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Sarafi-Reinach, Trina R., Tali Melkman, Oliver Hobert, and Piali Sengupta. "The lin-11 LIM homeobox gene specifies olfactory and chemosensory neuron fates in C. elegans." Development 128, no. 17 (September 1, 2001): 3269–81. http://dx.doi.org/10.1242/dev.128.17.3269.
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Chemosensory neuron diversity in C. elegans arises from the action of transcription factors that specify different aspects of sensory neuron fate. In the AWB and AWA olfactory neurons, the LIM homeobox gene lim-4 and the nuclear hormone receptor gene odr-7 are required to confer AWB and AWA-specific characteristics respectively, and to repress an AWC olfactory neuron-like default fate. Here, we show that AWA neuron fate is also regulated by a member of the LIM homeobox gene family, lin-11. lin-11 regulates AWA olfactory neuron differentiation by initiating expression of odr-7, which then autoregulates to maintain expression. lin-11 also regulates the fate of the ASG chemosensory neurons, which are the lineal sisters of the AWA neurons. We show that lin-11 is expressed dynamically in the AWA and ASG neurons, and that misexpression of lin-11 is sufficient to promote an ASG, but not an AWA fate, in a subset of neuron types. Our results suggest that differential temporal regulation of lin-11, presumably together with its interaction with asymmetrically segregated factors, results in the generation of the distinct AWA and ASG sensory neuron types. We propose that a LIM code may be an important contributor to the generation of functional diversity in a subset of olfactory and chemosensory neurons in C. elegans.
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Van de Bittner, Genevieve C., Misha M. Riley, Luxiang Cao, Janina Ehses, Scott P. Herrick, Emily L. Ricq, Hsiao-Ying Wey, et al. "Nasal neuron PET imaging quantifies neuron generation and degeneration." Journal of Clinical Investigation 127, no. 2 (January 23, 2017): 681–94. http://dx.doi.org/10.1172/jci89162.
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Torben-Nielsen, Ben, Karl Tuyls, and Eric Postma. "EvOL-Neuron: Neuronal morphology generation." Neurocomputing 71, no. 4-6 (January 2008): 963–72. http://dx.doi.org/10.1016/j.neucom.2007.02.016.
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Ensini, M., T. N. Tsuchida, H. G. Belting, and T. M. Jessell. "The control of rostrocaudal pattern in the developing spinal cord: specification of motor neuron subtype identity is initiated by signals from paraxial mesoderm." Development 125, no. 6 (March 15, 1998): 969–82. http://dx.doi.org/10.1242/dev.125.6.969.
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The generation of distinct classes of motor neurons is an early step in the control of vertebrate motor behavior. To study the interactions that control the generation of motor neuron subclasses in the developing avian spinal cord we performed in vivo grafting studies in which either the neural tube or flanking mesoderm were displaced between thoracic and brachial levels. The positional identity of neural tube cells and motor neuron subtype identity was assessed by Hox and LIM homeodomain protein expression. Our results show that the rostrocaudal identity of neural cells is plastic at the time of neural tube closure and is sensitive to positionally restricted signals from the paraxial mesoderm. Such paraxial mesodermal signals appear to control the rostrocaudal identity of neural tube cells and the columnar subtype identity of motor neurons. These results suggest that the generation of motor neuron subtypes in the developing spinal cord involves the integration of distinct rostrocaudal and dorsoventral patterning signals that derive, respectively, from paraxial and axial mesodermal cell groups.
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McKenna, William L., Christian F. Ortiz-Londono, Thomas K. Mathew, Kendy Hoang, Sol Katzman, and Bin Chen. "Mutual regulation between Satb2 and Fezf2 promotes subcerebral projection neuron identity in the developing cerebral cortex." Proceedings of the National Academy of Sciences 112, no. 37 (August 31, 2015): 11702–7. http://dx.doi.org/10.1073/pnas.1504144112.
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Generation of distinct cortical projection neuron subtypes during development relies in part on repression of alternative neuron identities. It was reported that the special AT-rich sequence-binding protein 2 (Satb2) is required for proper development of callosal neuron identity and represses expression of genes that are essential for subcerebral axon development. Surprisingly, Satb2 has recently been shown to be necessary for subcerebral axon development. Here, we unravel a previously unidentified mechanism underlying this paradox. We show that SATB2 directly activates transcription of forebrain embryonic zinc finger 2 (Fezf2) and SRY-box 5 (Sox5), genes essential for subcerebral neuron development. We find that the mutual regulation between Satb2 and Fezf2 enables Satb2 to promote subcerebral neuron identity in layer 5 neurons, and to repress subcerebral characters in callosal neurons. Thus, Satb2 promotes the development of callosal and subcerebral neurons in a cell context-dependent manner.
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WANG, LEI, PEI-JI LIANG, PU-MING ZHANG, and YI-HONG QIU. "ADAPTATION-DEPENDENT SYNCHRONIZATION TRANSITIONS AND BURST GENERATIONS IN ELECTRICALLY COUPLED NEURAL NETWORKS." International Journal of Neural Systems 24, no. 08 (November 20, 2014): 1450033. http://dx.doi.org/10.1142/s0129065714500336.
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A typical feature of neurons is their ability to encode neural information dynamically through spike frequency adaptation (SFA). Previous studies of SFA on neuronal synchronization were mainly concentrated on the correlated firing between neuron pairs, while the synchronization of neuron populations in the presence of SFA is still unclear. In this study, the influence of SFA on the population synchronization of neurons was numerically explored in electrically coupled networks, with regular, small-world, and random connectivity, respectively. The simulation results indicate that cross-correlation indices decrease significantly when the neurons have adaptation compared with those of nonadapting neurons, similar to previous experimental observations. However, the synchronous activity of population neurons exhibits a rather complex adaptation-dependent manner. Specifically, synchronization strength of neuron populations changes nonmonotonically, depending on the degree of adaptation. In addition, single neurons in the networks can switch from regular spiking to bursting with the increase of adaptation degree. Furthermore, the connection probability among neurons exhibits significant influence on the population synchronous activity, but has little effect on the burst generation of single neurons. Accordingly, the results may suggest that synchronous activity and burst firing of population neurons are both adaptation-dependent.
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Abbott, L. F., E. Marder, and S. L. Hooper. "Oscillating Networks: Control of Burst Duration by Electrically Coupled Neurons." Neural Computation 3, no. 4 (December 1991): 487–97. http://dx.doi.org/10.1162/neco.1991.3.4.487.
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The pyloric network of the stomatogastric ganglion in crustacea is a central pattern generator that can produce the same basic rhythm over a wide frequency range. Three electrically coupled neurons, the anterior burster (AB) neuron and two pyloric dilator (PD) neurons, act as a pacemaker unit for the pyloric network. The functional characteristics of the pacemaker network are the result of electrical coupling between neurons with quite different intrinsic properties, each contributing a basic feature to the complete circuit. The AB neuron, a conditional oscillator, plays a dominant role in rhythm generation. In the work described here, we manipulate the frequency of the AB neuron both isolated and electrically coupled to the PD neurons. Physiological and modeling studies indicate that the PD neurons play an important role in regulating the duration of the bursts produced by the pacemaker unit.
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Gawthrop, Charles Stroud, Kavitha Challagulla, Annette Vu, Lynne Bianchi, Kate F. Barald, and John A. Germiller. "R440 – Generation of Neuron-Like Cells in Spiral Ganglion Cultures." Otolaryngology–Head and Neck Surgery 139, no. 2_suppl (August 2008): P191—P192. http://dx.doi.org/10.1016/j.otohns.2008.05.596.
