resulting spike trains are then again time-reversed: these are the “reverse noise” responses. The forward and reverse responses were then analyzed with the coincidence count methods we have introduced earlier. Latency measurements derived from correlograms between forward and reverse noise responses show maxima at twice the latency value measured with other methods, as expected. Correlograms were often asymmetric but, at low-characteristic frequencies, were well-predicted by crosscorrelation of the reverse-correlation function and its reverse. We conclude that reverse noise provides an easy and reliable means to estimate latency of auditory nerve and brainstem neurons.
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Oakley, R. A., A. S. Garner, T. H. Large, and E. Frank. "Muscle sensory neurons require neurotrophin-3 from peripheral tissues during the period of normal cell death." Development 121, no. 5 (May 1, 1995): 1341–50. http://dx.doi.org/10.1242/dev.121.5.1341.
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To determine if muscle sensory neurons require neurotrophin-3 (NT3) during the period of normal cell death, we used an NT3-specific antiserum to deplete NT3 from peripheral tissues during this period in chick embryos. DiI staining of dorsal roots indicated that limb injections of anti-NT3 reduced the spinal projection of muscle spindle afferents. In contrast, injection of the antiserum into the spinal cord had no demonstrable effect, indicating that the reduced projection following limb injection was due to peripheral blockade of NT3 signaling. Counts of neurons retrogradely labeled from muscle and cutaneous nerves showed that peripheral blockade of NT3 selectively reduced the survival of muscle sensory neurons without affecting the survival of cutaneous sensory neurons or motoneurons. In situ hybridization with trkC probes indicated that, during the period of cell death, most large diameter muscle sensory neurons express trkC transcripts, whereas few cutaneous neurons express this receptor for NT3. We conclude that large diameter muscle afferents, including spindle afferents, require NT3 from peripheral tissues to survive the normal period of sensory neuron death in vivo.
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Cass, Stephen P., Paul Davidson, and Harry Goshgarian. "Survival of the Vestibular Nerve after Labyrinthectomy in the Cat." Otolaryngology–Head and Neck Surgery 101, no. 4 (October 1989): 459–65. http://dx.doi.org/10.1177/019459988910100409.
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Temporal bone studies in cat, monkey, and man demonstrate that the cell bodies of the primary vestibular neurons located in Scarpa's ganglion persist after labyrlnthectomy. However, it is not known whether the centrally directed axon process of deafferented vestibular neurons survive or degenerate after labyrinthectomy. If the central axon were to persist, then the primary vestibular neuron could influence vestibular compensation or produce symptoms of vestibular dysfunction. In the present study the temporal bones and brain stem of four cats were prepared for light microscopic examination with hematoxylin-eosin, silver, and trichrome connective tissue stains. Cell counts within Scarpa's ganglion were performed. After labyrinthectomy, many intact axons were demonstrated in the brain stem, a finding that correlated with survival of neurons in Scarpa's ganglion. This study provides anatomic evidence that primary vestibular neurons that survive labyrinthectomy may retain their central axon processes. The persistence of this neural pathway and data from behavioral studies in the cat suggest that vestibular neurons may affect vestibular compensation after labyrinthectomy. Deafferented vestibular neurons may play a role in human vestibular compensation and dysfunction.
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Rullán Buxó, Camille E., and Jonathan W. Pillow. "Poisson balanced spiking networks." PLOS Computational Biology 16, no. 11 (November 20, 2020): e1008261. http://dx.doi.org/10.1371/journal.pcbi.1008261.
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An important problem in computational neuroscience is to understand how networks of spiking neurons can carry out various computations underlying behavior. Balanced spiking networks (BSNs) provide a powerful framework for implementing arbitrary linear dynamical systems in networks of integrate-and-fire neurons. However, the classic BSN model requires near-instantaneous transmission of spikes between neurons, which is biologically implausible. Introducing realistic synaptic delays leads to an pathological regime known as “ping-ponging”, in which different populations spike maximally in alternating time bins, causing network output to overshoot the target solution. Here we document this phenomenon and provide a novel solution: we show that a network can have realistic synaptic delays while maintaining accuracy and stability if neurons are endowed with conditionally Poisson firing. Formally, we propose two alternate formulations of Poisson balanced spiking networks: (1) a “local” framework, which replaces the hard integrate-and-fire spiking rule within each neuron by a “soft” threshold function, such that firing probability grows as a smooth nonlinear function of membrane potential; and (2) a “population” framework, which reformulates the BSN objective function in terms of expected spike counts over the entire population. We show that both approaches offer improved robustness, allowing for accurate implementation of network dynamics with realistic synaptic delays between neurons. Both Poisson frameworks preserve the coding accuracy and robustness to neuron loss of the original model and, moreover, produce positive correlations between similarly tuned neurons, a feature of real neural populations that is not found in the deterministic BSN. This work unifies balanced spiking networks with Poisson generalized linear models and suggests several promising avenues for future research.
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Lee, Jennifer K., Bing Wang, Michael Reyes, Jillian S. Armstrong, Ewa Kulikowicz, Polan T. Santos, Jeong-Hoo Lee, Raymond C. Koehler, and Lee J. Martin. "Hypothermia and Rewarming Activate a Macroglial Unfolded Protein Response Independent of Hypoxic-Ischemic Brain Injury in Neonatal Piglets." Developmental Neuroscience 38, no. 4 (2016): 277–94. http://dx.doi.org/10.1159/000448585.
