Journal articles on the topic 'Primary neuron'

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1

Sun, Wensheng, Ellisha N. Marongelli, Paul V. Watkins, and Dennis L. Barbour. "Decoding sound level in the marmoset primary auditory cortex." Journal of Neurophysiology 118, no. 4 (October 1, 2017): 2024–33. http://dx.doi.org/10.1152/jn.00670.2016.

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Neurons that respond favorably to a particular sound level have been observed throughout the central auditory system, becoming steadily more common at higher processing areas. One theory about the role of these level-tuned or nonmonotonic neurons is the level-invariant encoding of sounds. To investigate this theory, we simulated various subpopulations of neurons by drawing from real primary auditory cortex (A1) neuron responses and surveyed their performance in forming different sound level representations. Pure nonmonotonic subpopulations did not provide the best level-invariant decoding; instead, mixtures of monotonic and nonmonotonic neurons provided the most accurate decoding. For level-fidelity decoding, the inclusion of nonmonotonic neurons slightly improved or did not change decoding accuracy until they constituted a high proportion. These results indicate that nonmonotonic neurons fill an encoding role complementary to, rather than alternate to, monotonic neurons. NEW & NOTEWORTHY Neurons with nonmonotonic rate-level functions are unique to the central auditory system. These level-tuned neurons have been proposed to account for invariant sound perception across sound levels. Through systematic simulations based on real neuron responses, this study shows that neuron populations perform sound encoding optimally when containing both monotonic and nonmonotonic neurons. The results indicate that instead of working independently, nonmonotonic neurons complement the function of monotonic neurons in different sound-encoding contexts.
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2

Shin, Seung Min, Yongsong Cai, Brandon Itson-Zoske, Chensheng Qiu, Xu Hao, Hongfei Xiang, Quinn H. Hogan, and Hongwei Yu. "Enhanced T-type calcium channel 3.2 activity in sensory neurons contributes to neuropathic-like pain of monosodium iodoacetate-induced knee osteoarthritis." Molecular Pain 16 (January 2020): 174480692096380. http://dx.doi.org/10.1177/1744806920963807.

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The monosodium iodoacetate knee osteoarthritis model has been widely used for the evaluation of osteoarthritis pain, but the pathogenesis of associated chronic pain is not fully understood. The T-type calcium channel 3.2 (CaV3.2) is abundantly expressed in the primary sensory neurons, in which it regulates neuronal excitability at both the somata and peripheral terminals and facilitates spontaneous neurotransmitter release at the spinal terminals. In this study, we investigated the involvement of primary sensory neuron-CaV3.2 activation in monosodium iodoacetate osteoarthritis pain. Knee joint osteoarthritis pain was induced by intra-articular injection of monosodium iodoacetate (2 mg) in rats, and sensory behavior was evaluated for 35 days. At that time, knee joint structural histology, primary sensory neuron injury, and inflammatory gliosis in lumbar dorsal root ganglia, and spinal dorsal horn were examined. Primary sensory neuron-T-type calcium channel current by patch-clamp recording and CaV3.2 expression by immunohistochemistry and immunoblots were determined. In a subset of animals, pain relief by CaV3.2 inhibition after delivery of CaV3.2 inhibitor TTA-P2 into sciatic nerve was investigated. Knee injection of monosodium iodoacetate resulted in osteoarthritis histopathology, weight-bearing asymmetry, sensory hypersensitivity of the ipsilateral hindpaw, and inflammatory gliosis in the ipsilateral dorsal root ganglia, sciatic nerve, and spinal dorsal horn. Neuronal injury marker ATF-3 was extensively upregulated in primary sensory neurons, suggesting that neuronal damage was beyond merely knee-innervating primary sensory neurons. T-type current in dissociated primary sensory neurons from lumbar dorsal root ganglia of monosodium iodoacetate rats was significantly increased, and CaV3.2 protein levels in the dorsal root ganglia and spinal dorsal horn ipsilateral to monosodium iodoacetate by immunoblots were significantly increased, compared to controls. Perineural application of TTA-P2 into the ipsilateral sciatic nerve alleviated mechanical hypersensitivity and weight-bearing asymmetry in monosodium iodoacetate osteoarthritis rats. Overall, our findings demonstrate an elevated CaV3.2 expression and enhanced function of primary sensory neuron-T channels in the monosodium iodoacetate osteoarthritis pain. Further study is needed to delineate the importance of dysfunctional primary sensory neuron-CaV3.2 in osteoarthritis pain.
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3

Reyes, Laura D., Tessa Harland, Roger L. Reep, Chet C. Sherwood, and Bob Jacobs. "Golgi Analysis of Neuron Morphology in the Presumptive Somatosensory Cortex and Visual Cortex of the Florida Manatee (Trichechus manatus latirostris)." Brain, Behavior and Evolution 87, no. 2 (2016): 105–16. http://dx.doi.org/10.1159/000445495.

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The current study investigates neuron morphology in presumptive primary somatosensory (S1) and primary visual (V1) cortices of the Florida manatee (Trichechus manatus latirostris) as revealed by Golgi impregnation. Sirenians, including manatees, have an aquatic lifestyle, a large body size, and a relatively large lissencephalic brain. The present study examines neuron morphology in 3 cortical areas: in S1, dorsolateral cortex area 1 (DL1) and cluster cortex area 2 (CL2) and in V1, dorsolateral cortex area 4 (DL4). Neurons exhibited a variety of morphological types, with pyramidal neurons being the most common. The large variety of neuron types present in the manatee cortex was comparable to that seen in other eutherian mammals, except for rodents and primates, where pyramid-shaped neurons predominate. A comparison between pyramidal neurons in S1 and V1 indicated relatively greater dendritic branching in S1. Across all 3 areas, the dendritic arborization pattern of pyramidal neurons was also similar to that observed previously in the afrotherian rock hyrax, cetartiodactyls, opossums, and echidnas but did not resemble the widely bifurcated dendrites seen in the large-brained African elephant. Despite adaptations for an aquatic environment, manatees did not share specific neuron types such as tritufted and star-like neurons that have been found in cetaceans. Manatees exhibit an evolutionarily primitive pattern of cortical neuron morphology shared with most other mammals and do not appear to have neuronal specializations for an aquatic niche.
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4

Turner, Emily C., Nicole A. Young, Jamie L. Reed, Christine E. Collins, David K. Flaherty, Mariana Gabi, and Jon H. Kaas. "Distributions of Cells and Neurons across the Cortical Sheet in Old World Macaques." Brain, Behavior and Evolution 88, no. 1 (2016): 1–13. http://dx.doi.org/10.1159/000446762.

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According to previous research, cell and neuron densities vary across neocortex in a similar manner across primate taxa. Here, we provide a more extensive examination of this effect in macaque monkeys. We separated neocortex from the underlying white matter in 4 macaque monkey hemispheres (1 Macaca nemestrina, 2 Macaca radiata, and 1 Macaca mulatta), manually flattened the neocortex, and divided it into smaller tissue pieces for analysis. The number of cells and neurons were determined for each piece across the cortical sheet using flow cytometry. Primary visual cortex had the most densely packed neurons and primary motor cortex had the least densely packed neurons. With respect to differences in brain size between cases, there was little variability in the total cell and neuron numbers within specific areas, and overall trends were similar to what has been previously described in Old World baboons and other primates. The average hemispheric total cell number per hemisphere ranged from 2.9 to 3.7 billion, while the average total neuron number ranged from 1.3 to 1.7 billion neurons. The visual cortex neuron densities were predictably higher, ranging from 18.2 to 34.7 million neurons/cm2 in macaques, in comparison to a range of 9.3-17.7 million neurons/cm2 across cortex as a whole. The results support other evidence that neuron surface densities vary across the cortical sheet in a predictable pattern within and across primate taxa.
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5

Sutter, M. L., and C. E. Schreiner. "Physiology and topography of neurons with multipeaked tuning curves in cat primary auditory cortex." Journal of Neurophysiology 65, no. 5 (May 1, 1991): 1207–26. http://dx.doi.org/10.1152/jn.1991.65.5.1207.

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1. The physiology and topography of single neuron responses along the isofrequency domain of the middle- and high-frequency portions [characteristic frequencies (CFs) greater than 4 kHz] of the primary auditory cortex (AI) were investigated in the barbiturate-anesthetized cat. Single neurons were recorded at several locations along the extent of isofrequency contours, defined from initial multiple-unit mapping. For each neuron a high-resolution excitatory tuning curve was determined, and for some neurons high-resolution two-tone tuning curves were recorded to measure inhibitory/suppressive areas. 2. A physiologically distinct population of neurons was found in the dorsal part of cat AI. These neurons exhibited two or three distinct excitatory frequency ranges, whereas most neurons in AI responded with excitation to a single narrow frequency range. These were called multipeaked neurons because of the shape of their tuning curves. At frequencies between the excitatory regions, the multipeaked neurons were inhibited or unresponsive. 3. Multipeaked neurons exhibited several distinct threshold minima in their frequency tuning curves. Most of the multipeaked neurons (88%) displayed two frequency minima, whereas the rest exhibited three minima. 4. The frequency separation between threshold minima was less than 1 octave in 71% of the double-peaked neurons recorded. Occasionally, the frequency peaks of these neurons closely corresponded to a response to second and third harmonics without a response to the fundamental frequency. 5. Multipeaked neurons exhibited a wide range of total bandwidths (highest excitatory frequency minus lowest excitatory frequency expressed in octaves). Bandwidths of the isolated peaks within the same neuron were also quite variable. 6. Response latencies to tones with frequencies within each peak of a multipeaked neuron could vary considerably. In 71% (17) of the neurons, tones corresponding to the high-frequency peak (CFh) elicited a longer response latency (greater than 4 ms) than those corresponding to the low-frequency peak (CF1). 7. Inhibitory/suppressive bands, as demonstrated with a two-tone paradigm, were often present between the peaks. Typically, neurons with excitatory peaks of similar response latencies showed an inhibitory band located between the peaks. 8. Ninety percent of the topographically localized multipeaked neurons were in the dorsal part of AI (greater than 1 mm dorsal to the maximum in the sharpness-of-tuning map). Although these neurons were restricted to dorsal AI, only 35% of neurons in this region were multipeaked. 9. Multipeaked neurons could show decreased response latencies and thresholds to two-tone combinations.(ABSTRACT TRUNCATED AT 400 WORDS)
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6

Cao, Jinyan, and John Meitzen. "Perinatal activation of ERα and ERβ but not GPER-1 masculinizes female rat caudate-putamen medium spiny neuron electrophysiological properties." Journal of Neurophysiology 125, no. 6 (June 1, 2021): 2322–38. http://dx.doi.org/10.1152/jn.00063.2021.