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Problem Development of the auditory nerve is dependent on neurotrophic factors. Neurotrophins BDNF and NT-3 are critical in the later stages of development. More recently, a substance secreted by the early inner ear, otocyst-derived factor (ODF), was shown to stimulate development of primitive auditory neurons at the earliest stages. We hypothesized that this powerful neurotrophic substance might be capable of regenerating auditory neurons in the mature animal. Methods Cultured neurons and whole explants from neonatal mouse spiral ganglia were incubated with either BDNF or supernatant from an ODF-secreting cell line. Results Exposure to ODF resulted in large numbers of cells which stained with neuronal markers, and had neuronal morphology. Though they appeared somewhat different from the native spiral ganglion neurons seen in BDNF-treated cultures, they were present in vastly greater numbers, and appeared to arise from within the proliferating, migrating glial cell populations growing along with the neurons. These cells were not seen in cultures containing either control serum or BDNF. Addition of beta-bungarotoxin, a neurotoxin, to spiral ganglia just after harvest destroyed the native neurons, which did not regenerate upon addition of BDNF. However, many of the new neuron-like cells were observed after rescue with ODF, suggesting they represented a newly regenerated population of cells. Conclusion These data suggest that the components of ODF have the potential to regenerate neuronal cells, possibly from precursors or stem cells existing within the supporting cell populations of the auditory nerve. Significance The ability to regenerate auditory neurons would have exciting implications on the design and function of cochlear implants. Work continues in our lab to better define the properties of these new cells, and to isolate ODF's active component growth factors. Support Commonwealth of Pennsylvania's Tobacco Formula Fund.
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Clarkson, Jenny, Su Young Han, Richard Piet, Timothy McLennan, Grace M. Kane, Jamie Ng, Robert W. Porteous, et al. "Definition of the hypothalamic GnRH pulse generator in mice." Proceedings of the National Academy of Sciences 114, no. 47 (November 6, 2017): E10216—E10223. http://dx.doi.org/10.1073/pnas.1713897114.
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The pulsatile release of luteinizing hormone (LH) is critical for mammalian fertility. However, despite several decades of investigation, the identity of the neuronal network generating pulsatile reproductive hormone secretion remains unproven. We use here a variety of optogenetic approaches in freely behaving mice to evaluate the role of the arcuate nucleus kisspeptin (ARNKISS) neurons in LH pulse generation. Using GCaMP6 fiber photometry, we find that the ARNKISS neuron population exhibits brief (∼1 min) synchronized episodes of calcium activity occurring as frequently as every 9 min in gonadectomized mice. These ARNKISS population events were found to be near-perfectly correlated with pulsatile LH secretion. The selective optogenetic activation of ARNKISS neurons for 1 min generated pulses of LH in freely behaving mice, whereas inhibition with archaerhodopsin for 30 min suppressed LH pulsatility. Experiments aimed at resetting the activity of the ARNKISS neuron population with halorhodopsin were found to reset ongoing LH pulsatility. These observations indicate the ARNKISS neurons as the long-elusive hypothalamic pulse generator driving fertility.
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Martinez-Morales, J. R., J. A. Barbas, E. Marti, P. Bovolenta, D. Edgar, and A. Rodriguez-Tebar. "Vitronectin is expressed in the ventral region of the neural tube and promotes the differentiation of motor neurons." Development 124, no. 24 (December 15, 1997): 5139–47. http://dx.doi.org/10.1242/dev.124.24.5139.
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The extracellular matrix protein vitronectin and its mRNA are present in the embryonic chick notochord, floor plate and in the ventral neural tube at the time position of motor neuron generation. When added to cultures of neural tube explants of developmental stage 9, vitronectin promotes the generation of motor neurons in the absence of either notochord or exogenously added Sonic hedgehog. Conversely, the neutralisation of endogenous vitronectin with antibodies inhibits over 90% motor neuron differentiation in co-cultured neural tube/notochord explants, neural tube explants cultured in the presence of Sonic hedgehog, and in committed (stage 13) neural tube explants. Furthermore, treatment of embryos with anti-vitronectin antibodies results in a substantial and specific reduction in the number of motor neurons generated in vivo. These results demonstrate that vitronectin stimulates the differentiation of motor neurons in vitro and in vivo. Since the treatment of stage 9 neural tube explants with Sonic hedgehog resulted in induction of vitronectin mRNA expression before the expression of floor plate markers, we conclude that vitronectin may act either as a downstream effector in the signalling cascade induced by Sonic hedgehog, or as a synergistic factor that increases Shh-induced motor neuron differentiation.
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Michalikova, Martina, Michiel W. H. Remme, Dietmar Schmitz, Susanne Schreiber, and Richard Kempter. "Spikelets in pyramidal neurons: generating mechanisms, distinguishing properties, and functional implications." Reviews in the Neurosciences 31, no. 1 (December 18, 2019): 101–19. http://dx.doi.org/10.1515/revneuro-2019-0044.
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Abstract Spikelets are small spike-like depolarizations that are found in somatic recordings of many neuron types. Spikelets have been assigned important functions, ranging from neuronal synchronization to the regulation of synaptic plasticity, which are specific to the particular mechanism of spikelet generation. As spikelets reflect spiking activity in neuronal compartments that are electrotonically distinct from the soma, four modes of spikelet generation can be envisaged: (1) dendritic spikes or (2) axonal action potentials occurring in a single cell as well as action potentials transmitted via (3) gap junctions or (4) ephaptic coupling in pairs of neurons. In one of the best studied neuron type, cortical pyramidal neurons, the origins and functions of spikelets are still unresolved; all four potential mechanisms have been proposed, but the experimental evidence remains ambiguous. Here we attempt to reconcile the scattered experimental findings in a coherent theoretical framework. We review in detail the various mechanisms that can give rise to spikelets. For each mechanism, we present the biophysical underpinnings as well as the resulting properties of spikelets and compare these predictions to experimental data from pyramidal neurons. We also discuss the functional implications of each mechanism. On the example of pyramidal neurons, we illustrate that several independent spikelet-generating mechanisms fulfilling vastly different functions might be operating in a single cell.
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Elsen, Frank P., and Jan-Marino Ramirez. "Postnatal Development Differentially Affects Voltage-Activated Calcium Currents in Respiratory Rhythmic Versus Nonrhythmic Neurons of the Pre-Bötzinger Complex." Journal of Neurophysiology 94, no. 2 (August 2005): 1423–31. http://dx.doi.org/10.1152/jn.00237.2005.
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The mammalian respiratory network reorganizes during early postnatal life. We characterized the postnatal developmental changes of calcium currents in neurons of the pre-Bötzinger complex (pBC), the presumed site for respiratory rhythm generation. The pBC contains not only respiratory rhythmic (R) but also nonrhythmic neurons (nR). Both types of neurons express low- and high-voltage-activated (LVA and HVA) calcium currents. This raises the interesting issue: do calcium currents of the two co-localized neuron types have similar developmental profiles? To address this issue, we used the whole cell patch-clamp technique to compare in transverse slices of mice LVA and HVA calcium current amplitudes of the two neuron populations (R and nR) during the first and second postnatal week (P0–P16). The amplitude of HVA currents did not significantly change in R pBC-neurons (P0–P16), but it significantly increased in nR pBC-neurons during P8–P16. The dehydropyridine (DHP)-sensitive current amplitudes did not significantly change during the early postnatal development, suggesting that the observed amplitude changes in nR pBC-neurons are caused by (DHP) insensitive calcium currents. The ratio between HVA calcium current amplitudes dramatically changed during early postnatal development: At P0–P3, current amplitudes were significantly larger in R pBC-neurons, whereas at P8–P16, current amplitudes were significantly larger in nR pBC-neurons. Our results suggest that calcium currents in pBC neurons are differentially altered during postnatal development and that R pBC-neurons have fully expressed calcium currents early during postnatal development. This may be critical for stable respiratory rhythm generation in the underlying rhythm generating network.