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Therapeutic hypothermia provides incomplete neuroprotection after hypoxia-ischemia (HI)-induced brain injury in neonates. We previously showed that cortical neuron and white matter apoptosis are promoted by hypothermia and early rewarming in a piglet model of HI. The unfolded protein response (UPR) may be one of the potential mediators of this cell death. Here, neonatal piglets underwent HI or sham surgery followed by 29 h of normothermia, 2 h of normothermia + 27 h of hypothermia or 18 h of hypothermia + rewarming. Piglets recovered for 29 h. Immunohistochemistry for endoplasmic reticulum to nucleus signaling-1 protein (ERN1), a marker of UPR activation, was used to determine the ratios of ERN1+ macroglia and neurons in the motor subcortical white matter and cerebral cortex. The ERN1+ macroglia were immunophenotyped as oligodendrocytes and astrocytes by immunofluorescent colabeling. Temperature (p = 0.046) and HI (p < 0.001) independently affected the ratio of ERN1+ macroglia. In sham piglets, sustained hypothermia (p = 0.011) and rewarming (p = 0.004) increased the ERN1+ macroglia ratio above that in normothermia. HI prior to hypothermia diminished the UPR. Ratios of ERN1+ macroglia correlated with white matter apoptotic profile counts in shams (r = 0.472; p = 0.026), thereby associating UPR activation with white matter apoptosis during hypothermia and rewarming. Accordingly, macroglial cell counts decreased in shams that received sustained hypothermia (p = 0.009) or rewarming (p = 0.007) compared to those in normothermic shams. HI prior to hypothermia neutralized the macroglial cell loss. Neither HI nor temperature affected ERN1+ neuron ratios. In summary, delayed hypothermia and rewarming activate the macroglial UPR, which is associated with white matter apoptosis. HI may decrease the macroglial endoplasmic reticulum stress response after hypothermia and rewarming.
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Güner, Güneş, and Figen Söylemezoğlu. "Morphometry in Classification of Hippocampal Sclerosis." Acta Medica 53, no. 3 (September 26, 2022): 227–32. http://dx.doi.org/10.32552/2022.actamedica.690.
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Hippocampal sclerosis (HS) is evaluated in 3 categories by the latest (2013) ILAE classification. The distinction between these categories rely on the histopathological assessment of pyramidal neuron loss in 4 CA sectors. In order to evaluate neuron loss assessment done manually by a neuropathologist, cell counts were carried out from representative photomicrographs of each section. NeuN immunohistochemistry was applied on hippocampus sections of 28 samples of epilepsy surgery, photographed at x100 magnification to represent each of the 4 sectors, and neuron density was calculated per photo. This density data was compared to the pathology reports’ diagnoses. HS type 1 cases were predominant (n=23) with few type 2 and type 3 cases (3 and 2, respectively). Percentage of neuron loss calculated per photos, ILAE classification guidelines and pathological diagnoses rendered without any calculation were relatively well-correlated; with HS type 2 and 3 displaying slight changes from recommendations. Data also display accurate pathological diagnoses of HS without special equipment or cell density calculation. HS types 2 and 3 in Turkey may display variant cell density properties which may warrant further clarification.
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Wiese, Ashley J., Michael Rathbun, Mark T. Butt, Shelle A. Malkmus, Philip J. Richter, Kent G. Osborn, Qinghao Xu, et al. "Intrathecal Substance P-Saporin in the Dog." Anesthesiology 119, no. 5 (November 1, 2013): 1163–77. http://dx.doi.org/10.1097/aln.0b013e3182a95164.
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Abstract Background: Neurokinin-1 receptors (NK1-rs) located on superficial dorsal horn neurons are essential for integration of nociceptive input. Intrathecal injection of substance P-saporin (SP-SAP) leads to local loss of spinal NK1-r (+) neurons suggesting its potential as a therapeutic agent for chronic pain. The authors determined, in a canine model, effects of lumbar intrathecal SP-SAP. Methods: Distribution of SP-SAP and Saporin was determined in plasma, lumbar cerebrospinal fluid, and tissue. Safety of intrathecal SP-SAP was determined in four groups (six dogs each) administered 0 (0.9% saline), 1.5, 15, or 150 µg SP-SAP through lumbar intrathecal catheters. Behavioral, physiologic, and biochemical variables were assessed. Spinal tissues were collected at 7 and approximately 90 days, or earlier if significant morbidity developed, and analyzed for NK1-r (+) neuron loss and histopathology. Results: SP-SAP and Saporin were detectable in lumbar cerebrospinal fluid for up to 4 and 24 h, respectively. Animals receiving intrathecal saline, 1.5, or 15 µg of SP-SAP showed no persistent neurologic deficits. Three animals receiving 150 µg of SP-SAP developed pelvic limb paraparesis and were euthanized prematurely. Immunohistochemistry and in situ hybridization cell counts confirmed a significant reduction in NK1-r (+) in superficial dorsal horn neurons from lumbar spinal cord after intrathecal administration of 15 and 150 µg of SP-SAP. A significant loss of NK1-r neurons in the lumbar ventral horn occurred only with 150-µg SP-SAP. Conclusion: Intrathecal 15-µg SP-SAP reduced dorsal, but not ventral, NK1-r (+) neurons at the spinal level of delivery with minimal side effects, whereas 150-µg SP-SAP resulted in motor neuron toxicity.
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van Kann, Elisabeth, Bruno Cozzi, Patrick R. Hof, and Helmut H. A. Oelschläger. "Qualitative and Quantitative Analysis of Primary Neocortical Areas in Selected Mammals." Brain, Behavior and Evolution 90, no. 3 (2017): 193–210. http://dx.doi.org/10.1159/000477431.