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This study is the first to demonstrate that estradiol and estrogen receptor α and β stimulation during early development sexually differentiates the electrophysiological properties of caudate-putamen medium spiny neurons, the primary output neuron of the striatal regions. Overall, this evidence provides new insight into the neuroendocrine mechanism by which caudate-putamen neuron electrophysiology is sexually differentiated and demonstrates the powerful action of early hormone exposure upon individual neuron electrophysiology.
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7

Han, Jingfeng, Weiping Tao, Wei Cui, and Jiawei Chen. "Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons." Oxidative Medicine and Cellular Longevity 2022 (January 18, 2022): 1–16. http://dx.doi.org/10.1155/2022/6298786.

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Background. Hypoxia may induce mitochondrial abnormality, which is associated with a variety of clinical phenotypes in the central nervous system. Propofol is an anesthetic agent with neuroprotective property. We examined whether and how propofol protected hypoxia-induced mitochondrial abnormality in neurons. Methods. Primary rat hippocampal neurons were exposed to propofol followed by hypoxia treatment. Neuron viability, mitochondrial morphology, mitochondrial permeability transition pore (mPTP) opening, mitochondrial membrane potential (MMP), and adenosine triphosphate (ATP) production were measured. Mechanisms including reactive oxygen species (ROS), extracellular regulated protein kinase (ERK), protein kinase A (PKA), HIF-1α, Drp1, Fis1, Mfn1, Mfn2, and Opa1 were investigated. Results. Hypoxia increased intracellular ROS production and induced mPTP opening, while reducing ATP production, MMP values, and neuron viability. Hypoxia impaired mitochondrial dynamic balance by increasing mitochondrial fragmentation. Further, hypoxia induced the translocation of HIF-1α and increased the expression of Drp1, while having no effect on Fis1 expression. In addition, hypoxia induced the phosphorylation of ERK and Drp1ser616, while reducing the phosphorylation of PKA and Drp1ser637. Importantly, we demonstrated all these effects were attenuated by pretreatment of neurons with 50 μM propofol, antioxidant α-tocopherol, and ROS scavenger ebselen. Besides, hypoxia, propofol, α-tocopherol, or ebselen had no effect on the expression of Mfn1, Mfn2, and Opa1. Conclusions. In rat hippocampal neurons, hypoxia induced oxidative stress, caused mitochondrial dynamic imbalance and malfunction, and reduced neuron viability. Propofol protected mitochondrial abnormality and neuron viability via antioxidant property, and the molecular mechanisms involved HIF-1α-mediated Drp1 expression and ERK/PKA-mediated Drp1 phosphorylation.
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8

Carandini, Matteo, Horace B. Barlow, Lawrence P. O'keefe, Allen B. Poirson, and J. Anthony Movshon. "Adaptation to contingencies in macaque primary visual cortex." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, no. 1358 (August 29, 1997): 1149–54. http://dx.doi.org/10.1098/rstb.1997.0098.

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We tested the hypothesis that neurons in the primary visual cortex adapt selectively to contingencies in the attributes of visual stimuli. We recorded from single neurons in macaque V1 and measured the effects of adaptation either to the sum of two gratings (compound stimulus) or to the individual gratings. According to our hypothesis, there would be a component of adaptation that is specific to the compound stimulus. In a first series of experiments, the two gratings differed in orientation. One grating had optimal orientation and the other was orthogonal to it, and therefore did not activate the neuron under study. These experiments provided evidence in favour of our hypothesis. In most cells adaptation to the compound stimulus reduced responses to the compound stimulus more than it reduced responses to the optimal grating, and adaptation to the optimal grating reduced responses to the optimal grating more than it reduced responses to the compound stimulus. This suggests that a component of adaptation was specific to (and caused by) the simultaneous presence of the two orientations in the compound stimulus. To test whether V1 neurons could adapt to other contingencies in the stimulus attributes, we performed a second series of experiments, in which the component gratings were parallel but differed in spatial frequency, and were both effective in activating the neuron under study. These experiments failed to reveal convincing contingent effects of adaptation, suggesting that neurons cannot adapt equally well to all types of contingency.
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9

Hardwick, Laura J. A., and Anna Philpott. "xNgn2 induces expression of predominantly sensory neuron markers in Xenopus whole embryo ectoderm but induces mixed subtype expression in isolated ectoderm explants." Wellcome Open Research 3 (November 8, 2018): 144. http://dx.doi.org/10.12688/wellcomeopenres.14911.1.

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Proneural basic-helix-loop-helix (bHLH) proteins, such as Neurogenin2 (Ngn2) and Ascl1, are critical regulators at the onset of neuronal differentiation. Endogenously they have largely complementary expression patterns, and have conserved roles in the specification of distinct neuronal subtypes. In Xenopus embryos, xNgn2 is the master regulator of primary neurogenesis forming sensory, inter- and motor neurons within the neural plate, while xAscl1 is the master regulator of autonomic neurogenesis, forming noradrenergic neurons in the antero-ventral region of the embryo. Here we characterise neuronal subtype identity of neurons induced by xNgn2 in the ectoderm of whole Xenopus embryos in comparison with xAscl1, and in ectodermal “animal cap” explants. We find that the transcriptional cascades mediating primary and autonomic neuron formation are distinct, and while xNgn2 and xAscl1 can upregulate genes associated with a non-endogenous cascade, this expression is spatially restricted within the embryo. xNgn2 is more potent than xAscl1 at inducing primary neurogenesis as assayed by neural-β-tubulin. In ectoderm of the intact embryo, these induced primary neurons have sensory characteristics with no upregulation of motor neuron markers. In contrast, xNgn2 is able to up-regulate both sensory and motor neuron markers in naïve ectoderm of animal cap explants, suggesting a non-permissive environment for motor identity in the patterned ectoderm of the whole embryo.
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10

Wang, Xiao-Jing, Yinghui Liu, Maria V. Sanchez-Vives, and David A. McCormick. "Adaptation and Temporal Decorrelation by Single Neurons in the Primary Visual Cortex." Journal of Neurophysiology 89, no. 6 (June 2003): 3279–93. http://dx.doi.org/10.1152/jn.00242.2003.

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Limiting redundancy in the real-world sensory inputs is of obvious benefit for efficient neural coding, but little is known about how this may be accomplished by biophysical neural mechanisms. One possible cellular mechanism is through adaptation to relatively constant inputs. Recent investigations in primary visual (V1) cortical neurons have demonstrated that adaptation to prolonged changes in stimulus contrast is mediated in part through intrinsic ionic currents, a Ca2+-activated K+ current ( IKCa) and especially a Na+-activated K+ current ( IKNa). The present study was designed to test the hypothesis that the activation of adaptation ionic currents may provide a cellular mechanism for temporal decorrelation in V1. A conductance-based neuron model was simulated, which included an IKCa and an IKNa. We show that the model neuron reproduces the adaptive behavior of V1 neurons in response to high contrast inputs. When the stimulus is stochastic with 1/ f 2 or 1/ f-type temporal correlations, these autocorrelations are greatly reduced in the output spike train of the model neuron. The IKCa is effective at reducing positive temporal correlations at approximately 100-ms time scale, while a slower adaptation mediated by IKNa is effective in reducing temporal correlations over the range of 1–20 s. Intracellular injection of stochastic currents into layer 2/3 and 4 (pyramidal and stellate) neurons in ferret primary visual cortical slices revealed neuronal responses that exhibited temporal decorrelation in similarity with the model. Enhancing the slow afterhyperpolarization resulted in a strengthening of the decorrelation effect. These results demonstrate the intrinsic membrane properties of neocortical neurons provide a mechanism for decorrelation of sensory inputs.
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Fornaro, Michele, Stefania Raimondo, Jennifer M. Lee, and Maria Giuseppina Giacobini-Robecchi. "Neuron-specific Hu proteins sub-cellular localization in primary sensory neurons." Annals of Anatomy - Anatomischer Anzeiger 189, no. 3 (May 2007): 223–28. http://dx.doi.org/10.1016/j.aanat.2006.11.004.

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12

DILIEGRO, I., A. CESTELLI, G. BARBIERI, and A. GIALLONGO. "Expression of neuron-specific enolase in primary cultures of rat neurons." Cell Biology International Reports 14 (September 1990): 153. http://dx.doi.org/10.1016/0309-1651(90)90714-a.

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13

Hogan, Quinn H. "Labat Lecture: The Primary Sensory Neuron." Regional Anesthesia and Pain Medicine 35, no. 3 (May 2010): 306–11. http://dx.doi.org/10.1097/aap.0b013e3181d2375e.