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Sapolsky, Robert M. "Second generation questions about senescent neuron loss." Neurobiology of Aging 8, no. 6 (November 1987): 547–48. http://dx.doi.org/10.1016/0197-4580(87)90128-x.
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KATORI, YUICHI, ERIC J. LANG, MIHO ONIZUKA, MITSUO KAWATO, and KAZUYUKI AIHARA. "QUANTITATIVE MODELING OF SPATIO-TEMPORAL DYNAMICS OF INFERIOR OLIVE NEURONS WITH A SIMPLE CONDUCTANCE-BASED MODEL." International Journal of Bifurcation and Chaos 20, no. 03 (March 2010): 583–603. http://dx.doi.org/10.1142/s0218127410025909.
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Inferior olive (IO) neurons project to the cerebellum and contribute to motor control. They can show intriguing spatio-temporal dynamics with rhythmic and synchronized spiking. IO neurons are connected to their neighbors via gap junctions to form an electrically coupled network, and so it is considered that this coupling contributes to the characteristic dynamics of this nucleus. Here, we demonstrate that a gap junction-coupled network composed of simple conductance-based model neurons (a simplified version of a Hodgkin–Huxley type neuron) reproduce important aspects of IO activity. The simplified phenomenological model neuron facilitated the analysis of the single cell and network properties of the IO while still quantitatively reproducing the spiking patterns of complex spike activity observed by simultaneous recording in anesthetized rats. The results imply that both intrinsic bistability of each neuron and gap junction coupling among neurons play key roles in the generation of the spatio-temporal dynamics of IO neurons.
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Ghahari, Alireza, and John D. Enderle. "A Physiological Neural Controller of a Muscle Fiber Oculomotor Plant in Horizontal Monkey Saccades." ISRN Ophthalmology 2014 (May 7, 2014): 1–19. http://dx.doi.org/10.1155/2014/406210.
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A neural network model of biophysical neurons in the midbrain is presented to drive a muscle fiber oculomotor plant during horizontal monkey saccades. Neural circuitry, including omnipause neuron, premotor excitatory and inhibitory burst neurons, long lead burst neuron, tonic neuron, interneuron, abducens nucleus, and oculomotor nucleus, is developed to examine saccade dynamics. The time-optimal control strategy by realization of agonist and antagonist controller models is investigated. In consequence, each agonist muscle fiber is stimulated by an agonist neuron, while an antagonist muscle fiber is unstimulated by a pause and step from the antagonist neuron. It is concluded that the neural network is constrained by a minimum duration of the agonist pulse and that the most dominant factor in determining the saccade magnitude is the number of active neurons for the small saccades. For the large saccades, however, the duration of agonist burst firing significantly affects the control of saccades. The proposed saccadic circuitry establishes a complete model of saccade generation since it not only includes the neural circuits at both the premotor and motor stages of the saccade generator, but also uses a time-optimal controller to yield the desired saccade magnitude.
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Xing, Yuan, Nan Zhang, Wei Zhang, and Lei-Ming Ren. "Bupivacaine Indirectly Potentiates Glutamate-induced Intracellular Calcium Signaling in Rat Hippocampal Neurons by Impairing Mitochondrial Function in Cocultured Astrocytes." Anesthesiology 128, no. 3 (March 1, 2018): 539–54. http://dx.doi.org/10.1097/aln.0000000000002003.
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Abstract Background Bupivacaine induces central neurotoxicity at lower blood concentrations than cardiovascular toxicity. However, central sensitivity to bupivacaine is poorly understood. The toxicity mechanism might be related to glutamate-induced excitotoxicity in hippocampal cells. Methods The intracellular free Ca2+ concentration ([Ca2+]i), mitochondrial membrane potential, and reactive oxygen species generation were measured by fluorescence and two-photon laser scanning microscopy in fetal rat hippocampal neurons and astrocytes. Results In astrocyte/neuron cocultures, 300 μM bupivacaine inhibited glutamate-induced increases in [Ca2+]i in astrocytes by 40% (P < 0.0001; n = 20) but significantly potentiated glutamate-induced increases in [Ca2+]i in neurons by 102% (P = 0.0007; n = 10). Ropivacaine produced concentration-dependent effects similar to bupivacaine (0.3 to 300 μM). Tetrodotoxin did not mimic bupivacaine’s effects. In pure cell cultures, bupivacaine did not affect glutamate-induced increases in [Ca2+]i in neurons but did inhibit increased [Ca2+]i in astrocytes. Moreover, bupivacaine produced a 61% decrease in the mitochondrial membrane potential (n = 20) and a 130% increase in reactive oxygen species generation (n = 15) in astrocytes. Cyclosporin A treatment suppressed bupivacaine’s effects on [Ca2+]i, mitochondrial membrane potential, and reactive oxygen species generation. When astrocyte/neuron cocultures were incubated with 500 μM dihydrokainic acid (a specific glutamate transporter–1 inhibitor), bupivacaine did not potentiate glutamate-induced increases in [Ca2+]i in neurons but still inhibited glutamate-induced increases in [Ca2+]i in astrocytes. Conclusions In primary rat hippocampal astrocyte and neuron cocultures, clinically relevant concentrations of bupivacaine selectively impair astrocytic mitochondrial function, thereby suppressing glutamate uptake, which indirectly potentiates glutamate-induced increases in [Ca2+]i in neurons.
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Otsuka, Takeshi, Takafumi Abe, Takahisa Tsukagawa, and Wen-Jie Song. "Conductance-Based Model of the Voltage-Dependent Generation of a Plateau Potential in Subthalamic Neurons." Journal of Neurophysiology 92, no. 1 (July 2004): 255–64. http://dx.doi.org/10.1152/jn.00508.2003.
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Because the subthalamic nucleus (STN) acts as a driving force of the basal ganglia, it is important to know how the activities of STN neurons are regulated. Previously, we have reported that a subset of STN neurons generates a plateau potential in a voltage-dependent manner. These plateau potentials can be evoked only when the cell is hyperpolarized. Here, to examine the mechanism of the voltage-dependent generation of the plateau potential in STN neurons, we constructed a conductance-based model of the plateau-generating STN neuron based on experimental observations and compared simulation results with recordings in slices. The model consists of a single compartment containing a Na+ current, a delayed-rectifier K+ current, an A-type K+ current, an L-like long-lasting Ca2+ current, a T-type Ca2+ current, a Ca2+-dependent K+ current, and a leak current. Our simulation results showed that a plateau potential in the model could be induced in a voltage-dependent manner that depended on the inactivation properties of L-like long-lasting Ca2+ current. The model could also reproduce the generation of a plateau potential as a rebound potential after termination of hyperpolarizing current injection. In addition, we tested the stability of simulated plateau potentials against inhibitory perturbation and found that the model showed similar properties observed for the plateau potentials of STN neurons in slices. The effects of K+ channel blockade by TEA and intracellular Ca2+ ion chelation by BAPTA on the plateau duration were also tested in the model and were found to match experimental observations. Thus our STN neuron model could qualitatively reproduce a number of experimental observations on plateau potentials. Our results suggest that the inactivation of L-type Ca2+ channels plays an important role in the voltage-dependent generation of the plateau potential.