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The present study focuses on the relationship between neocortical structures and functional aspects in three selected mammalian species. Our aim was to compare cortical layering and neuron density in the projection areas (somatomotor, M1; somatosensory, S1; auditory, A1; and visual, V1; each in a wider sense). Morphological and design-based stereological analysis was performed in the wild boar (Sus scrofa scrofa) as a representative terrestrial hoofed animal (artiodactyl) and the common dolphin (Delphinus delphis) as a highly derived related aquatic mammal (cetartiodactyl). For comparison, we included the human (Homo sapiens) as a well-documented anthropoid primate. In the cortex of many mammals, layer IV (inner granular layer) is the main target of specific thalamocortical inputs while layers III and V are the main origins of neocortical projections. Because the fourth layer is indistinct or mostly lacking in the primary neocortex of the wild boar and dolphins, respectively, we analyzed the adjacent layers III and V in these animals. In the human, all the three layers were investigated separately. The stereological data show comparatively low neuron densities in all areas of the wild boar and high cell counts in the human (as expected), particularly in the primary visual cortex. The common dolphin, in general, holds an intermediate position in terms of neuron density but exhibits higher values than the human in a few layers. With respect to the situation in the wild boar, stereological neuron counts in the dolphin are consistently higher, with a maximum in layer III of the visual cortex. The extended auditory neocortical field in dolphins and the hypertrophic auditory pathway indicate secondary neurobiological adaptations to their aquatic habitat during evolution. The wild boar, however, an omnivorous quadruped terrestrial mammal, shows striking specializations as to the sensorimotor neurobiology of the snout region.
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Uylings, H. B. M., K. Zilles, and G. Rajkowska. "Optimal Staining Methods for Delineation of Cortical Areas and Neuron Counts in Human Brains." NeuroImage 9, no. 4 (April 1999): 439–45. http://dx.doi.org/10.1006/nimg.1999.0417.
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Hurley, Laura M., and George D. Pollak. "Serotonin Effects on Frequency Tuning of Inferior Colliculus Neurons." Journal of Neurophysiology 85, no. 2 (February 1, 2001): 828–42. http://dx.doi.org/10.1152/jn.2001.85.2.828.
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We investigated the modulatory effects of serotonin on the tuning of 114 neurons in the central nucleus of the inferior colliculus (ICc) of Mexican free-tailed bats and how serotonin-induced changes in tuning influenced responses to complex signals. We obtained a “response area” for each neuron, defined as the frequency range that evoked discharges and the spike counts evoked by those frequencies at a constant intensity. We then iontophoretically applied serotonin and compared response areas obtained before and during the application of serotonin. In 58 cells, we also assessed how serotonin-induced changes in response areas correlated with changes in the responses to brief frequency-modulated (FM) sweeps whose structure simulated natural echolocation calls. Serotonin profoundly changed tone-evoked spike counts in 60% of the neurons (68/114). In most neurons, serotonin exerted a gain control, facilitating or depressing the responses to all frequencies in their response areas. In many cells, serotonergic effects on tones were reflected in the responses to FM signals. The most interesting effects were in those cells in which serotonin selectively changed the responsiveness to only some frequencies in the neuron's response area and had little or no effect on other frequencies. This caused predictable changes in responses to the more complex FM sweeps whose spectral components passed through the neurons' response areas. Our results suggest that serotonin, whose release varies with behavioral state, functionally reconfigures the circuitry of the IC and may modulate the perception of acoustic signals under different behavioral states.
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Kaur, Gurveen, Beerinder Singh, Himisha Beltran, Naveed Hassan Akhtar, David M. Nanus, and Scott T. Tagawa. "Circulating tumor cell (CTC) enumeration in patients with metastatic neuroendocrine prostate cancer (NEPC) and castration-resistant prostate cancer (CRPC)." Journal of Clinical Oncology 32, no. 4_suppl (February 1, 2014): 204. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.204.
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204 Background: Neuroendocrine prostate cancer (NEPC) is an aggressive variant of prostate cancer. Circulating tumor cell (CTC) counts as measured by CellSearch are prognostic for large groups with metastatic prostate cancer (PC), but are not well described in NEPC. Methods: With institutional review board approval, we retrospectively identified patients with metastatic PC and available CTC enumeration (CellSearch methodology) and compared counts/7.5 mL blood and overall survival (OS), measured from the first recorded CTC count until death or last follow up. Entry criteria for clinical trials were used to define NEPC, including histology (small cell/neuroendocrine carcinoma or adenocarcinoma with more than 50% NE staining), serum chromogranin greater than 5x ULN and/or neuron specific enolase greater than 2x ULN, and/or predominant liver/brain metastases with lack of prostate-specific antigen [Beltran ASCO 2013, clinicaltrials.gov NCT01799278 ]. Frequency of detectable and unfavorable counts was tabulated and OS was compared across groups. Results: Sixty one patients were identified: 21 NEPC with median age 73.7 and 40 patients with castration-resistant prostate cancer (CRPC) with median age 73.9 over contemporary time periods 2009 to 2012. Median OS for the entire group was 22.6 months (mo), with a trend for shorter OS in NEPC (20.7 mo) than CRPC (22.7 mo), p=0.11. 47.6% of NEPC and 55% of CRPC had detectable CTC counts (p=0.58); 38.1% of NEPC and 40.0% of CRPC had greater than or equal to five CTCs (p=0.89). CTC counts of 0 to 4 versus greater than or equal to five were prognostic for both groups: NEPC with 0 to 4 CTCs had median OS of 22.6 versus 6.6 mo for CTCs greater than or equal to 5 (p<0.001) and CRPC with 0 to 4 CTCs median OS not reached (mean 40.6 mo) versus 11.2 mo for those with greater than or equal to five CTCs (p<0.001). Conclusions: Patients with NEPC have similar frequency of detectable and elevated CTC counts by CellSearch methodology as compared to an overall CRPC population. CTC counts are prognostic for both groups.