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14

Strayer, Amy L., Cassandra N. Dennys-Rivers, Karina C. Ricart, Narae Bae, Joseph S. Beckman, Maria Clara Franco, and Alvaro G. Estevez. "Ligand-independent activation of the P2X7 receptor by Hsp90 inhibition stimulates motor neuron apoptosis." Experimental Biology and Medicine 244, no. 11 (May 29, 2019): 901–14. http://dx.doi.org/10.1177/1535370219853798.

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Activation of the extracellular ATP ionotropic receptor P2X7 stimulates motor neuron apoptosis, whereas its inhibition in cell and animal models of amyotrophic lateral sclerosis can be protective. These observations suggest that P2X7 receptor activation is relevant to motor neuron disease and that it could be targeted for therapeutic development. Heat shock protein 90 (Hsp90) is an integral regulatory component of the P2X7 receptor complex, antagonizing ligand-induced receptor activation. Here, we show that the repressive activity of Hsp90 on P2X7 receptor activation in primary motor neurons is highly sensitive to inhibition. Primary motor neurons in culture are 100-fold more sensitive to Hsp90 inhibition by geldanamycin than other neuronal populations. Pharmacological inhibition and down-regulation of the P2X7 receptor prevented motor neuron apoptosis triggered by Hsp90 inhibition, which occurred in the absence of extracellular ATP. These observations suggest that inhibition of a seemingly motor neuron specific pool of Hsp90 leads to ligand independent activation of P2X7 receptor and motor neuron death. Downstream of Hsp90 inhibition, P2X7 receptor activated the phosphatase and tensin homolog (TPEN), which in turn suppressed the pro-survival phosphatidyl inositol 3 kinase (PI3K)/Akt pathway, leading to Fas-dependent motor neuron apoptosis. Conditions altering the interaction between P2X7 receptor and Hsp90, such as recruitment of Hsp90 to other subcellular compartments under stress conditions, or nitration following oxidative stress can induce motor neuron death. These findings may have broad implications in neurodegenerative disorders, including amyotrophic lateral sclerosis, in which activation of P2X7 receptor may be involved in both autonomous and non-autonomous motor neurons death. Impact statement Here we show that a motor neuron specific pool of Hsp90 that is highly sensitive to geldanamycin inhibition represses ligand-independent activation of P2X7 receptor and is critical to motor neuron survival. Activation of P2X7 receptor by Hsp90 inhibition triggers motor neuron apoptosis through the activation of PTEN, which in turn inhibits the PI3 kinase/Akt survival pathway. Thus, inhibition of Hsp90 for therapeutic applications may have the unexpected negative consequence of decreasing the activity of trophic pathways in motor neurons. The inhibition of Hsp90 as a therapeutic approach may require the identification of the Hsp90 complexes involved in pathogenic processes and the development of inhibitors selective for these complexes.
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Course, Meredith M., and Xinnan Wang. "Transporting mitochondria in neurons." F1000Research 5 (July 18, 2016): 1735. http://dx.doi.org/10.12688/f1000research.7864.1.

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Neurons demand vast and vacillating supplies of energy. As the key contributors of this energy, as well as primary pools of calcium and signaling molecules, mitochondria must be where the neuron needs them, when the neuron needs them. The unique architecture and length of neurons, however, make them a complex system for mitochondria to navigate. To add to this difficulty, mitochondria are synthesized mainly in the soma, but must be transported as far as the distant terminals of the neuron. Similarly, damaged mitochondria—which can cause oxidative stress to the neuron—must fuse with healthy mitochondria to repair the damage, return all the way back to the soma for disposal, or be eliminated at the terminals. Increasing evidence suggests that the improper distribution of mitochondria in neurons can lead to neurodegenerative and neuropsychiatric disorders. Here, we will discuss the machinery and regulatory systems used to properly distribute mitochondria in neurons, and how this knowledge has been leveraged to better understand neurological dysfunction.
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16

Reed, Jamie L., Pierre Pouget, Hui-Xin Qi, Zhiyi Zhou, Melanie R. Bernard, Mark J. Burish, and Jon H. Kaas. "Effects of spatiotemporal stimulus properties on spike timing correlations in owl monkey primary somatosensory cortex." Journal of Neurophysiology 108, no. 12 (December 15, 2012): 3353–69. http://dx.doi.org/10.1152/jn.00414.2011.

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The correlated discharges of cortical neurons in primary somatosensory cortex are a potential source of information about somatosensory stimuli. One aspect of neuronal correlations that has not been well studied is how the spatiotemporal properties of tactile stimuli affect the presence and magnitude of correlations. We presented single- and dual-point stimuli with varying spatiotemporal relationships to the hands of three anesthetized owl monkeys and recorded neuronal activity from 100-electrode arrays implanted in primary somatosensory cortex. Correlation magnitudes derived from joint peristimulus time histogram (JPSTH) analysis of single neuron pairs were used to determine the level of spike timing correlations under selected spatiotemporal stimulus conditions. Correlated activities between neuron pairs were commonly observed, and the proportions of correlated pairs tended to decrease with distance between the recorded neurons. Distance between stimulus sites also affected correlations. When stimuli were presented simultaneously at two sites, ∼37% of the recorded neuron pairs showed significant correlations when adjacent phalanges were stimulated, and ∼21% of the pairs were significantly correlated when nonadjacent digits were stimulated. Spatial proximity of paired stimuli also increased the average correlation magnitude. Stimulus onset asynchronies in the paired stimuli had small effects on the correlation magnitude. These results show that correlated discharges between neurons at the first level of cortical processing provide information about the relative locations of two stimuli on the hand.
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Penniyaynen, V. A., S. A. Podzorova, S. G. Terekhin, B. V. Krylov, and V. B. Plakhova. "THE GABA-ERGIC SYSTEM DOES NOT CONTROL THE NOCICEPTIVE RESPONSES OF PRIMARY SENSORY NEURON." Medical academic journal 19, no. 1S (December 15, 2019): 44–45. http://dx.doi.org/10.17816/maj191s144-45.

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The aim of the study was to elucidate the molecular mechanisms of the interconnection of the GABA-ergic and nociceptive systems at the level of the peripheral division of the CNS. The data obtained indicate that GABA does not affect the activation gating device of the NaV1.8 channel of the primary sensory neuron responsible for coding pain signals.This agent in a wide range of concentrations also does not affect the growth of neurites of sensory neurons of embryonic nervous tissue. These results confirm our assumption, expressed earlier that the asynaptic membrane of the primary nociceptive neuron is not under the control of the GABA-ergic system.
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Alles, Sascha R. A., Filipe Nascimento, Rafael Luján, Ana P. Luiz, Queensta Millet, M. Ali Bangash, Sonia Santana-Varela, et al. "Sensory neuron–derived NaV1.7 contributes to dorsal horn neuron excitability." Science Advances 6, no. 8 (February 2020): eaax4568. http://dx.doi.org/10.1126/sciadv.aax4568.

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Expression of the voltage-gated sodium channel NaV1.7 in sensory neurons is required for pain sensation. We examined the role of NaV1.7 in the dorsal horn of the spinal cord using an epitope-tagged NaV1.7 knock-in mouse. Immuno–electron microscopy showed the presence of NaV1.7 in dendrites of superficial dorsal horn neurons, despite the absence of mRNA. Rhizotomy of L5 afferent nerves lowered the levels of NaV1.7 in the dorsal horn. Peripheral nervous system–specific NaV1.7 null mutant mice showed central deficits, with lamina II dorsal horn tonic firing neurons more than halved and single spiking neurons more than doubled. NaV1.7 blocker PF05089771 diminished excitability in dorsal horn neurons but had no effect on NaV1.7 null mutant mice. These data demonstrate an unsuspected functional role of primary afferent neuron-generated NaV1.7 in dorsal horn neurons and an expression pattern that would not be predicted by transcriptomic analysis.
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Bajramovic, Jeffrey J., Sylvia Münter, Sylvie Syan, Ulf Nehrbass, Michel Brahic, and Daniel Gonzalez-Dunia. "Borna Disease Virus Glycoprotein Is Required for Viral Dissemination in Neurons." Journal of Virology 77, no. 22 (November 15, 2003): 12222–31. http://dx.doi.org/10.1128/jvi.77.22.12222-12231.2003.

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ABSTRACT Borna disease virus (BDV) is a nonsegmented negative-strand RNA virus with a tropism for neurons. Infection with BDV causes neurological diseases in a wide variety of animal species. Although it is known that the virus spreads from neuron to neuron, assembled viral particles have never been visualized in the brains of infected animals. This has led to the hypothesis that BDV spreads as nonenveloped ribonucleoproteins (RNP) rather than as enveloped viral particles. We assessed whether the viral envelope glycoprotein (GP) is required for neuronal dissemination of BDV by using primary cultures of rat hippocampal neurons. We show that upon in vitro infection, BDV replicated and spread efficiently in this system. Despite rapid virus dissemination, very few infectious viral particles were detectable in the culture. However, neutralizing antibodies directed against BDV-GP inhibited BDV spread. In addition, interference with BDV-GP processing by inhibiting furin-mediated cleavage of the glycoprotein blocked virus spread. Finally, antisense treatment with peptide nucleic acids directed against BDV-GP mRNA inhibited BDV dissemination, marking BDV-GP as an attractive target for antiviral therapy against BDV. Together, our results demonstrate that the expression and correct processing of BDV-GP are necessary for BDV dissemination in primary cultures of rat hippocampal neurons, arguing against the hypothesis that the virus spreads from neuron to neuron in the form of nonenveloped RNP.
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Sutter, M. L., and C. E. Schreiner. "Topography of intensity tuning in cat primary auditory cortex: single-neuron versus multiple-neuron recordings." Journal of Neurophysiology 73, no. 1 (January 1, 1995): 190–204. http://dx.doi.org/10.1152/jn.1995.73.1.190.