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Koiwa, Shiromizu, Adachi, Ikejiri, Nakatani, Tanaka, and Nishimura. "Generation of a Triple-Transgenic Zebrafish Line for Assessment of Developmental Neurotoxicity during Neuronal Differentiation." Pharmaceuticals 12, no. 4 (September 24, 2019): 145. http://dx.doi.org/10.3390/ph12040145.
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: The developing brain is extremely sensitive to many chemicals. Exposure to neurotoxicants during development has been implicated in various neuropsychiatric and neurological disorders, including autism spectrum disorders and schizophrenia. Various screening methods have been used to assess the developmental neurotoxicity (DNT) of chemicals, with most assays focusing on cell viability, apoptosis, proliferation, migration, neuronal differentiation, and neuronal network formation. However, assessment of toxicity during progenitor cell differentiation into neurons, astrocytes, and oligodendrocytes often requires immunohistochemistry, which is a reliable but labor-intensive and time-consuming assay. Here, we report the development of a triple-transgenic zebrafish line that expresses distinct fluorescent proteins in neurons (Cerulean), astrocytes (mCherry), and oligodendrocytes (mCitrine), which can be used to detect DNT during neuronal differentiation. Using in vivo fluorescence microscopy, we could detect DNT by 6 of the 10 neurotoxicants tested after exposure to zebrafish from 12 h to 5 days’ post-fertilization. Moreover, the chemicals could be clustered into three main DNT groups based on the fluorescence pattern: (i) inhibition of neuron and oligodendrocyte differentiation and stimulation of astrocyte differentiation; (ii) inhibition of neuron and oligodendrocyte differentiation; and (iii) inhibition of neuron and astrocyte differentiation, which suggests that reporter expression reflects the toxicodynamics of the chemicals. Thus, the triple-transgenic zebrafish line developed here may be a useful tool to assess DNT during neuronal differentiation.
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Bukinich, Anna Aleksandrovna, and Petr Dmitriyevich Shabanov. "The human brain is working in the system of dual coding: a hypothesis." Reviews on Clinical Pharmacology and Drug Therapy 11, no. 2 (June 15, 2013): 52–56. http://dx.doi.org/10.17816/rcf11252-56.
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How the human brain is working is up to now unclear. Using singular neuron as an object, and pharmacological agents as a tool the neuron activity in general in the mammalian CNS has been described. The basis of all investigations was the study of dimmer (heteromer) structures associated with G-coupled receptor proteins on the surfaces of neuron membranes isolated from the own usual circle. We can organize the recombinant movement by means of physiological concentrations of pharmacological reagents if these processes were lasting in the network neurons native brain. That is, the ideal conditions for the processes generation in the neural impulse were reconstructed.
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Ostrovskiy, Valeriy, Denis Butusov, Artur Karimov, and Valeriy Andreev. "DISCRETIZATION EFFECTS DURING NUMERICAL INVESTIGATION OF HODGKIN-HUXLEY NEURON MODEL." Bulletin of Bryansk state technical university 2019, no. 12 (December 19, 2019): 94–101. http://dx.doi.org/10.30987/1999-8775-2019-2019-12-94-101.
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Computer design is a valuable tool in the course of designing neuro-morphic systems. In particular it allows investigating basic mechanisms of neuron pulse activities in networks. For computer modeling it is necessary to digitize a continuous model of the system by means of the application of discrete operators able to keep basic properties of a prototype. But the accuracy of discrete models may decrease because of negative effects caused by the type of the method used, by a discretization pitch and errors in rounding off.
This fact is significant for the analysis of non-linear systems to which belong the models of biological neurons. As a possible solution of the problem may be the development of specialized tools for the analysis of dynamic systems with the focus upon numerical methods used. In this paper by the example of the modeling of the neuron described by Hodgkin-Huxley classical equations there is considered a set of widespread methods for ODU solution. In the course of investigations there are shown possible negative consequences of incorrect use of some discrete operators. In the paper the results of two sets of computer experiments are presented. The first ones determine the limitations for the practical use of the methods of the first accuracy order during modeling neurons in the mode of resonance generation of action potentials. The second ones show discretization effects connected with chaotic modes of neurons functioning: incorrect behavior of discrete models which is manifested in the emergence of chaotic transition processes. The investigation results may be used at the formation of modeling tool packages both, non-linear dynamic systems in the whole, and neuro-morphic systems in particular.
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Zhang, Shu-Zhen, Li-Xiang Ma, Wen-Jing Qian, Hong-Fu Li, Zhong-Feng Wang, Hong-Xia Wang, and Zhi-Ying Wu. "Modeling Neurological Disease by Rapid Conversion of Human Urine Cells into Functional Neurons." Stem Cells International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/2452985.
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Somatic cells can be directly converted into functional neurons by ectopic expression of defined factors and/or microRNAs. Since the first report of conversion mouse embryonic fibroblasts into functional neurons, the postnatal mouse, and human fibroblasts, astroglia, hepatocytes, and pericyte-derived cells have been converted into functional dopaminergic and motor neurons bothin vitroandin vivo. However, it is invasive to get all these materials. In the current study, we provide a noninvasive approach to obtain directly reprogrammed functional neurons by overexpression of the transcription factors Ascl1, Brn2, NeuroD, c-Myc, and Myt1l in human urine cells. These induced neuronal (iN) cells could express multiple neuron-specific proteins and generate action potentials. Moreover, urine cells from Wilson’s disease (WD) patient could also be directly converted into neurons. In conclusion, generation of iN cells from nonneural lineages is a feasible and befitting approach for neurological disease modeling.
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Stark, Eran, Lisa Roux, Ronny Eichler, and György Buzsáki. "Local generation of multineuronal spike sequences in the hippocampal CA1 region." Proceedings of the National Academy of Sciences 112, no. 33 (August 3, 2015): 10521–26. http://dx.doi.org/10.1073/pnas.1508785112.
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Sequential activity of multineuronal spiking can be observed during theta and high-frequency ripple oscillations in the hippocampal CA1 region and is linked to experience, but the mechanisms underlying such sequences are unknown. We compared multineuronal spiking during theta oscillations, spontaneous ripples, and focal optically induced high-frequency oscillations (“synthetic” ripples) in freely moving mice. Firing rates and rate modulations of individual neurons, and multineuronal sequences of pyramidal cell and interneuron spiking, were correlated during theta oscillations, spontaneous ripples, and synthetic ripples. Interneuron spiking was crucial for sequence consistency. These results suggest that participation of single neurons and their sequential order in population events are not strictly determined by extrinsic inputs but also influenced by local-circuit properties, including synapses between local neurons and single-neuron biophysics.
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Khurram, Obaid U., Matthew J. Fogarty, Sabhya Rana, Pangdra Vang, Gary C. Sieck, and Carlos B. Mantilla. "Diaphragm muscle function following midcervical contusion injury in rats." Journal of Applied Physiology 126, no. 1 (January 1, 2019): 221–30. http://dx.doi.org/10.1152/japplphysiol.00481.2018.