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Mathern, Gary W., James K. Pretorius, and Thomas L. Babb. "Quantified patterns of mossy fiber sprouting and neuron densities in hippocampal and lesional seizures." Journal of Neurosurgery 82, no. 2 (February 1995): 211–19. http://dx.doi.org/10.3171/jns.1995.82.2.0211.
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✓ Quantified hippocampal mossy fiber synaptic reorganization and neuron losses were measured to determine the pathological features associated with epileptogenic fascia dentata. Twenty-five patients with temporal lobe epilepsy (TLE) were classified as having either mesial temporal sclerosis (MTS; 16 patients), with seizure genesis in the hippocampus, or temporal mass lesions (nine patients), with seizures that were probably extrahippocampal. Neo-Timm's histochemistry identified mossy fiber sprouting, and aberrant fascia dentata puncta densities were objectively measured by light microscopic analysis on an image-analysis computer. Neuron densities determined cell losses and the two seizure groups were compared to control specimens obtained from autopsies. Results showed significantly greater fascia dentata mossy fiber puncta densities and neuron losses in TLE patients compared to autopsy specimens (p < 0.026). Furthermore, there were significant differences between the two seizure groups: 1) mossy fiber puncta densities in the inner molecular layer were significantly greater in MTS compared to lesions (p < 0.02), and 2) mossy fiber puncta densities were greater in the inner molecular layer than in the stratum granulosum in 14 of 16 MTS patients (88%) compared to four of nine patients with lesions (44%, p < 0.01). Neuron densities were significantly different comparing MTS, lesion and control groups for stratum granulosum (p = 0.0001) and Ammon's horn (p = 0.0001), with each group significantly different (p < 0.05) compared to another. All patients were either seizure-free or significantly improved 1 year or more after en bloc temporal lobectomy. There were no significant correlations between fascia dentata mossy fiber puncta densities and counts of hilar neurons, CA4 pyramids, granule cells, or years of seizures. This indicates that inner molecular layer mossy fiber puncta densities and neuron losses are greater in patients with MTS than in those with lesions, and mossy fiber sprouting probably contributes to the pathophysiology of hippocampal seizures. Furthermore, these data show that some patients with extrahippocampal lesions have mossy fiber sprouting similar to MTS patients, suggesting that hippocampi in lesion patients may be capable of epileptogenesis from synaptic reorganization.
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Jakobs, Tatjana C., Richard T. Libby, Yixin Ben, Simon W. M. John, and Richard H. Masland. "Retinal ganglion cell degeneration is topological but not cell type specific in DBA/2J mice." Journal of Cell Biology 171, no. 2 (October 24, 2005): 313–25. http://dx.doi.org/10.1083/jcb.200506099.
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Using a variety of double and triple labeling techniques, we have reevaluated the death of retinal neurons in a mouse model of hereditary glaucoma. Cell-specific markers and total neuron counts revealed no cell loss in any retinal neurons other than the ganglion cells. Within the limits of our ability to define cell types, no group of ganglion cells was especially vulnerable or resistant to degeneration. Retrograde labeling and neurofilament staining showed that axonal atrophy, dendritic remodeling, and somal shrinkage (at least of the largest cell types) precedes ganglion cell death in this glaucoma model. Regions of cell death or survival radiated from the optic nerve head in fan-shaped sectors. Collectively, the data suggest axon damage at the optic nerve head as an early lesion, and damage to axon bundles would cause this pattern of degeneration. However, the architecture of the mouse eye seems to preclude a commonly postulated source of mechanical damage within the nerve head.
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Yu, Xiong-jie, J. David Dickman, Gregory C. DeAngelis, and Dora E. Angelaki. "Neuronal thresholds and choice-related activity of otolith afferent fibers during heading perception." Proceedings of the National Academy of Sciences 112, no. 20 (May 4, 2015): 6467–72. http://dx.doi.org/10.1073/pnas.1507402112.
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How activity of sensory neurons leads to perceptual decisions remains a challenge to understand. Correlations between choices and single neuron firing rates have been found early in vestibular processing, in the brainstem and cerebellum. To investigate the origins of choice-related activity, we have recorded from otolith afferent fibers while animals performed a fine heading discrimination task. We find that afferent fibers have similar discrimination thresholds as central cells, and the most sensitive fibers have thresholds that are only twofold or threefold greater than perceptual thresholds. Unlike brainstem and cerebellar nuclei neurons, spike counts from afferent fibers do not exhibit trial-by-trial correlations with perceptual decisions. This finding may reflect the fact that otolith afferent responses are poorly suited for driving heading perception because they fail to discriminate self-motion from changes in orientation relative to gravity. Alternatively, if choice probabilities reflect top-down inference signals, they are not relayed to the vestibular periphery.
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Pawlas, Zbyněk, Lev B. Klebanov, Martin Prokop, and Petr Lansky. "Parameters of Spike Trains Observed in a Short Time Window." Neural Computation 20, no. 5 (May 2008): 1325–43. http://dx.doi.org/10.1162/neco.2007.01-07-442.
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We study the estimation of statistical moments of interspike intervals based on observation of spike counts in many independent short time windows. This scenario corresponds to the situation in which a target neuron occurs. It receives information from many neurons and has to respond within a short time interval. The precision of the estimation procedures is examined. As the model for neuronal activity, two examples of stationary point processes are considered: renewal process and doubly stochastic Poisson process. Both moment and maximum likelihood estimators are investigated. Not only the mean but also the coefficient of variation is estimated. In accordance with our expectations, numerical studies confirm that the estimation of mean interspike interval is more reliable than the estimation of coefficient of variation. The error of estimation increases with increasing mean interspike interval, which is equivalent to decreasing the size of window (less events are observed in a window) and with decreasing the number of neurons (lower number of windows).