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1. We studied the spatial distributions of amplitude tuning (monotonicity of rate-level functions) and response threshold of single neurons along the dorsoventral extent of cat primary auditory cortex (AI). To pool data across animals, we used the multiple-unit map of monotonicity as a frame of reference. Amplitude selectivity of multiple units is known to vary systematically along isofrequency contours, which run roughly in the dorsoventral direction. Clusters sharply tuned for intensity (i.e., "nonmonotonic" clusters) are located near the center of the contour. A second nonmonotonic region can be found several millimeters dorsal to the center. We used the locations of these two nonmonotonic regions as reference points to normalize data across animals. Additionally, to compare this study to sharpness of frequency tuning results, we also used multiple-unit bandwidth (BW) maps as references to pool data. 2. The multiple-unit amplitude-related topographies recorded in previous studies were confirmed. Pooled multiple-unit maps closely approximated the previously reported individual case maps when the multiple-unit monotonicity or the map of bandwidth (in octaves) of pure tones to which a cell responds 40 dB above minimum threshold were used as the pooling reference. When the map of bandwidth (in octaves) of pure tones to which a cell responds 10 dB above minimum threshold map was used as part of the measure, the pooled spatial pattern of multiple-unit activity was degraded. 3. Single neurons exhibited nonmonotonic rate-level functions more frequently than multiple units. Although common in single-neuron recordings (28%), strongly nonmonotonic recordings (firing rates reduced by > 50% at high intensities) were uncommon (8%) in multiple-unit recordings. Intermediately nonmonotonic neurons (firing rates reduced between 20% and 50% at high intensities) occurred with nearly equal probability in single-neuron (28%) and multiple-unit (26%) recordings. The remaining recordings for multiple units (66%) and single units (44%) were monotonic (firing rates within 20% of the maximum at the highest tested intensity). 4. In ventral AI (AIv), the topography of monotonicity for single units was qualitatively similar to multiple units, although single units were on average more intensity selective. In dorsal AI (AId) we consistently found a spatial gradient for sharpness of intensity tuning for multiple units; however, for pooled single units in Aid there was no clear topographic gradient. 5. Response (intensity) thresholds of single neurons were not uniformly distributed across the dorsoventral extent of AI.(ABSTRACT TRUNCATED AT 400 WORDS)
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Panchin, Y. V., Y. I. Arshavsky, A. Selverston, and T. A. Cleland. "Lobster stomatogastric neurons in primary culture. I. Basic characteristics." Journal of Neurophysiology 69, no. 6 (June 1, 1993): 1976–92. http://dx.doi.org/10.1152/jn.1993.69.6.1976.

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1. A method for the isolation of stomatogastric neurons with neuropilar processes and an axon < or = 2 mm long is described. Isolated neurons adhered to an uncoated plastic surface and demonstrated neurite outgrowth for > or = 7-10 days in a simple medium (salt-adjusted Leibovitz-15). Neurite outgrowth started immediately after plating and was maximal during the first 2-3 days. The electrical activity of neurons and their responses to bath application of pilocarpine were studied between 2 and 10 days after plating. 2. Identified neurons [pyloric dilator (PD), pyloric (PY), and lateral pyloric (LP) neurons from the pyloric pattern generator as well as gastric mill (GM) and lateral posterior gastric (LPG) neurons from the gastric mill pattern generator], isolated with neuropilar processes and axons, behaved in general like corresponding neurons in the isolated stomatogastric ganglion (STG). PD neurons were tonically active or silent in culture; pilocarpine caused them to begin rhythmic activity, which at particular levels of imposed polarization was similar to the pyloric rhythm in vitro. PY and LP neurons were silent. Pilocarpine produced some rhythmicity in the PY neuron, whereas in LP neurons it decreased the firing threshold to depolarizing current and accentuated postinhibitory rebound. LPG neurons were tonically active. Pilocarpine depolarized the LPG neurons and accelerated their tonic activity; neuron hyperpolarization by current injection led to bursting pacemaker activity that was similar to the gastric rhythm in vitro. GM neurons were silent; pilocarpine did not cause them to generate rhythmic activity but did lower their thresholds to depolarizing current. Simultaneous recordings from the soma and axon under direct visual control demonstrated that the intrasomatic spikes (15-20 mV in amplitude) were attenuated action potentials generated in the axon. 3. Neurons isolated with short primary neurites, including those without any noticeable primary neurite (in contrast to neurons isolated with longer neuropilar processes and axons), never generated any kind of electrical activity immediately after extraction from the STG. After 2 days in culture, these "short-neurite" neurons became capable of generating different types of electrical activity (e.g., fast spikes with amplitudes of < or = 40-45 mV, plateau potentials, bursting potentials, etc.). The capability of isolated somata to generate electrical activity did not depend on whether or not the cell had adhered to the substrate and demonstrated neurite outgrowth.(ABSTRACT TRUNCATED AT 400 WORDS)
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22

Shen, Huaishuang, Minfeng Gan, Huilin Yang, and Jun Zou. "An integrated cell isolation and purification method for rat dorsal root ganglion neurons." Journal of International Medical Research 47, no. 7 (June 19, 2019): 3253–60. http://dx.doi.org/10.1177/0300060519855585.

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Objective Neurobiology studies are increasingly focused on the dorsal root ganglion (DRG), which plays an important role in neuropathic pain. Existing DRG neuron primary culture methods have considerable limitations, including challenging cell isolation and poor cell yield, which cause difficulty in signaling pathway studies. The present study aimed to establish an integrated primary culture method for DRG neurons. Methods DRGs were obtained from fetal rats by microdissection, and then dissociated with trypsin. The dissociated neurons were treated with 5-fluorouracil to promote growth of neurons from the isolated cells. Then, reverse transcription polymerase chain reaction and immunofluorescence assays were used to identify and purify DRG neurons. Results Isolated DRGs were successfully dissociated and showed robust growth as individual DRG neurons in neurobasal medium. Both mRNA and protein assays confirmed that DRG neurons expressed neurofilament-200 and neuron-specific enolase. Conclusions Highly purified, stable DRG neurons could be easily harvested and grown for extended periods by using this integrated cell isolation and purification method, which may help to elucidate the mechanisms underlying neuropathic pain.
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De Lorenzi, Davide, Marco Bernardini, and Marti Pumarola. "Primary hyperoxaluria (l-glyceric aciduria) in a cat." Journal of Feline Medicine and Surgery 7, no. 6 (December 2005): 357–61. http://dx.doi.org/10.1016/j.jfms.2005.03.007.

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A 7-month-old, male European cat was examined because of weakness and inappetence. The cat was dehydrated, polypnoeic and severely weak. Severe, generalised muscle atrophy was present. Spinal reflexes were all decreased to absent. Blood analysis and urinalysis showed several abnormalities, including intermittent hyperoxaluria. The l-gliceric acid concentration was remarkably increased. Electrodiagnostic tests of the peripheral nervous system were abnormal. At necropsy, generalised muscle atrophy was observed. Microscopically, both kidneys showed intraluminal birefringent oxalate crystals. Motor neuron degeneration and accumulation of neurofilaments were observed in the axons of the spinal motor neurons.
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Turner, Martin R., Richard J. Barohn, Philippe Corcia, John K. Fink, Matthew B. Harms, Matthew C. Kiernan, John Ravits, et al. "Primary lateral sclerosis: consensus diagnostic criteria." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 4 (February 6, 2020): 373–77. http://dx.doi.org/10.1136/jnnp-2019-322541.

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Primary lateral sclerosis (PLS) is a neurodegenerative disorder of the adult motor system. Characterised by a slowly progressive upper motor neuron syndrome, the diagnosis is clinical, after exclusion of structural, neurodegenerative and metabolic mimics. Differentiation of PLS from upper motor neuron-predominant forms of amyotrophic lateral sclerosis remains a significant challenge in the early symptomatic phase of both disorders, with ongoing debate as to whether they form a clinical and histopathological continuum. Current diagnostic criteria for PLS may be a barrier to therapeutic development, requiring long delays between symptom onset and formal diagnosis. While new technologies sensitive to both upper and lower motor neuron involvement may ultimately resolve controversies in the diagnosis of PLS, we present updated consensus diagnostic criteria with the aim of reducing diagnostic delay, optimising therapeutic trial design and catalysing the development of disease-modifying therapy.
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Reich, Daniel S., Ferenc Mechler, and Jonathan D. Victor. "Formal and Attribute-Specific Information in Primary Visual Cortex." Journal of Neurophysiology 85, no. 1 (January 1, 2001): 305–18. http://dx.doi.org/10.1152/jn.2001.85.1.305.

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We estimate the rates at which neurons in the primary visual cortex (V1) of anesthetized macaque monkeys transmit stimulus-related information in response to three types of visual stimulus. The stimuli—randomly modulated checkerboard patterns, stationary sinusoidal gratings, and drifting sinusoidal gratings—have very different spatiotemporal structures. We obtain the overall rate of information transmission, which we call formal information, by a direct method. We find the highest information rates in the responses of simple cells to drifting gratings (median: 10.3 bits/s, 0.92 bits/spike); responses to randomly modulated stimuli and stationary gratings transmit information at significantly lower rates. In general, simple cells transmit information at higher rates, and over a larger range, than do complex cells. Thus in the responses of V1 neurons, stimuli that are rapidly modulated do not necessarily evoke higher information rates, as might be the case with motion-sensitive neurons in area MT. By an extension of the direct method, we parse the formal information into attribute-specific components, which provide estimates of the information transmitted about contrast and spatiotemporal pattern. We find that contrast-specific information rates vary across neurons—about 0.3 to 2.1 bits/s or 0.05 to 0.22 bits/spike—but depend little on stimulus type. Spatiotemporal pattern-specific information rates, however, depend strongly on the type of stimulus and neuron (simple or complex). The remaining information rate, typically between 10 and 32% of the formal information rate for each neuron, cannot be unambiguously assigned to either contrast or spatiotemporal pattern. This indicates that some information concerning these two stimulus attributes is confounded in the responses of single neurons in V1. A model that considers a simple cell to consist of a linear spatiotemporal filter followed by a static rectifier predicts higher information rates than are found in real neurons and completely fails to replicate the performance of real cells in generating the confounded information.
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Wang, Wei, Jiqing Han, Tieran Zheng, Guibin Zheng, and Xingyu Zhou. "Speaker Verification via Modeling Kurtosis Using Sparse Coding." International Journal of Pattern Recognition and Artificial Intelligence 30, no. 03 (February 22, 2016): 1659008. http://dx.doi.org/10.1142/s0218001416590084.