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Midcervical spinal cord contusion injury results in tissue damage, disruption of spinal pathways, and motor neuron loss. Unilateral C4 contusion results in loss of 40%–50% of phrenic motor neurons ipsilateral to the injury (~25% of the total phrenic motor neuron pool). Over time after unilateral C4 contusion injury, diaphragm muscle (DIAm) electromyogram activity increases both contralateral and ipsilateral to the side of injury in rats, suggesting compensation because of increased activation of the surviving motor neurons. However, the impact of contusion injury on DIAm force generation is less clear. Transdiaphragmatic pressure (Pdi) was measured across motor behaviors over time after unilateral C4 contusion injury in adult male Sprague-Dawley rats. Maximum Pdi (Pdimax) was elicited by bilateral phrenic nerve stimulation at 7 days postinjury. We hypothesized that Pdimax is reduced following unilateral C4 contusion injury, whereas ventilatory behaviors of the DIAm are unimpaired. In support of our hypothesis, Pdimax was reduced by ~25% after unilateral C4 contusion, consistent with the extent of phrenic motor neuron loss following contusion injury. One day after contusion injury, the Pdi amplitude during airway occlusion was reduced from ~30 to ~20 cmH2O, but this reduction was completely reversed by 7 days postinjury. Ventilatory behaviors (~10 cmH2O), DIAm-specific force, and muscle fiber cross-sectional area did not differ between the laminectomy and contusion groups. These results indicate that the large reserve capacity for DIAm force generation allows for higher-force motor behaviors to be accomplished despite motor neuron loss, likely reflecting changes in motor unit recruitment. NEW & NOTEWORTHY Respiratory muscles such as the diaphragm generate the pressures necessary to accomplish a variety of motor behaviors ranging from ventilation to near-maximal expulsive behaviors. However, the impact of contusion injury on diaphragm pressure generation across behaviors is not clear. The present study shows that contusion injury impairs maximal pressure generation while preserving the ability of the diaphragm to accomplish lower-force motor behaviors, likely reflecting changes in diaphragm motor unit recruitment.
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Kim, Yong-Sik, and Chang-Hwan Park. "Dopamine Neuron Generation from Human Embryonic Stem Cells." International Journal of Stem Cells 4, no. 2 (November 30, 2011): 85–87. http://dx.doi.org/10.15283/ijsc.2011.4.2.85.
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MITSUI, Kazuo. "AUTONOMOUS GENERATION OF STRUCTURAL SYSTEMS BY NEURON MODEL." Proceedings of OPTIS 2002.5 (2002): 111–15. http://dx.doi.org/10.1299/jsmeoptis.2002.5.111.
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Onimaru, Hiroshi, Kayo Tsuzawa, Yoshimi Nakazono, and Wiktor A. Janczewski. "Midline section of the medulla abolishes inspiratory activity and desynchronizes pre-inspiratory neuron rhythm on both sides of the medulla in newborn rats." Journal of Neurophysiology 113, no. 7 (April 2015): 2871–78. http://dx.doi.org/10.1152/jn.00554.2014.
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Each half of the medulla contains respiratory neurons that constitute two generators that control respiratory rhythm. One generator consists of the inspiratory neurons in the pre-Bötzinger complex (preBötC); the other, the pre-inspiratory (Pre-I) neurons in the parafacial respiratory group (pFRG), rostral to the preBötC. We investigated the contribution of the commissural fibers, connecting the respiratory rhythm generators located on the opposite side of the medulla to the generation of respiratory activity in brain stem-spinal cord preparation from 0- to 1-day-old rats. Pre-I neuron activity and the facial nerve and/or first lumbar (L1) root activity were recorded as indicators of the pFRG-driven rhythm. Fourth cervical ventral root (C4) root and/or hypoglossal (XII) nerve activity were recorded as indicators of preBötC-driven inspiratory activity. We found that a midline section that interrupted crossed fibers rostral to the obex irreversibly eliminated C4 and XII root activity, whereas the Pre-I neurons, facial nerve, and L1 roots remained rhythmically active. The facial and contralateral L1 nerve activities were synchronous, whereas right and left facial (and right and left L1) nerves lost synchrony. Optical recordings demonstrated that pFRG-driven burst activity was preserved after a midline section, whereas the preBötC neurons were no longer rhythmic. We conclude that in newborn rats, crossed excitatory interactions (via commissural fibers) are necessary for the generation of inspiratory bursts but not for the generation of rhythmic Pre-I neuron activity.
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Khodr, Christina E., Sara Clark, Alex F. Bokov, Arlan Richardson, Randy Strong, David L. Hurley, and Carol J. Phelps. "Early Postnatal Administration of Growth Hormone Increases Tuberoinfundibular Dopaminergic Neuron Numbers in Ames Dwarf Mice." Endocrinology 151, no. 7 (May 12, 2010): 3277–85. http://dx.doi.org/10.1210/en.2009-1482.
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Hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons secrete dopamine, which inhibits pituitary prolactin (PRL) secretion. PRL has demonstrated neurotrophic effects on TIDA neuron development in PRL-, GH-, and TSH-deficient Ames (df/df) and Snell (dw/dw) dwarf mice. However, both PRL and PRL receptor knockout mice exhibit normal-sized TIDA neuron numbers, implying GH and/or TSH influence TIDA neuron development. The current study investigated the effect of porcine (p) GH on TIDA neuron development in Ames dwarf hypothalamus. Normal (DF/df) and dwarf mice were treated daily with pGH or saline beginning at 3 d of age for a period of 42 d. After treatment, brains were analyzed using catecholamine histofluorescence, tyrosine hydroxylase immunocytochemistry, and bromodeoxyuridine (BrdU) immunocytochemistry to detect BrdU incorporation. DF/df males and df/df treated with pGH experienced increased (P ≤ 0.01) weight gain compared with those treated with saline. DF/df had greater (P ≤ 0.01) TIDA neuron numbers than df/df, regardless of treatment. TIDA neuron number in pGH-treated df/df was greater (P ≤ 0.01) than in saline-treated df/df. Zona incerta and periventricular dopamine neurons were not affected by treatment or genotype. There was no effect of genotype or treatment on BrdU incorporation in the arcuate nucleus, median eminence, or periventricular region surrounding the third ventricle. Saline-treated df/df experienced decreased (P ≤ 0.05) dentate gyrus BrdU incorporation compared with saline-treated DF/df. In the lateral ventricle, pGH-treated males had greater BrdU immunoreactivity than pGH-treated females. The results show an effect of pGH on TIDA neuron development, although this effect is less potent than that of PRL, and likely GH-induced preservation of TIDA neurons rather than generation of new TIDA neurons via neurogenesis.
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Krolo, M., V. Tonkovic-Capin, A. G. Stucke, E. A. Stuth, F. A. Hopp, C. Dean, and E. J. Zuperku. "Subtype Composition and Responses of Respiratory Neurons in the Pre-Bötzinger Region to Pulmonary Afferent Inputs in Dogs." Journal of Neurophysiology 93, no. 5 (May 2005): 2674–87. http://dx.doi.org/10.1152/jn.01206.2003.