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Caldararo, Niccolo. "Anatomical Variation, Hominins, Species, and Self-Domestication." OBM Genetics 6, no. 1 (October 19, 2021): 1. http://dx.doi.org/10.21926/obm.genet.2201145.
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The evolution of hominins, members of the zoological tribe Hominini, has been a much-studied topic, and the construction of phylogenetic trees has been the key method in molecular evolutionary studies. How scientists determine the phylogenetic trees are governed by the assumptions they place on the construction of similarities and differences in morphological traits, the differences in the number of base pairs in the genomes, and the number of similar gene clusters that code for traits (haplotypes) or are error sequences (SNPs). Among the several methods employed for the construction of a phylogenetic tree, mathematical methods (utilized for sorting data, including fabrication of algorithms) are the most significant ones; also, the nature of population structuring plays an important role in the evolutionary process. In this paper, I will not only describe the drawbacks of current assumptions in hominin evolution during the Middle Pleistocene era (based on fossil evidence) but also the aspects of brain evolution and the self-domestication of our species. The evolution of the brain is usually associated with an increase in neurons and other types of cells associated with signal processing (connectivity) and memory. Assessing actual neuron counts in fossils is challenging; moreover, new research has shown decreased neuron numbers in the neocortex and demonstrated large counts in the cerebellum, leading to a decreased focus on brain size. The idea of increased brain size in the Pleistocene era without a substantial increase in the evidence of cognitive activity in complex behavior residues might be explained by increased myelination to provide additional insulation in Ice Age conditions and faster transition of signals due to increased competition for reduced food supplies. Other cold-adaptation features can also be noted. Such a model can provide a new approach to assess the apparent brain size reduction in the Upper Paleolithic period.
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Isla, Alberto, Bartolomé Bejarano, Carmen Morales, Concepción Pérez Conde, and Carlos Avendaño. "Anatomical and functional connectivity of the transected ulnar nerve after intercostal neurotization in cats." Journal of Neurosurgery 90, no. 6 (June 1999): 1057–63. http://dx.doi.org/10.3171/jns.1999.90.6.1057.
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Object. Acute transfer of three intercostal nerves to the ulnar nerve was performed in cats for histological and clinical evaluation of a distal muscle reinnervation.Methods. Infraclavicular intercostal-ulnar communications were created after dividing the motor branches of the upper intercostal nerves in 14 adult cats. Reinnervation of distal forelimb muscles in the ulnar territory was assessed by electromyographic (EMG) studies and motor function rating each month until 18 months postsurgery. In five of these treated animals, and in four controls, horseradish peroxidase (HRP) was applied to the ulnar or intercostal nerves to study the amount and distribution of retrograde motor neuron labeling in the spinal cord. Also, samples of reinnervated muscles and neurotized ulnar nerves were processed to assess regeneration.Simple ulnar transection without reconstruction led to permanent atrophy of ulnar muscles, lack of recovery according to EMG or clinical studies, and disappearance of the ulnar motor neuron pool. In contrast, ulnar neurotization with the intercostal nerves led to a high rate of functional recovery, which began 5 months postsurgery, and progressed from muscle activity synchronized with ventilatory movements to spontaneous movements that were independent of respiration. This recovery was accompanied by substantial retrograde labeling of intercostal motor neurons after HRP application in the ulnar nerve. Cell counts showed that practically the whole motor neuron pool of the involved intercostal nerves contributed to reinnervation of the transected ulnar nerve.Conclusions. These findings demonstrate that the use of intercostal nerves to neurotize long brachial plexus nerves can achieve long-lasting and successful reinnervation of distal forelimb muscles.
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Liu, Yang, Robert M. Grumbles, and Christine K. Thomas. "Electrical stimulation of transplanted motoneurons improves motor unit formation." Journal of Neurophysiology 112, no. 3 (August 1, 2014): 660–70. http://dx.doi.org/10.1152/jn.00806.2013.
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Motoneurons die following spinal cord trauma and with neurological disease. Intact axons reinnervate nearby muscle fibers to compensate for the death of motoneurons, but when an entire motoneuron pool dies, there is complete denervation. To reduce denervation atrophy, we have reinnervated muscles in Fisher rats from local transplants of embryonic motoneurons in peripheral nerve. Since growth of axons from embryonic neurons is activity dependent, our aim was to test whether brief electrical stimulation of the neurons immediately after transplantation altered motor unit numbers and muscle properties 10 wk later. All surgical procedures and recordings were done in anesthetized animals. The muscle consequences of motoneuron death were mimicked by unilateral sciatic nerve section. One week later, 200,000 embryonic day 14 and 15 ventral spinal cord cells, purified for motoneurons, were injected into the tibial nerve 10–15 mm from the gastrocnemii muscles as the only neuron source for muscle reinnervation. The cells were stimulated immediately after transplantation for up to 1 h using protocols designed to examine differential effects due to pulse number, stimulation frequency, pattern, and duration. Electrical stimulation that included short rests and lasted for 1 h resulted in higher motor unit counts. Muscles with higher motor unit counts had more reinnervated fibers and were stronger. Denervated muscles had to be stimulated directly to evoke contractions. These results show that brief electrical stimulation of embryonic neurons, in vivo, has long-term effects on motor unit formation and muscle force. This muscle reinnervation provides the opportunity to use patterned electrical stimulation to produce functional movements.
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Förstl, Hans, Alistair Burns, Raymond Levy, Nigel Cairns, Philip Luthert, and Peter Lantos. "Neuropathological Correlates of Behavioural Disturbance in Confirmed Alzheimer's Disease." British Journal of Psychiatry 163, no. 3 (September 1993): 364–68. http://dx.doi.org/10.1192/bjp.163.3.364.