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This paper proposes a new model for speaker verification by employing kurtosis statistical method based on sparse coding of human auditory system. Since only a small number of neurons in primary auditory cortex are activated in encoding acoustic stimuli and sparse independent events are used to represent the characteristics of the neurons. Each individual dictionary is learned from individual speaker samples where dictionary atoms correspond to the cortex neurons. The neuron responses possess statistical properties of acoustic signals in auditory cortex so that the activation distribution of individual speaker’s neurons is approximated as the characteristics of the speaker. Kurtosis is an efficient approach to measure the sparsity of the neuron from its activation distribution, and the vector composed of the kurtosis of every neuron is obtained as the model to characterize the speaker’s voice. The experimental results demonstrate that the kurtosis model outperforms the baseline systems and an effective identity validation function is achieved desirably.
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Ch'ng, T. H., P. G. Spear, F. Struyf, and L. W. Enquist. "Glycoprotein D-Independent Spread of Pseudorabies Virus Infection in Cultured Peripheral Nervous System Neurons in a Compartmented System." Journal of Virology 81, no. 19 (July 25, 2007): 10742–57. http://dx.doi.org/10.1128/jvi.00981-07.

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ABSTRACT The molecular mechanisms underlying the directional neuron-to-epithelial cell transport of herpesvirus particles during infection are poorly understood. To study the role of the viral glycoprotein D (gD) in the directional spread of herpes simplex virus (HSV) and pseudorabies virus (PRV) infection, a culture system consisting of sympathetic neurons or epithelial cells in different compartments was employed. We discovered that PRV infection could spread efficiently from neurons to cells and back to neurons in the absence of gD, the viral ligand required for entry of extracellular particles. Unexpectedly, PRV infection can also spread transneuronally via axo-axonal contacts. We show that this form of interaxonal spread between neurons is gD independent and is not mediated by extracellular virions. We also found that unlike PRV gD, HSV-1 gD is required for neuron-to-cell spread of infection. Neither of the host cell gD receptors (HVEM and nectin-1) is required in target primary fibroblasts for neuron-to-cell spread of HSV-1 or PRV infection.
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Yoshioka, Takashi, Jonathan B. Levitt, and Jennifer S. Lund. "Independence and merger of thalamocortical channels within macaque monkey primary visual cortex: Anatomy of interlaminar projections." Visual Neuroscience 11, no. 3 (May 1994): 467–89. http://dx.doi.org/10.1017/s0952523800002406.

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AbstractAn important issue in understanding the function of primary visual cortex in the macaque monkey is how the several efferent neuron groups projecting to extrastriate cortex acquire their different response properties. To assist our understanding of this issue, we have compared the anatomical distribution of VI intrinsic relays that carry information derived from magno- (M) and parvocellular (P) divisions of the dorsal lateral geniculate nucleus between thalamic recipient neurons and interareal efferent neuron groups within area VI. We used small, iontophoretic injections of biocytin placed in individual cortical laminae of area VI to trace orthograde and retrograde inter- and intralaminar projections. In either the same or adjacent sections, the tissue was reacted for cytochrome oxidase (CO), which provides important landmarks for different efferent neuron populations located in CO rich blobs and CO poor interblobs in laminae ⅔, as well as defining clear boundaries for the populations of efferent neurons in laminae 4A and 4B. This study shows that the interblobs, but not the blobs, receive direct input from thalamic recipient 4C neurons; the interblobs receive relays from mid 4C neurons (believed to receive convergent M and P inputs), while blobs receive indirect inputs from either M or P (or both) pathways through layers 4B (which receives M relays from layer 4Cα) and 4A (which receives P relays directly from the thalamus as well as from layer 4Cβ). The property of orientation selectivity, most prominent in the interblob regions and in layer 4B, may have a common origin from oriented lateral projections made by mid 4C spiny stellate neurons. While layer 4B efferents may emphasize M characteristics and layer 4A efferents emphasize P characteristics, the dendrites of their constituent pyramidal neurons may provide anatomical access to the other channel since both blob and interblob regions in layers ⅔ have anatomical access to M and P driven relays, despite functional differences in the way these properties may be expressed in the two compartments.
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Reyes, Laura D., Cheryl D. Stimpson, Kanika Gupta, Mary Ann Raghanti, Patrick R. Hof, Roger L. Reep, and Chet C. Sherwood. "Neuron Types in the Presumptive Primary Somatosensory Cortex of the Florida Manatee (Trichechus manatus latirostris)." Brain, Behavior and Evolution 86, no. 3-4 (2015): 210–31. http://dx.doi.org/10.1159/000441964.

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Within afrotherians, sirenians are unusual due to their aquatic lifestyle, large body size and relatively large lissencephalic brain. However, little is known about the neuron type distributions of the cerebral cortex in sirenians within the context of other afrotherians and aquatic mammals. The present study investigated two cortical regions, dorsolateral cortex area 1 (DL1) and cluster cortex area 2 (CL2), in the presumptive primary somatosensory cortex (S1) in Florida manatees (Trichechus manatus latirostris) to characterize cyto- and chemoarchitecture. The mean neuron density for both cortical regions was 35,617 neurons/mm3 and fell within the 95% prediction intervals relative to brain mass based on a reference group of afrotherians and xenarthrans. Densities of inhibitory interneuron subtypes labeled against calcium-binding proteins and neuropeptide Y were relatively low compared to afrotherians and xenarthrans and also formed a small percentage of the overall population of inhibitory interneurons as revealed by GAD67 immunoreactivity. Nonphosphorylated neurofilament protein-immunoreactive (NPNFP-ir) neurons comprised a mean of 60% of neurons in layer V across DL1 and CL2. DL1 contained a higher percentage of NPNFP-ir neurons than CL2, although CL2 had a higher variety of morphological types. The mean percentage of NPNFP-ir neurons in the two regions of the presumptive S1 were low compared to other afrotherians and xenarthrans but were within the 95% prediction intervals relative to brain mass, and their morphologies were comparable to those found in other afrotherians and xenarthrans. Although this specific pattern of neuron types and densities sets the manatee apart from other afrotherians and xenarthrans, the manatee isocortex does not appear to be explicitly adapted for an aquatic habitat. Many of the features that are shared between manatees and cetaceans are also shared with a diverse array of terrestrial mammals and likely represent highly conserved neural features. A comparative study across manatees and dugongs is necessary to determine whether these traits are specific to one or more of the manatee species, or can be generalized to all sirenians.
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30

Faust, Anne, Apoorva Kandakatla, Yolandi van der Merwe, Tanchen Ren, Luai Huleihel, George Hussey, Juan Diego Naranjo, Scott Johnson, Stephen Badylak, and Michael Steketee. "Urinary bladder extracellular matrix hydrogels and matrix-bound vesicles differentially regulate central nervous system neuron viability and axon growth and branching." Journal of Biomaterials Applications 31, no. 9 (March 9, 2017): 1277–95. http://dx.doi.org/10.1177/0885328217698062.

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Central nervous system neurons often degenerate after trauma due to the inflammatory innate immune response to injury, which can lead to neuronal cell death, scarring, and permanently lost neurologic function. Extracellular matrix bioscaffolds, derived by decellularizing healthy tissues, have been widely used in both preclinical and clinical studies to promote positive tissue remodeling, including neurogenesis, in numerous tissues, with extracellular matrix from homologous tissues often inducing more positive responses. Extracellular matrix hydrogels are liquid at room temperature and enable minimally invasive extracellular matrix injections into central nervous system tissues, before gelation at 37℃. However, few studies have analyzed how extracellular matrix hydrogels influence primary central nervous system neuron survival and growth, and whether central nervous system and non-central nervous system extracellular matrix specificity is critical to neuronal responses. Urinary bladder extracellular matrix hydrogels increase both primary hippocampal neuron survival and neurite growth to similar or even greater extents, suggesting extracellular matrix from non-homologous tissue sources, such as urinary bladder matrix-extracellular matrix, may be a more economical and safer alternative to developing central nervous system extracellular matrices for central nervous system applications. Additionally, we show matrix-bound vesicles derived from urinary bladder extracellular matrix are endocytosed by hippocampal neurons and positively regulate primary hippocampal neuron neurite growth. Matrix-bound vesicles carry protein and RNA cargos, including noncoding RNAs and miRNAs that map to the human genome and are known to regulate cellular processes. Thus, urinary bladder matrix-bound vesicles provide natural and transfectable cargoes which offer new experimental tools and therapeutic applications to study and treat central nervous system neuron injury.
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31

Holmstrom, Lars, Patrick D. Roberts, and Christine V. Portfors. "Responses to Social Vocalizations in the Inferior Colliculus of the Mustached Bat Are Influenced by Secondary Tuning Curves." Journal of Neurophysiology 98, no. 6 (December 2007): 3461–72. http://dx.doi.org/10.1152/jn.00638.2007.