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The brain stem pre-Bötzinger complex (pre-BC) plays an important role in respiratory rhythm generation. However, it is not clear what function each subpopulation of neurons in the pre-BC serves. The purpose of the present studies was to identify neuronal subpopulations of the canine pre-BC and to characterize the neuronal responses of subpopulations to experimentally imposed changes in inspiratory (I) and expiratory (E) phase durations. Lung inflations and electrical stimulation of the cervical vagus nerve were used to produce changes in respiratory phase timing via the Hering-Breuer reflex. Multibarrel micropipettes were used to record neuronal activity and for pressure microejection in decerebrate, paralyzed, ventilated dogs. The pre-BC region was functionally identified by eliciting tachypneic phrenic neural responses to localized microejections of dl-homocysteic acid. Antidromic stimulation and spike-triggered averaging techniques were used to identify bulbospinal and cranial motoneurons, respectively. The results indicate that the canine pre-BC region consists of a heterogeneous mixture of propriobulbar I and E neuron subpopulations. The neuronal responses to ipsi-, contra-, and bilateral pulmonary afferent inputs indicated that I and E neurons with decrementing patterns were the only neurons with responses consistently related to phase duration. Late-I neurons were excited, but most other types of I neurons were inhibited or unresponsive. E neurons with augmenting or parabolic discharge patters were inhibited by ipsilateral inputs but excited by contra- and bilateral inputs. Late-E neurons were more frequently encountered and were inhibited by ipsi- and bilateral inputs, but excited by contralateral inputs. The results suggest that only a limited number of neuron subpopulations may be involved in rhythmogenesis, whereas many neuron types may be involved in motor pattern generation.
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Wang, Xiu Qing, Zeng Guang Hou, Min Tan, Yong Ji Wang, and Fei Xie. "Mobile Robots' Wall-Following Controller Based on Probabilistic Spiking Neuron Model." Advanced Materials Research 588-589 (November 2012): 1547–51. http://dx.doi.org/10.4028/www.scientific.net/amr.588-589.1547.
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This paper focuses on the third generation of neural networks- Spiking neural networks (SNNs), the novel Spiking neuron model- probabilistic Spiking neuron model (pSNM), and their applications. pSNM is used in mobile robots' behavior control, and a novel mobile robots' wall-following controller based on pSNM is proposed. In the pSNM controller, Spiking time-delayed coding is used for the sensory neurons of the input layer and pSNM is used for the motor neurons in the output layer. Thorpe and Hebbian learning rules are used in the controller. The experimental results show that the controller can control the mobile robots to follow the wall clockwise and counterclockwise successfully. The structure of the controller is simple, and the controller can study online.
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Paraíso-Luna, Juan, José Aguareles, Ricardo Martín, Ane C. Ayo-Martín, Samuel Simón-Sánchez, Daniel García-Rincón, Carlos Costas-Insua, et al. "Endocannabinoid signalling in stem cells and cerebral organoids drives differentiation to deep layer projection neurons via CB1 receptors." Development 147, no. 24 (November 9, 2020): dev192161. http://dx.doi.org/10.1242/dev.192161.
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ABSTRACTThe endocannabinoid (eCB) system, via the cannabinoid CB1 receptor, regulates neurodevelopment by controlling neural progenitor proliferation and neurogenesis. CB1 receptor signalling in vivo drives corticofugal deep layer projection neuron development through the regulation of BCL11B and SATB2 transcription factors. Here, we investigated the role of eCB signalling in mouse pluripotent embryonic stem cell-derived neuronal differentiation. Characterization of the eCB system revealed increased expression of eCB-metabolizing enzymes, eCB ligands and CB1 receptors during neuronal differentiation. CB1 receptor knockdown inhibited neuronal differentiation of deep layer neurons and increased upper layer neuron generation, and this phenotype was rescued by CB1 re-expression. Pharmacological regulation with CB1 receptor agonists or elevation of eCB tone with a monoacylglycerol lipase inhibitor promoted neuronal differentiation of deep layer neurons at the expense of upper layer neurons. Patch-clamp analyses revealed that enhancing cannabinoid signalling facilitated neuronal differentiation and functionality. Noteworthy, incubation with CB1 receptor agonists during human iPSC-derived cerebral organoid formation also promoted the expansion of BCL11B+ neurons. These findings unveil a cell-autonomous role of eCB signalling that, via the CB1 receptor, promotes mouse and human deep layer cortical neuron development.
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Orbán, Gergő, Tamás Kiss, and Péter Érdi. "Intrinsic and Synaptic Mechanisms Determining the Timing of Neuron Population Activity During Hippocampal Theta Oscillation." Journal of Neurophysiology 96, no. 6 (December 2006): 2889–904. http://dx.doi.org/10.1152/jn.01233.2005.
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Hippocampal theta (3–8 Hz) is a major electrophysiological activity in rodents, which can be found in primates and humans as well. During theta activity, pyramidal cells and different classes of interneurons were shown to discharge at different phases of the extracellular theta. A recent in vitro study has shown that theta-frequency oscillation can be elicited in a hippocampal CA1 slice by the activation of metabotropic glutamate receptors with similar pharmacological and physiological profile that was found in vivo. We constructed a conductance based three-population network model of the hippocampal CA1 region to study the specific roles of neuron types in the generation of the in vitro theta oscillation and the emergent network properties. Interactions between pairs of neuron populations were studied systematically to assess synchronization and delay properties. We showed that the circuitry consisting of pyramidal cells and two types of hippocampal interneurons [basket and oriens lacunosum-moleculare (O-LM) neurons] was able to generate coherent theta-frequency population oscillation. Furthermore, we found that hyperpolarization-activated nonspecific cation current in pyramidal cells, but not in O-LM neurons, plays an important role in the timing of spike generation, and thus synchronization of pyramidal cells. The model was shown to exhibit the same phase differences between neuron population activities found in vivo, supporting the idea that these patterns of activity are determined internal to the hippocampus.
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Paul, D. H., and B. Mulloney. "Nonspiking local interneuron in the motor pattern generator for the crayfish swimmeret." Journal of Neurophysiology 54, no. 1 (July 1, 1985): 28–39. http://dx.doi.org/10.1152/jn.1985.54.1.28.
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We describe a type of nonspiking premotor local interneuron (interneuron IA) in the abdominal nervous system of Pacifasticus leniusculus. All of its branches are restricted to one side of the midline. These interneurons are identifiable and occur as bilateral pairs, one neuron on each side of abdominal ganglia 3, 4, and 5. The membrane potential of interneuron IA oscillated in phase with the swimmeret rhythm, a motor pattern generated in each of these ganglia, because the neuron received postsynaptic potentials in phase with the rhythm. Sustained hyperpolarization of an individual interneuron IA initiated generation of the swimmeret rhythm in all the ganglia of a quiescent nervous system. Sustained depolarization stopped the swimmeret rhythm in all the active ganglia of a nervous system that was generating the rhythm. Currents injected into one interneuron reset the rhythm. Comparisons of the shapes of the IA interneurons in different ganglia showed that they are similar to each other and distinct from other local interneurons in these ganglia. Interneuron IA has a large integrative segment and relatively few branches that are largely restricted to the lateral neuropil, to which all other kinds of swimmeret neurons also project. We conclude that this interneuron occurs only once in each hemiganglion in abdominal segments 3, 4, and 5, and that it is identifiable. Furthermore, this interneuron is an essential component of the circuit in each hemiganglion that generates the swimmeret rhythm. The interneuron was dye coupled to a particular identifiable motor neuron and not to any other neurons. The motor neuron was not dye-coupled to any other local interneurons. The ability of this motor neuron to reset the rhythm is attributed to its being electrically coupled to interneuron IA in its ganglion.