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Clinico-pathological correlations were examined in 54 patients with neuropathologically verified Alzheimer's disease (AD) who were part of a prospective study. Behavioural disturbance was documented using an expanded version of the Stockton Geriatric Rating Scale (SGRS). The subscores for physical disability (P), apathy (A) and communication failure (C) (summation score PAC) were closely correlated and were high in most patients during the late stages of illness. High PAC scores correlated with an earlier onset and longer duration of illness, lower brain weight, more severe tangle pathology in the parahippocampal gyrus and the frontal and parietal neocortex, and lower neuron counts in the hippocampus and basal nucleus of Meynert. Features of the Klüver-Bucy syndrome (range behaviour and hypermetamorphosis) were significantly associated with lower counts of large neurons in the parahippocampal gyrus and parietal neocortex, but not with more severe plaque or tangle formation or with neuronal loss in the subcortical nuclei. No correction was made for multiple comparisons. These findings may signify decreased cortical inhibition in patients with relatively well preserved subcortical structures who show features suggestive of the Klüver-Bucy syndrome. High PAC scores on the SGRS could reflect more advanced and widespread cerebral pathology in the end stages of AD.
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Bauer, Eric E., Achim Klug, and George D. Pollak. "Spectral Determination of Responses to Species-Specific Calls in the Dorsal Nucleus of the Lateral Lemniscus." Journal of Neurophysiology 88, no. 4 (October 1, 2002): 1955–67. http://dx.doi.org/10.1152/jn.2002.88.4.1955.
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This study evaluated how neurons in the dorsal nucleus of the lateral lemniscus (DNLL) in Mexican free-tailed bats respond to both tone bursts and species-specific calls. Up to 20 calls were presented to each neuron, of which 18 were social communication and 2 were echolocation calls. We also measured excitatory response regions (ERRs): the range of tone burst frequencies that evoked discharges at a fixed intensity. Neurons were unselective for one or another call in that each neuron responded to any call so long as the call had energy that encroached on its ERR. Additionally, responses were evoked by the same set of calls, and with similar spike counts, when they were presented normally or reversed. By convolving activity in the ERRs with the spectrogram of each call, we showed that responses to tones accurately predicted discharge patterns evoked by species-specific calls. DNLL cells are remarkably homogeneous in that neurons having similar BFs responded to each of the species-specific calls with similar response profiles. The homogeneity was further illustrated by the ability to accurately predict the response profiles of a particular DNLL cell to species-specific calls from the ERR of another similarly tuned DNLL cell. Thus DNLL neurons tuned to the same or similar frequencies responded to species-specific calls with latencies and temporal discharge patterns that were so similar as to be virtually interchangeable. What this suggests is that DNLL responses evoked by complex sounds can be largely explained by a simple summation of the excitation in each neuron's ERR. Finally, superimposing the spectrograms of each call on the responses evoked by that call revealed that the DNLL population response re-creates both the spectral and the temporal features of each signal.
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Schmidt, Richard H., and M. Sean Grady. "Loss of forebrain cholinergic neurons following fluid-percussion injury: implications for cognitive impairment in closed head injury." Journal of Neurosurgery 83, no. 3 (September 1995): 496–502. http://dx.doi.org/10.3171/jns.1995.83.3.0496.
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✓ Disturbances in memory, concentration, and problem solving are common after even mild to moderate traumatic brain injury. Because these functions are mediated in part by forebrain cholinergic and catecholaminergic innervation, in this study the authors sought to determine if experimental concussive injury produces detectable morphological damage to these systems. Fluid-percussion head injury, sufficient to cause a 13- to 14-minute loss of righting reflex, was produced in rats that had been anesthetized with halothane. Injury was delivered either at midline or 2 mm off midline and compared with appropriate sham-injured controls. After 11 to 15 days, the rat brains were stained in serial sections for choline acetyltransferase, tyrosine hydroxylase, dopamine β-hydroxylase, acetylcholinesterase, and nicotinamide adenine dinucleotide phosphate diaphorase. Cell counts were determined for the entire population of ventrobasal forebrain cholinergic cells. Midline injury produced a bilateral loss of cholinergic neurons averaging 36% in area Ch1 (medial septal nucleus), 45% in Ch2 (nucleus of the diagonal band of Broca), and 41% in Ch4 (nucleus basalis of Meynart), (p ≤ 0.05). Lateralized injury resulted in cholinergic neuron loss of similar magnitude ipsilaterally (p ≤ 0.05), but a smaller contralateral loss of between 11% and 28%. No loss of neurons was detected in the pontomesencephalic cholinergic groups Ch5 and Ch6. There was no visible effect of head injury on forebrain dopamine or noradrenergic innervation. A significant and apparently selective loss of ventrobasal forebrain cholinergic neurons following brief concussive injury in rats is demonstrated in this study. This type of injury is known to produce significant disturbance in cognitive tasks linked to neocortical and hippocampal cholinergic function. It remains to be determined how this neuron loss occurs, whether it can be prevented with neuroprotective agents, how it affects innervation in target tissues, and whether it occurs in human victims of traumatic brain injury.
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Faulkes, Zen, and Gerald S. Pollack. "Effects of Inhibitory Timing on Contrast Enhancement in Auditory Circuits in Crickets (Teleogryllus oceanicus)." Journal of Neurophysiology 84, no. 3 (September 1, 2000): 1247–55. http://dx.doi.org/10.1152/jn.2000.84.3.1247.