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Neurons in the inferior colliculus (IC) of the mustached bat integrate input from multiple frequency bands in a complex fashion. These neurons are important for encoding the bat's echolocation and social vocalizations. The purpose of this study was to quantify the contribution of complex frequency interactions on the responses of IC neurons to social vocalizations. Neural responses to single tones, two-tone pairs, and social vocalizations were recorded in the IC of the mustached bat. Three types of data driven stimulus-response models were designed for each neuron from single tone and tone pair stimuli to predict the responses of individual neurons to social vocalizations. The first model was generated only using the neuron's primary frequency tuning curve, whereas the second model incorporated the entire hearing range of the animal. The extended model often predicted responses to many social vocalizations more accurately for multiply tuned neurons. One class of multiply tuned neuron that likely encodes echolocation information also responded to many of the social vocalizations, suggesting that some neurons in the mustached bat IC have dual functions. The third model included two-tone frequency tunings of the neurons. The responses to vocalizations were better predicted by the two-tone models when the neuron had inhibitory frequency tuning curves that were not near the neuron's primary tuning curve. Our results suggest that complex frequency interactions in the IC determine neural responses to social vocalizations and some neurons in IC have dual functions that encode both echolocation and social vocalization signals.
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32

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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33

MIFTAHOF, ROUSTEM, and N. R. AKHMADEEV. "COMPUTER SIMULATION OF COTRANSMISSION BY EXCITATORY AMINO ACIDS AND ACETYLCHOLINE IN THE ENTERIC NERVOUS SYSTEM." Journal of Mechanics in Medicine and Biology 07, no. 02 (June 2007): 229–46. http://dx.doi.org/10.1142/s0219519407002261.

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The role of cotransmission by α-amino-3-hydroxy-5-methyl-4-isoxalose propionic acid (AMPA), L-aspartate, N-methyl-D-aspartate (NMDA), and acetylcholine (ACh) as well as the coexpression of AMPA, NMDA, and nicotinic ACh (nACh) receptors on the electrophysiological activity of the primary sensory (AH) and motor (S) neurons of the enteric nervous system are numerically assessed. Results of computer simulations showed that AMPA and L-Asp alone can induce fast action potentials of short duration on AH and S neurons. Costimulation of nACh and AMPA receptors on the soma of the S neuron resulted in periodic spiking activity. A characteristic biphasic response was recorded from the AH neuron after coactivation of AMPA and NMDA receptors. Glutamate alone acting on NMDA receptors caused prolonged depolarization of the AH neuron and failed to depolarize the S neuron. Cojoint stimulation of the AMPA or nACh receptors was required to produce the effect of glutamate. The overall electrical response of neurons to the activation of NMDA receptors was long-term depolarization. Acetylcholine, AMPA, and glutamate acting alone or cojointly enhanced phasic contraction of the longitudinal smooth muscle. Treatment of neurons with AMPA, NMDA, and nACh receptor antagonists revealed intricate properties of the AH and S neurons. Application of MK-801, D-AP5, and CPP reduced the excitability of the AH neuron and totally abolished electrical activity in the S neuron. The information gained into the cotransmission by excitatory amino acids and acetylcholine in the enteric nervous system may be beneficial in the development of novel effective therapeutics to treat diseases associated with altered visceral nociception, i.e. irritable bowel syndrome.
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Sabourin, Patrick, and Gerald S. Pollack. "Behaviorally Relevant Burst Coding in Primary Sensory Neurons." Journal of Neurophysiology 102, no. 2 (August 2009): 1086–91. http://dx.doi.org/10.1152/jn.00370.2009.

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Bursts of action potentials in sensory interneurons are believed to signal the occurrence of particularly salient stimulus features. Previous work showed that bursts in an identified, ultrasound-tuned interneuron (AN2) of the cricket Teleogryllus oceanicus code for conspicuous increases in amplitude of an ultrasound stimulus, resulting in behavioral responses that are interpreted as avoidance of echolocating bats. We show that the primary sensory neurons that inform AN2 about high-frequency acoustic stimuli also produce bursts. As is the case for AN2, bursts in sensory neurons perform better as feature detectors than isolated, nonburst, spikes. Bursting is temporally correlated between sensory neurons, suggesting that on occurrence of a salient stimulus feature, AN2 will receive strong synaptic input in the form of coincident bursts, from several sensory neurons, and that this might result in bursting in AN2. Our results show that an important feature of the temporal structure of interneuron spike trains can be established at the earliest possible level of sensory processing, i.e., that of the primary sensory neuron.
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Zhang, Mengliang, and Kevin D. Alloway. "Stimulus-Induced Intercolumnar Synchronization of Neuronal Activity in Rat Barrel Cortex: A Laminar Analysis." Journal of Neurophysiology 92, no. 3 (September 2004): 1464–78. http://dx.doi.org/10.1152/jn.01272.2003.

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We used cross-correlation analysis to characterize the coordination of stimulus-induced neuronal activity in the primary somatosensory barrel cortex of isoflurane-anesthetized rats. On each trial, multiple whiskers were simultaneously deflected at frequencies that corresponded to 2, 5, 8, or 11 Hz. Among 476 neuron pairs that we examined, 342 (71.8%) displayed significant peaks of synchronized activity that exceeded the 99.9% confidence limits. The incidence and strength of these functional associations varied across different cortical layers. Only 52.9% of neuron pairs in layer IV displayed synchronized responses, whereas 84.1% of the infragranular neuron pairs were synchronized during whisker stimulation. Neuronal synchronization was strongest in the infragranular layers, weakest in layer IV, and varied according to the columnar configuration of the neuron pairs. Thus correlation coefficients were largest for neuron pairs in the same whisker barrel row but were smallest for neurons in different rows and arcs. Spontaneous activity in the infragranular layers was also synchronized to a greater degree than in the other layers. Although infragranular neuron pairs displayed similar amounts of synchronization in response to each stimulus frequency, granular and supragranular neurons were synchronized mainly during stimulation at 2 or 5 Hz. These results are consistent with previous studies indicating that infragranular neurons have intrinsic properties that facilitate synchronized activity, and they suggest that neuronal synchronization plays an important role in transmitting sensory information to other cortical or subcortical brain regions.
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Pero, Maria Elena, Laura Cortese, Vincenzo Mastellone, Raffaella Tudisco, Nadia Musco, Anna Scandurra, Biagio D’Aniello, Giuseppe Vassalotti, Francesca Bartolini, and Pietro Lombardi. "Effects of a Nutritional Supplement on Cognitive Function in Aged Dogs and on Synaptic Function of Primary Cultured Neurons." Animals 9, no. 7 (June 27, 2019): 393. http://dx.doi.org/10.3390/ani9070393.

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The objective of this research was to investigate the efficacy of DìSeniorTM, a nutraceutical formulated to improve cognitive functions in elderly dogs. To this purpose, some clinical and metabolic investigations and a spatial navigation test were performed in treated and untreated dogs. Moreover, the nutraceutical was also tested on primary hippocampal neuron cultures. Results showed no adverse effects on the dogs’ health and a positive effect on learning. In vitro effects on neuron cultures showed an increase in the level of cFOS in treated neurons compared with the vehicle, suggesting that DiSeniorTM has also a positive effect on neuronal functions. Overall, this study suggests that DiSeniorTM can exert a beneficial effect on aged dogs by preventing the negative effects of aging on cognition. Further studies are needed to assess the mechanisms by which it acts on neurons and the specific effect of the different components alone or combined.
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Schieber, Marc H., and Gil Rivlis. "Partial Reconstruction of Muscle Activity From a Pruned Network of Diverse Motor Cortex Neurons." Journal of Neurophysiology 97, no. 1 (January 2007): 70–82. http://dx.doi.org/10.1152/jn.00544.2006.

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Primary motor cortex (M1) neurons traditionally have been viewed as “upper motor neurons” that directly drive spinal motoneuron pools, particularly during finger movements. We used spike-triggered averages (SpikeTAs) of electromyographic (EMG) activity to select M1 neurons whose spikes signaled the arrival of input in motoneuron pools, and examined the degree of similarity between the activity patterns of these M1 neurons and their target muscles during 12 individuated finger and wrist movements. Neuron–EMG similarity generally was low. Similarity was unrelated to the strength of the SpikeTA effect, to whether the effect was pure versus synchrony, or to the number of muscles influenced by the neuron. Nevertheless, the sum of M1 neuron activity patterns, each weighted by the sign and strength of its SpikeTA effect, could be more similar to the EMG than the average similarity of individual neurons. Significant correlations between the weighted sum of M1 neuron activity patterns and EMG were obtained in six of 17 muscles, but showed R2 values ranging from only 0.26 to 0.42. These observations suggest that additional factors—including inputs from sources other than M1 and nonlinear summation of inputs to motoneuron pools—also contributed substantially to EMG activity patterns. Furthermore, although each of these M1 neurons produced SpikeTA effects with a significant peak or trough 6–16 ms after the triggering spike, shifting the weighted sum of neuron activity to lead the EMG by 40–60 ms increased their similarity, suggesting that the influence of M1 neurons that produce SpikeTA effects includes substantial synaptic integration that in part may reach the motoneuron pools over less-direct pathways.
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Yang, Guang, and Jinxin Shi. "miRNA-130a-3p targets sphingosine-1-phosphate receptor 1 to activate the microglial and astrocytes and to promote neural injury under the high glucose condition." Open Medicine 17, no. 1 (January 1, 2022): 2117–29. http://dx.doi.org/10.1515/med-2022-0565.