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Burtscher, Ingo, Marta Tarquis-Medina, Ciro Salinno, Silvia Schirge, Julia Beckenbauer, Mostafa Bakhti, and Heiko Lickert. "Generation of a Novel Nkx6-1 Venus Fusion Reporter Mouse Line." International Journal of Molecular Sciences 22, no. 7 (March 26, 2021): 3434. http://dx.doi.org/10.3390/ijms22073434.
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Nkx6-1 is a member of the Nkx family of homeodomain transcription factors (TFs) that regulates motor neuron development, neuron specification and pancreatic endocrine and β-cell differentiation. To facilitate the isolation and tracking of Nkx6-1-expressing cells, we have generated a novel Nkx6-1 Venus fusion (Nkx6-1-VF) reporter allele. The Nkx6-1-VF knock-in reporter is regulated by endogenous cis-regulatory elements of Nkx6-1 and the fluorescent protein fusion does not interfere with the TF function, as homozygous mice are viable and fertile. The nuclear localization of Nkx6-1-VF protein reflects the endogenous Nkx6-1 protein distribution. During embryonic pancreas development, the reporter protein marks the pancreatic ductal progenitors and the endocrine lineage, but is absent in the exocrine compartment. As expected, the levels of Nkx6-1-VF reporter are upregulated upon β-cell differentiation during the major wave of endocrinogenesis. In the adult islets of Langerhans, the reporter protein is exclusively found in insulin-secreting β-cells. Importantly, the Venus reporter activities allow successful tracking of β-cells in live-cell imaging and their specific isolation by flow sorting. In summary, the generation of the Nkx6-1-VF reporter line reflects the expression pattern and dynamics of the endogenous protein and thus provides a unique tool to study the spatio-temporal expression pattern of this TF during organ development and enables isolation and tracking of Nkx6-1-expressing cells such as pancreatic β-cells, but also neurons and motor neurons in health and disease.
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Ashida, Go, Kousuke Abe, Kazuo Funabiki, and Masakazu Konishi. "Passive Soma Facilitates Submillisecond Coincidence Detection in the Owl's Auditory System." Journal of Neurophysiology 97, no. 3 (March 2007): 2267–82. http://dx.doi.org/10.1152/jn.00399.2006.
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Neurons of the avian nucleus laminaris (NL) compute the interaural time difference (ITD) by detecting coincident arrivals of binaural signals with submillisecond accuracy. The cellular mechanisms for this temporal precision have long been studied theoretically and experimentally. The myelinated axon initial segment in the owl's NL neuron and small somatic spikes observed in auditory coincidence detector neurons of various animals suggest that spikes in the NL neuron are generated at the first node of Ranvier and that the soma passively receives back-propagating spikes. To investigate the significance of the “passive soma” structure, we constructed a two-compartment NL neuron model, consisting of a cell body and a first node, and systematically changed the excitability of each compartment. Here, we show that a neuron with a less active soma achieves higher ITD sensitivity and higher noise tolerance with lower energy costs. We also investigate the biophysical mechanism of the computational advantage of the “passive soma” structure by performing sub- and suprathreshold analyses. Setting a spike initiation site with high sodium conductance, not in the large soma but in the small node, serves to amplify high-frequency input signals and to reduce the impact and the energy cost of spike generation. Our results indicate that the owl's NL neuron uses a “passive soma” design for computational and metabolic reasons.
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Hedwig, Berthold. "Control of Cricket Stridulation by a Command Neuron: Efficacy Depends on the Behavioral State." Journal of Neurophysiology 83, no. 2 (February 1, 2000): 712–22. http://dx.doi.org/10.1152/jn.2000.83.2.712.
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Crickets use different song patterns for acoustic communication. The stridulatory pattern-generating networks are housed within the thoracic ganglia but are controlled by the brain. This descending control of stridulation was identified by intracellular recordings and stainings of brain neurons. Its impact on the generation of calling song was analyzed both in resting and stridulating crickets and during cercal wind stimulation, which impaired the stridulatory movements and caused transient silencing reactions. A descending interneuron in the brain serves as a command neuron for calling-song stridulation. The neuron has a dorsal soma position, anterior dendritic processes, and an axon that descends in the contralateral connective. The neuron is present in each side of the CNS. It is not activated in resting crickets. Intracellular depolarization of the interneuron so that its spike frequency is increased to 60–80 spikes/s reliably elicits calling-song stridulation. The spike frequency is modulated slightly in the chirp cycle with the maximum activity in phase with each chirp. There is a high positive correlation between the chirp repetition rate and the interneuron's spike frequency. Only a very weak correlation, however, exists between the syllable repetition rate and the interneuron activity. The effectiveness of the command neuron depends on the activity state of the cricket. In resting crickets, experimentally evoked short bursts of action potentials elicit only incomplete calling-song chirps. In crickets that previously had stridulated during the experiment, short elicitation of interneuron activity can trigger sustained calling songs during which the interneuron exhibits a spike frequency of ∼30 spikes/s. During sustained calling songs, the command neuron activity is necessary to maintain the stridulatory behavior. Inhibition of the interneuron stops stridulation. A transient increase in the spike frequency of the interneuron speeds up the chirp rate and thereby resets the timing of the chirp pattern generator. The interneuron also is excited by cercal wind stimulation. Cercal wind stimulation can impair the pattern of chirp and syllable generation, but these changes are not reflected in the discharge pattern of the command neuron. During wind-evoked silencing reactions, the activity of the calling-song command neuron remains unchanged, but under these conditions, its activity is no longer sufficient to maintain stridulation. Therefore stridulation can be suppressed by cercal inputs from the terminal ganglia without directly inhibiting the descending command activity.
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Yamazaki, Tadashi, and Shigeru Tanaka. "Robust Reservoir Generation by Correlation-Based Learning." Advances in Artificial Neural Systems 2009 (October 27, 2009): 1–7. http://dx.doi.org/10.1155/2009/467128.
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Reservoir computing (RC) is a new framework for neural computation. A reservoir is usually a recurrent neural network with fixed random connections. In this article, we propose an RC model in which the connections in the reservoir are modifiable. Specifically, we consider correlation-based learning (CBL), which modifies the connection weight between a given pair of neurons according to the correlation in their activities. We demonstrate that CBL enables the reservoir to reproduce almost the same spatiotemporal activity patterns in response to an identical input stimulus in the presence of noise. This result suggests that CBL enhances the robustness in the generation of the spatiotemporal activity pattern against noise in input signals. We apply our RC model to trace eyeblink conditioning. The reservoir bridged the gap of an interstimulus interval between the conditioned and unconditioned stimuli, and a readout neuron was able to learn and express the timed conditioned response.
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Seminary, Emily R., Stephanie Santarriaga, Lynn Wheeler, Marie Mejaki, Jenica Abrudan, Wendy Demos, Michael T. Zimmermann, et al. "Motor Neuron Generation from iPSCs from Identical Twins Discordant for Amyotrophic Lateral Sclerosis." Cells 9, no. 3 (February 28, 2020): 571. http://dx.doi.org/10.3390/cells9030571.