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In crickets ( Teleogryllus oceanicus), the paired auditory interneuron Omega Neuron 1 (ON1) responds to sounds with frequencies in the range from 3 to 40 kHz. The neuron is tuned to frequencies similar to that of conspecific songs (4.5 kHz), but its latency is longest for these same frequencies by a margin of 5–10 ms. Each ON1 is strongly excited by input from the ipsilateral ear and inhibits contralateral auditory neurons that are excited by the contralateral ear, including the interneurons ascending neurons 1 and 2 (AN1 and AN2). We investigated the functional consequences of ON1's long latency to cricket-like sound and the resulting delay in inhibition of AN1 and AN2. Using dichotic stimuli, we controlled the timing of contralateral inhibition of the ANs relative to their excitation by ipsilateral stimuli. Advancing the stimulus to the ear driving ON1 relative to that driving the ANs “subtracted” ON1's additional latency to 4.5 kHz. This had little effect on the spike counts of AN1 and AN2. The response latencies of these neurons, however, increased markedly. This is because in the absence of a delay in ON1's response, inhibition arrived at AN1 and AN2 early enough to abolish the first spikes in their responses. This also increased the variability of AN1 latency. This suggests that one possible function of the delay in ON1's response may be to protect the precise timing of the onset of response in the contralateral AN1, thus preserving interaural difference in response latency as a reliable potential cue for sound localization. Hyperpolarizing ON1 removed all detectable contralateral inhibition of AN1 and AN2, suggesting that ON1 is the main, if not the only, source of contralateral inhibition.
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Geisler, W. S., D. G. Albrecht, R. J. Salvi, and S. S. Saunders. "Discrimination performance of single neurons: rate and temporal-pattern information." Journal of Neurophysiology 66, no. 1 (July 1, 1991): 334–62. http://dx.doi.org/10.1152/jn.1991.66.1.334.
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1. A new method of measuring the performance of neurons in sensory discrimination tasks was developed and then applied to single-neuron responses recorded in the auditory nerve of chinchilla and in the striate visual cortex of cat. 2. Most previous methods of measuring discrimination performance have employed decision rules that involve comparing the total counts of action potentials (spikes) produced by two different stimuli. Such measures ignore response pattern and hence may not reflect all the information transmitted by a neuron. The proposed method attempts to measure all (or most) of the transmitted information by constructing descriptive models of the neuron's response to each stimulus in the discrimination experiment; these descriptive models consist of measured probability distributions of the spike counts in small time bins. The measured probability distributions are then used to define an optimal decision rule (an ideal observer) for discriminating the two stimuli. Finally, discrimination performance is measured by applying this decision rule to novel presentations of the same two stimuli. 3. Intensity and temporal-phase discrimination were measured for three neurons in the auditory nerve of chinchilla. The discrimination stimuli were low-frequency pure tones of 70-ms duration. Intensity thresholds were found to be 5–20 dB lower at low intensities using the new pattern method compared with the traditional counting method. The pattern method led to better performance because it utilized both rate and temporal pattern information. Phase discrimination performance using the counting method was at chance because the average spike rate did not change with phase. On the other hand, using the pattern method, phase discrimination thresholds were found to decrease with intensity, often reaching values equivalent to 30–40 microseconds of temporal offset. These thresholds are as good as or better than behavioral thresholds in chinchilla. 4. Contrast and temporal-phase discrimination were measured for three neurons in the striate visual cortex of cat. The discrimination stimuli were drifting sine-wave gratings of 100- to 160-ms duration. Contrast discrimination functions measured by the pattern method and the counting method were found to be essentially identical. Phase discrimination using the counting method was at chance. However, using the pattern method, phase thresholds were found to decrease with contrast, reaching values equivalent to 7 ms of temporal offset for the two simple cells. 5. Our results suggest that temporal response pattern carries substantial information for intensity and phase discrimination in the auditory nerve and for phase discrimination in the striate visual cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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Yao, Runhong, Kazuhiro Nishii, Naoki Aizu, Takumi Kito, Kazuyoshi Sakai, and Kouji Yamada. "Maintenance of the Amygdala-Hippocampal Circuit Function with Safe and Feasible Shaking Exercise Therapy in SAMP-10 Mice." Dementia and Geriatric Cognitive Disorders Extra 11, no. 2 (May 19, 2021): 114–21. http://dx.doi.org/10.1159/000515957.
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<b><i>Introduction:</i></b> Patients with dementia show reduced adaptive, behavioral, and physiological responses to environmental threats. Physical exercise is expected to delay brain aging, maintain cognitive function and, consequently, help dementia patients face threats and protect themselves skillfully. <b><i>Methods:</i></b> To confirm this, we aimed to investigate the effects of the shaking exercise on the avoidance function in the senescence-accelerated mouse-prone strain-10 (SAMP-10) model at the behavioral and tissue levels. SAMP-10 mice were randomized into 2 groups: a control group and a shaking group. The avoidance response (latency) of the mice was evaluated using a passive avoidance task. The degree of amygdala and hippocampal aging was evaluated based on the brain morphology. Subsequently, the association between avoidance response and the degree of amygdala-hippocampal aging was evaluated. <b><i>Results:</i></b> Regarding the passive avoidance task, the shaking group showed a longer latency period than the control group (<i>p</i> < 0.05), even and low intensity staining of ubiquitinated protein, and had a higher number of and larger neurons than those of the control group. The difference between the groups was more significant in the BA region of the amygdala and the CA1 region of the hippocampus (staining degree: <i>p</i> < 0.05, neuron size: <i>p</i> < 0.01, neuron counts: <i>p</i> < 0.01) than in other regions. <b><i>Conclusions:</i></b> The shaking exercise prevents nonfunctional protein (NFP) accumulation, neuron atrophy, and neuron loss; delays the aging of the amygdala and hippocampus; and maintains the function of the amygdala-hippocampal circuit. It thus enhances emotional processing and cognition functions, the memory of threats, the skillful confrontation of threats, and proper self-protection from danger.