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Abstract As a common complication of diabetes, diabetic pain neuropathy (DPN) is caused by neuron intrinsic and extrinsic factors. Neuron intrinsic factors include neuronal apoptosis and oxidative stress, while extrinsic factors are associated with glial activation. The present study was performed to reveal the functions of miR-130a-3p in apoptosis and oxidative stress of the high glucose (HG)-stimulated primary neurons as well as in the activation of microglial and astrocytes. Primary neurons, microglial, and astrocytes were isolated from newborn mice. Apoptosis was assessed by flow cytometry analysis and western blotting. Reactive oxygen species and glutathione levels were assessed to determine the oxidative stress. Markers of glial cells were detected by immunofluorescence staining. The results revealed that miR-130a-3p deficiency alleviated apoptosis and oxidative stress of HG-stimulated neurons as well as suppressed microglial and astrocyte activation. Moreover, sphingosine-1-phosphate receptor 1 (S1PR1) was found as a target downstream of miR-130a-3p. S1PR1 knockdown partially rescued the inhibitory effects of silenced miR-130a-3p on neuronal injury and glial activation. In conclusion, miR-130a-3p targets S1PR1 to activate the microglial and astrocytes and to promote apoptosis and oxidative stress of the HG-stimulated primary neurons. These findings may provide a novel insight into DPN treatment.
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39

Di Liegro, Italia, Alessandro Cestelli, Giovanna Barbieri, and Agata Giallongo. "Developmental changes of neuron-specific enolase mRNA in primary cultures of rat neurons." Cellular and Molecular Neurobiology 11, no. 2 (April 1991): 289–94. http://dx.doi.org/10.1007/bf00769041.

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40

Head, Brian P., Yue Hu, J. Cameron Finley, Michelle D. Saldana, Jacqueline A. Bonds, Atsushi Miyanohara, Ingrid R. Niesman, et al. "Neuron-targeted Caveolin-1 Protein Enhances Signaling and Promotes Arborization of Primary Neurons." Journal of Biological Chemistry 286, no. 38 (July 28, 2011): 33310–21. http://dx.doi.org/10.1074/jbc.m111.255976.

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41

Jovanovic, Predrag, Yidan Wang, Jean-Philippe Vit, Edward Novinbakht, Nancy Morones, Elliot Hogg, Michele Tagliati, and Celine E. Riera. "Sustained chemogenetic activation of locus coeruleus norepinephrine neurons promotes dopaminergic neuron survival in synucleinopathy." PLOS ONE 17, no. 3 (March 22, 2022): e0263074. http://dx.doi.org/10.1371/journal.pone.0263074.

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Dopaminergic neuron degeneration in the midbrain plays a pivotal role in motor symptoms associated with Parkinson’s disease. However, non-motor symptoms of Parkinson’s disease and post-mortem histopathology confirm dysfunction in other brain areas, including the locus coeruleus and its associated neurotransmitter norepinephrine. Here, we investigate the role of central norepinephrine-producing neurons in Parkinson’s disease by chronically stimulating catecholaminergic neurons in the locus coeruleus using chemogenetic manipulation. We show that norepinephrine neurons send complex axonal projections to the dopaminergic neurons in the substantia nigra, confirming physical communication between these regions. Furthermore, we demonstrate that increased activity of norepinephrine neurons is protective against dopaminergic neuronal depletion in human α-syn A53T missense mutation over-expressing mice and prevents motor dysfunction in these mice. Remarkably, elevated norepinephrine neurons action fails to alleviate α-synuclein aggregation and microgliosis in the substantia nigra suggesting the presence of an alternate neuroprotective mechanism. The beneficial effects of high norepinephrine neuron activity might be attributed to the action of norepinephrine on dopaminergic neurons, as recombinant norepinephrine treatment increased primary dopaminergic neuron cultures survival and neurite sprouting. Collectively, our results suggest a neuroprotective mechanism where noradrenergic neurons activity preserves the integrity of dopaminergic neurons, which prevents synucleinopathy-dependent loss of these cells.
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42

Schreiner, C. E., and M. L. Sutter. "Topography of excitatory bandwidth in cat primary auditory cortex: single-neuron versus multiple-neuron recordings." Journal of Neurophysiology 68, no. 5 (November 1, 1992): 1487–502. http://dx.doi.org/10.1152/jn.1992.68.5.1487.

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1. The spatial distribution of the sharpness of tuning of single neurons along the dorsoventral extent of primary auditory cortex (AI) was studied. A sharpness of tuning gradient was initially obtained with multiple-unit recordings, and in combination with the cochleotopic organization, served as a frame of reference for the locations of single neurons. The frequency selectivity or "integrated excitatory bandwidth" of multiple units varied systematically along the dorsoventral extent of AI. The most sharply tuned unit clusters were found at the approximate center of the dorsoventral extent. A gradual broadening of the integrated excitatory bandwidth in both dorsal and ventral directions was consistently seen. 2. The multiple-unit measures of the bandwidth 10 (BW10) and 40 dB (BW40) above minimum threshold, pooled across several animals and expressed in octaves, were similar to those described within individual cases in cats. As in the individual animals, the bandwidth maps were V shaped with minima located at the approximate center of the dorsal-ventral extent of AI. The location of the minimum in the multiple-unit bandwidth map (i.e., the most sharply tuned area) was used as a reference point to pool single-neuron data across animals. 3. For single neurons, the dorsal half of the BW40 distribution showed a gradient paralleling that found for multiple units. For both single and multiple units, the average excitatory bandwidth increased at a rate of approximately 0.27 octaves/mm from the center of AI toward the dorsal fringe. Differing from the dorsal half of AI, the ventral half of AI showed no clear BW40 gradient for single units along its dorsoventral extent. At 40 dB above minimum threshold, most ventral neurons encountered were sharply tuned. By contrast, the multiple-unit BW40 showed a gradient similar to the dorsal half with 0.23 octaves/mm increasing from the center toward the ventral border of AI. 4. For single neurons, BW10 showed no clear systematic spatial distribution in AI. Neither the dorsal nor the ventral gradient was significantly different from zero slope, although the dorsal half showed a trend toward increasing BW10s. Contrasting single neurons, both dorsal and ventral halves of AI showed BW10 slopes for multiple units confirming a V-shaped map of the integrated excitatory bandwidth within the dorsoventral extent of AI. 5. On the basis of the distribution of the integrated (multiple-unit) excitatory bandwidth, AI was parceled into three regions: the dorsal gradient, the ventral gradient, and the central, narrowly tuned area.(ABSTRACT TRUNCATED AT 400 WORDS)
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43

WEBB, BEN S., CHRIS J. TINSLEY, NICK E. BARRACLOUGH, AMANDA PARKER, and ANDREW M. DERRINGTON. "Gain control from beyond the classical receptive field in primate primary visual cortex." Visual Neuroscience 20, no. 3 (May 2003): 221–30. http://dx.doi.org/10.1017/s0952523803203011.

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Gain control is a salient feature of information processing throughout the visual system. Heeger (1991, 1992) described a mechanism that could underpin gain control in primary visual cortex (V1). According to this model, a neuron's response is normalized by dividing its output by the sum of a population of neurons, which are selective for orientations covering a broad range. Gain control in this scheme is manifested as a change in the semisaturation constant (contrast gain) of a V1 neuron. Here we examine how flanking and annular gratings of the same or orthogonal orientation to that preferred by a neuron presented beyond the receptive field modulate gain in V1 neurons in anesthetized marmosets (Callithrix jacchus). To characterize how gain was modulated by surround stimuli, the Michaelis–Menten equation was fitted to response versus contrast functions obtained under each stimulus condition. The modulation of gain by surround stimuli was modelled best as a divisive reduction in response gain. Response gain varied with the orientation of surround stimuli, but was reduced most when the orientation of a large annular grating beyond the classical receptive field matched the preferred orientation of neurons. The strength of surround suppression did not vary significantly with retinal eccentricity or laminar distribution. In the marmoset, as in macaques (Angelucci et al., 2002a, b), gain control over the sort of distances reported here (up to 10 deg) may be mediated by feedback from extrastriate areas.
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44

Levi, Rafael, Otar Akanyeti, Aleksander Ballo, and James C. Liao. "Frequency response properties of primary afferent neurons in the posterior lateral line system of larval zebrafish." Journal of Neurophysiology 113, no. 2 (January 15, 2015): 657–68. http://dx.doi.org/10.1152/jn.00414.2014.

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The ability of fishes to detect water flow with the neuromasts of their lateral line system depends on the physiology of afferent neurons as well as the hydrodynamic environment. Using larval zebrafish ( Danio rerio), we measured the basic response properties of primary afferent neurons to mechanical deflections of individual superficial neuromasts. We used two types of stimulation protocols. First, we used sine wave stimulation to characterize the response properties of the afferent neurons. The average frequency-response curve was flat across stimulation frequencies between 0 and 100 Hz, matching the filtering properties of a displacement detector. Spike rate increased asymptotically with frequency, and phase locking was maximal between 10 and 60 Hz. Second, we used pulse train stimulation to analyze the maximum spike rate capabilities. We found that afferent neurons could generate up to 80 spikes/s and could follow a pulse train stimulation rate of up to 40 pulses/s in a reliable and precise manner. Both sine wave and pulse stimulation protocols indicate that an afferent neuron can maintain their evoked activity for longer durations at low stimulation frequencies than at high frequencies. We found one type of afferent neuron based on spontaneous activity patterns and discovered a correlation between the level of spontaneous and evoked activity. Overall, our results establish the baseline response properties of lateral line primary afferent neurons in larval zebrafish, which is a crucial step in understanding how vertebrate mechanoreceptive systems sense and subsequently process information from the environment.
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Antonsen, Brian L., and Donald H. Edwards. "Mechanisms of Serotonergic Facilitation of a Command Neuron." Journal of Neurophysiology 98, no. 6 (December 2007): 3494–504. http://dx.doi.org/10.1152/jn.00331.2007.

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The lateral giant (LG) command neuron of crayfish responds to an attack directed at the abdomen by triggering a single highly stereotyped escape tail flip. Experimentally applied serotonin (5-hydroxytrptamine, 5-HT) can increase or decrease LG's excitability, depending on the concentration, rate, and duration of 5-HT application. Here we describe three physiological mechanisms that mediate serotonergic facilitation of LG. Two processes strengthen electrical coupling between the primary mechanosensory afferent neurons and LG: first, an early increase in the conductance of electrical synapses between primary afferent neurons and LG dendrites and second, an early increase in the membrane resistance of LG dendrites. The increased coupling facilitates LG's synaptic response and it promotes recruitment of weakly excited afferent neurons to contribute to the response. Third, a delayed increase in the membrane resistance of proximal regions of LG increases the cell's input resistance near the initial segment. Together these mechanisms contribute to serotonergic facilitation of LG's response.
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Shin, Grace Ji-eun, Maria Elena Pero, Luke A. Hammond, Anita Burgos, Atul Kumar, Samantha E. Galindo, Tanguy Lucas, Francesca Bartolini, and Wesley B. Grueber. "Integrins protect sensory neurons in models of paclitaxel-induced peripheral sensory neuropathy." Proceedings of the National Academy of Sciences 118, no. 15 (April 5, 2021): e2006050118. http://dx.doi.org/10.1073/pnas.2006050118.

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Chemotherapy-induced peripheral neuropathy (CIPN) is a major side effect from cancer treatment with no known method for prevention or cure in clinics. CIPN often affects unmyelinated nociceptive sensory terminals. Despite the high prevalence, molecular and cellular mechanisms that lead to CIPN are still poorly understood. Here, we used a genetically tractableDrosophilamodel and primary sensory neurons isolated from adult mouse to examine the mechanisms underlying CIPN and identify protective pathways. We found that chronic treatment ofDrosophilalarvae with paclitaxel caused degeneration and altered the branching pattern of nociceptive neurons, and reduced thermal nociceptive responses. We further found that nociceptive neuron-specific overexpression of integrins, which are known to support neuronal maintenance in several systems, conferred protection from paclitaxel-induced cellular and behavioral phenotypes. Live imaging and superresolution approaches provide evidence that paclitaxel treatment causes cellular changes that are consistent with alterations in endosome-mediated trafficking of integrins. Paclitaxel-induced changes in recycling endosomes precede morphological degeneration of nociceptive neuron arbors, which could be prevented by integrin overexpression. We used primary dorsal root ganglia (DRG) neuron cultures to test conservation of integrin-mediated protection. We show that transduction of a human integrin β-subunit 1 also prevented degeneration following paclitaxel treatment. Furthermore, endogenous levels of surface integrins were decreased in paclitaxel-treated mouse DRG neurons, suggesting that paclitaxel disrupts recycling in vertebrate sensory neurons. Altogether, our study supports conserved mechanisms of paclitaxel-induced perturbation of integrin trafficking and a therapeutic potential of restoring neuronal interactions with the extracellular environment to antagonize paclitaxel-induced toxicity in sensory neurons.
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Hu, Xiaolin, and Zhigang Zeng. "Bridging the Functional and Wiring Properties of V1 Neurons Through Sparse Coding." Neural Computation 34, no. 1 (January 1, 2022): 104–37. http://dx.doi.org/10.1162/neco_a_01453.

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Abstract The functional properties of neurons in the primary visual cortex (V1) are thought to be closely related to the structural properties of this network, but the specific relationships remain unclear. Previous theoretical studies have suggested that sparse coding, an energy-efficient coding method, might underlie the orientation selectivity of V1 neurons. We thus aimed to delineate how the neurons are wired to produce this feature. We constructed a model and endowed it with a simple Hebbian learning rule to encode images of natural scenes. The excitatory neurons fired sparsely in response to images and developed strong orientation selectivity. After learning, the connectivity between excitatory neuron pairs, inhibitory neuron pairs, and excitatory-inhibitory neuron pairs depended on firing pattern and receptive field similarity between the neurons. The receptive fields (RFs) of excitatory neurons and inhibitory neurons were well predicted by the RFs of presynaptic excitatory neurons and inhibitory neurons, respectively. The excitatory neurons formed a small-world network, in which certain local connection patterns were significantly overrepresented. Bidirectionally manipulating the firing rates of inhibitory neurons caused linear transformations of the firing rates of excitatory neurons, and vice versa. These wiring properties and modulatory effects were congruent with a wide variety of data measured in V1, suggesting that the sparse coding principle might underlie both the functional and wiring properties of V1 neurons.
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Ishiguro, Shinichi, Tetsuro Shinada, Zhou Wu, Mayumi Karimazawa, Michimasa Uchidate, Eiji Nishimura, Yoko Yasuno, et al. "A novel cyclic peptide (Naturido) modulates glia–neuron interactions in vitro and reverses ageing-related deficits in senescence-accelerated mice." PLOS ONE 16, no. 1 (January 27, 2021): e0245235. http://dx.doi.org/10.1371/journal.pone.0245235.

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The use of agents that target both glia and neurons may represent a new strategy for the treatment of ageing disorders. Here, we confirmed the presence of the novel cyclic peptide Naturido that originates from a medicinal fungus (Isaria japonica) grown on domestic silkworm (Bombyx mori). We found that Naturido significantly enhanced astrocyte proliferation and activated the single copy gene encoding the neuropeptide VGF and the neuron-derived NGF gene. The addition of the peptide to the culture medium of primary hippocampal neurons increased dendrite length, dendrite number and axon length. Furthermore, the addition of the peptide to primary microglial cultures shifted CGA-activated microglia towards anti-inflammatory and neuroprotective phenotypes. These findings of in vitro glia–neuron interactions led us to evaluate the effects of oral administration of the peptide on brain function and hair ageing in senescence-accelerated mice (SAMP8). In vivo analyses revealed that spatial learning ability and hair quality were improved in Naturido-treated mice compared with untreated mice, to the same level observed in the normal ageing control (SAMR1). These data suggest that Naturido may be a promising glia–neuron modulator for the treatment of not only senescence, but also Alzheimer’s disease and other neurodegenerative diseases.
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49

Liu, Qing-shan, Ran Deng, Shuran Li, Xu Li, Keqin Li, Gulibanumu Kebaituli, Xueli Li, and Rui Liu. "Ellagic acid protects against neuron damage in ischemic stroke through regulating the ratio of Bcl-2/Bax expression." Applied Physiology, Nutrition, and Metabolism 42, no. 8 (August 2017): 855–60. http://dx.doi.org/10.1139/apnm-2016-0651.

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An oxygen-glucose deprivation and reoxygenation model in primary cultured rat cortical neurons was developed for this study to investigate the effects of ellagic acid (EA), a low-molecular-weight polyphenol, on neuron cells and their function, and to evaluate whether EA can be safely utilized by humans as a functional food or therapeutic agent. Administration of EA significantly decreased the volume of cerebrum infarction and the neurological deficit scores of the rats; EA treatment also increased the number of Bcl-2-positive cells and the ratio of Bcl-2-positive to Bax-positive neurons in the semidarkness zone near the brain ischemic focus in the photothrombotic cerebral ischemia model. Treatment of EA resulted in increased neuron viability, cell nuclear integrity, and the ratio of Bcl-2/Bax expression in the primary cultured neuron model; EA treatment also lead to a decrease in the number of apoptotic cells. Our results therefore suggest a specific mechanism for the beneficial effects of EA, providing new insights into how it provides neuroprotection. To the best of our knowledge, these results represent new insights on the mechanisms of the brain cell protective activity of EA. Thus, EA may be used in functional foods or medicines to help treat nerve dysfunction, neurodegenerative disease, and aging.
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NOVIANTARI, ARIYANI, Masagus Zainuri, Ratih Rinendyaputri, and Ni Ketut Susilarini. "Simple Method to Isolation and Culture of Neuron Progenitor Cells (NPCs) from Whole Brain Post-Natal Rat." Health Science Journal of Indonesia 9, no. 2 (December 21, 2018): 63–69. http://dx.doi.org/10.22435/hsji.v9i2.644.

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Background: Using of neuron cells for in vitro neurobiology study is needed. Neuron cell can be obtained from a primary neuron or neuronal cell lines, depend on the aim of the study because both are not equivalent. Various methods are performed to obtain primary neurons from the cortical, hippocampal and whole brain of pre or neonatal rat. The limitations of neuron cells to proliferate so that is necessary to develop a method to isolate neuron progenitor cells (NPCs). The aim of the present study was to isolate NPCs from whole brain post-natal rat. Methods: Whole brain were obtained from neonates Sprague Dawley rat. There are 2 step to get NSC; first isolation by taking the brain into the 15 ml of tube with 1 ml of 0,05% trypsin EDTA for 400g brain (incubated in the 370C, 5% CO2 for 10 minutes), tirturation with adding 1 ml culture medium and 5 ml HBSS-glucose then filtered by 70μm pore size membrane and centrifuged 2000 rpm for 10 minutes. Second: remove of supernatant with add 1 ml of HBSS-Glucose and taking it into a tube with 35% and 65% concentration of Ficoll then centrifuged at 1800 g for 10 minutes then supernatant were replated twice with poly D lysine (100µg/ml). Characterization of progenitor neuron immunotype was checked by immunohistochemistry with positive marker (NeuN and MAP2) and flow cytometry (PSANCAM+ and A2B5 -). Results: In this study, our result show that this method does not take longer than one hours and > 95% cells that obtained are expressing PSANCAM+. After 4 days culture, cells exhibit positive for neuron marker as MAP2 and NeuN. Conclusion: The method that our develope to isolate neuron progenitor cell from whole-brain are more effective and more simple with high viability and purity.
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