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Acosta-Martínez, Maricedes, Ji Luo, Carol Elias, Andrew Wolfe, and Jon E. Levine. "Male-Biased Effects of Gonadotropin-Releasing Hormone Neuron-Specific Deletion of the Phosphoinositide 3-Kinase Regulatory Subunit p85α on the Reproductive Axis." Endocrinology 150, no. 9 (June 18, 2009): 4203–12. http://dx.doi.org/10.1210/en.2008-1753.
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Abstract GnRH neurosecretion is subject to regulation by insulin, IGF-I, leptin, and other neuroendocrine modulators whose effects may be conveyed by activation of phosphoinositide 3-kinase (PI3K)-mediated pathways. It is not known, however, whether any of these regulatory actions are exerted directly, via activation of PI3K in GnRH neurons, or whether they are primarily conveyed via effects on afferent circuitries governing GnRH neurosecretion. To investigate the role of PI3K signaling in GnRH neurons, we used conditional gene targeting to ablate expression of the major PI3K regulatory subunit, p85α, in GnRH neurons. Combined in situ hybridization and immunohistochemistry confirmed reduction of p85α mRNA expression in GnRH neurons of GnRH-p85α knockout (KO) animals. Females of both genotypes exhibited estrous cyclicity and had comparable serum LH, estradiol-17β, and FSH levels. In male GnRH-p85αKO mice, serum LH, testosterone, and sperm counts were significantly reduced compared with wild type. To investigate the role of the other major regulatory subunit, p85β, on the direct control of GnRH neuronal function, we generated mice with a GnRH-neuron-specific p85α deletion on a global βKO background. No additional reproductive effects in male or female mice were found, suggesting that p85β does not substitute p85 activity toward PI3K function in GnRH neurons. Our results suggest that p85α, and thus PI3K activity, participates in the control of GnRH neuronal activity in male mice. The sex-specific phenotype in these mice raises the possibility that PI3K activation during early development may establish sex differences in GnRH neuronal function.
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Huang, Xin, and Stephen G. Lisberger. "Circuit mechanisms revealed by spike-timing correlations in macaque area MT." Journal of Neurophysiology 109, no. 3 (February 1, 2013): 851–66. http://dx.doi.org/10.1152/jn.00775.2012.
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We recorded simultaneously from pairs of motion-sensitive neurons in the middle temporal cortex (MT) of macaque monkeys and used cross-correlations in the timing of spikes between neurons to gain insights into cortical circuitry. We characterized the time course and stimulus dependency of the cross-correlogram (CCG) for each pair of neurons and of the auto-correlogram (ACG) of the individual neurons. For some neuron pairs, the CCG showed negative flanks that emerged next to the central peak during stimulus-driven responses. Similar negative flanks appeared in the ACG of many neurons. Negative flanks were most prevalent and deepest when the neurons were driven to high rates by visual stimuli that moved in the neurons' preferred directions. The temporal development of the negative flanks in the CCG coincided with a parallel, modest reduction of the noise correlation between the spike counts of the neurons. Computational analysis of a model cortical circuit suggested that negative flanks in the CCG arise from the excitation-triggered mutual cross-inhibition between pairs of excitatory neurons. Intracortical recurrent inhibition and afterhyperpolarization caused by intrinsic outward currents, such as the calcium-activated potassium current of small conductance, can both contribute to the negative flanks in the ACG. In the model circuit, stronger intracortical inhibition helped to maintain the temporal precision between the spike trains of pairs of neurons and led to weaker noise correlations. Our results suggest a neural circuit architecture that can leverage activity-dependent intracortical inhibition to adaptively modulate both the synchrony of spike timing and the correlations in response variability.
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Arabzadeh, E. "Deciphering the Spike Train of a Sensory Neuron: Counts and Temporal Patterns in the Rat Whisker Pathway." Journal of Neuroscience 26, no. 36 (September 6, 2006): 9216–26. http://dx.doi.org/10.1523/jneurosci.1491-06.2006.
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Ueda, Masayuki, and S. Nowak Thaddeus. "Protective Preconditioning by Transient Global Ischemia in the Rat: Components of Delayed Injury Progression and Lasting Protection Distinguished by Comparisons of Depolarization Thresholds for Cell Loss at Long Survival Times." Journal of Cerebral Blood Flow & Metabolism 25, no. 8 (March 30, 2005): 949–58. http://dx.doi.org/10.1038/sj.jcbfm.9600107.
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Robust ischemic preconditioning has been shown in rodent brain, but there are concerns regarding the persistence of neuron protection. This issue was examined in rat hippocampus following 4-vessel occlusion (4-VO) ischemia, using DC shifts characteristic of ischemic depolarization to reproducibly define insult severity. Preconditioning ischemia producing 2 to 3.5 mins depolarization was followed at intervals of 2, 5, or 7 days by test insults of varied duration, after which CA1 counts were obtained at 1, 2, 4, or 12 weeks. Neuron loss in naive animals increased with depolarization time longer than 4 mins regardless of postischemic survival interval. Preconditioning 2, 5, or 7 days before test insults prolonged the injury threshold evaluated at 1 week survival to 15, 9, or 6 mins, respectively, showing robust protection and a rapid decay of the protected state. However, by 2 weeks survival after preconditioning at a 2-day interval, the injury threshold dramatically regressed from 15 to 9 mins. Thereafter protection remained relatively stable through 1 month, but slight progression of neuron injury was evident at 3 months. Inflammatory responses were seen in both naive and preconditioned hippocampi throughout this interval, appropriate to the extent of neuron injury. These studies show distinct components of transient and lasting protection after ischemic preconditioning. Finally, it was found that ischemic depolarization was delayed by approximately 1 min in optimally preconditioned rat hippocampus, in contrast to previous results in the gerbil, identifying one specific mechanism by which insult severity is reduced in this model.