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Amyotrophic lateral sclerosis (ALS) is a complex neurodegenerative disorder characterized by the loss of the upper and lower motor neurons. Approximately 10% of cases are caused by specific mutations in known genes, with the remaining cases having no known genetic link. As such, sporadic cases have been more difficult to model experimentally. Here, we describe the generation and differentiation of ALS induced pluripotent stem cells reprogrammed from discordant identical twins. Whole genome sequencing revealed no relevant mutations in known ALS-causing genes that differ between the twins. As protein aggregation is found in all ALS patients and is thought to contribute to motor neuron death, we sought to characterize the aggregation phenotype of the sporadic ALS induced pluripotent stem cells (iPSCs). Motor neurons from both twins had high levels of insoluble proteins that commonly aggregate in ALS that did not robustly change in response to exogenous glutamate. In contrast, established genetic ALS iPSC lines demonstrated insolubility in a protein- and genotype-dependent manner. Moreover, whereas the genetic ALS lines failed to induce autophagy after glutamate stress, motor neurons from both twins and independent controls did activate this protective pathway. Together, these data indicate that our unique model of sporadic ALS may provide key insights into disease pathology and highlight potential differences between sporadic and familial ALS.
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Lin, Xiaoli, Chanyi Lu, Makoto Ohmoto, Katarzyna Choma, Robert F. Margolskee, Ichiro Matsumoto, and Peihua Jiang. "R-spondin substitutes for neuronal input for taste cell regeneration in adult mice." Proceedings of the National Academy of Sciences 118, no. 2 (December 21, 2020): e2001833118. http://dx.doi.org/10.1073/pnas.2001833118.
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Taste bud cells regenerate throughout life. Taste bud maintenance depends on continuous replacement of senescent taste cells with new ones generated by adult taste stem cells. More than a century ago it was shown that taste buds degenerate after their innervating nerves are transected and that they are not restored until after reinnervation by distant gustatory ganglion neurons. Thus, neuronal input, likely via neuron-supplied factors, is required for generation of differentiated taste cells and taste bud maintenance. However, the identity of such a neuron-supplied niche factor(s) remains unclear. Here, by mining a published RNA-sequencing dataset of geniculate ganglion neurons and by in situ hybridization, we demonstrate that R-spondin-2, the ligand of Lgr5 and its homologs Lgr4/6 and stem-cell-expressed E3 ligases Rnf43/Znrf3, is expressed in nodose-petrosal and geniculate ganglion neurons. Using the glossopharyngeal nerve transection model, we show that systemic delivery of R-spondin via adenovirus can promote generation of differentiated taste cells despite denervation. Thus, exogenous R-spondin can substitute for neuronal input for taste bud cell replenishment and taste bud maintenance. Using taste organoid cultures, we show that R-spondin is required for generation of differentiated taste cells and that, in the absence of R-spondin in culture medium, taste bud cells are not generated ex vivo. Thus, we propose that R-spondin-2 may be the long-sought neuronal factor that acts on taste stem cells for maintaining taste tissue homeostasis.
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Roberts, A., M. J. Tunstall, and E. Wolf. "Properties of networks controlling locomotion and significance of voltage dependency of NMDA channels: stimulation study of rhythm generation sustained by positive feedback." Journal of Neurophysiology 73, no. 2 (February 1, 1995): 485–95. http://dx.doi.org/10.1152/jn.1995.73.2.485.
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1. We have built a realistic 24-neuron model based on data from the spinal pattern generator for swimming in Xenopus embryos with the use of the SWIM programs. The neurons have dendrite, soma, and axon compartments with voltage-gated Na+ and K+ channels. Dendritic synapses were modeled as modulated ionic conductances with currents that have different reversal levels. One of these conductances was voltage dependent to model N-methyl-D-aspartate ("NMDA") synapses in the presence of Mg2+. 2. In this model, rhythm generation is initiated by a brief excitation, depends on rebound from reciprocal inhibition, and is sustained by long-duration "NMDA-dependent" feedback excitation. 3. Without NMDA voltage dependency, rhythmic activity is stable over a wide range of synaptic conductances. Its frequency decreases with more inhibition and increases with more excitation. The introduction of normally distributed variation in soma size or excitatory synaptic conductance extends the lower stable frequency range. Without such variation the frequency of the 24-neuron model is the same as a 4-neuron model provided that the synaptic conductances for each neuron are the same. 4. The effect of introducing NMDA voltage dependency on rebound after negative current injections or synaptic inhibition was investigated in single depolarized model neurons. With NMDA voltage dependency, hyperpolarizations and rebound spike responses were increased. 5. Network activity with NMDA voltage dependency was similar to that without it, but inhibitory postsynaptic potentials (IPSPs) and spikes were larger, and frequencies were lower and more sensitive to changes in excitatory and inhibitory conductance. 6. We conclude that in the model, mutual reexcitation among excitatory spinal interneurons can sustain rhythm generation by positive feedback and that NMDA voltage dependency can enhance postinhibitory rebound, stabilize swimming activity and extend its lower frequency range, and steepen the dependency of frequency on synaptic drive.
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Rybak, Ilya A., Julian F. R. Paton, and James S. Schwaber. "Modeling Neural Mechanisms for Genesis of Respiratory Rhythm and Pattern. II. Network Models of the Central Respiratory Pattern Generator." Journal of Neurophysiology 77, no. 4 (April 1, 1997): 2007–26. http://dx.doi.org/10.1152/jn.1997.77.4.2007.
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Rybak, Ilya A., Julian F. R. Paton, and James S. Schwaber. Modeling neural mechanisms for genesis of respiratory rhythm and pattern. II. Network models of the central respiratory pattern generator. J. Neurophysiol. 77: 2007–2026, 1997. The present paper describes several models of the central respiratory pattern generator (CRPG) developed employing experimental data and current hypotheses for respiratory rhythmogenesis. Each CRPG model includes a network of respiratory neuron types (e.g., early inspiratory; ramp inspiratory; late inspiratory; decrementing expiratory; postinspiratory; stage II expiratory; stage II constant firing expiratory; preinspiratory) and simplified models of lung and pulmonary stretch receptors (PSR), which provide feedback to the respiratory network. The used models of single respiratory neurons were developed in the Hodgkin-Huxley style as described in the previous paper. The mechanism for termination of inspiration (the inspiratory off-switch) in all models operates via late-I neuron, which is considered to be the inspiratory off-switching neuron. Several two- and three-phase CRPG models have been developed using different accepted hypotheses of the mechanism for termination of expiration. The key elements in the two-phase models are the early-I and dec-E neurons. The expiratory off-switch mechanism in these models is based on the mutual inhibitory connections between early-I and dec-E and adaptive properties of the dec-E neuron. The difference between the two-phase models concerns the mechanism for ramp firing patterns of E2 neurons resulting either from the intrinsic neuronal properties of the E2 neuron or from disinhibition from the adapting dec-E neuron. The key element of the three-phase models is the pre-I neuron, which acts as the expiratory off-switching neuron. The three-phase models differ by the mechanisms used for termination of expiration and for the ramp firing patterns of E2 neurons. Additional CRPG models were developed employing a dual switching neuron that generates two bursts per respiratory cycle to terminate both inspiration and expiration. Although distinctly different each model generates a stable respiratory rhythm and shows physiologically plausible firing patterns of respiratory neurons with and without PSR feedback. Using our models, we analyze the roles of different respiratory neuron types and their interconnections for the respiratory rhythm and pattern generation. We also investigate the possible roles of intrinsic biophysical properties of different respiratory neurons in controlling the duration of respiratory phases and timing of switching between them. We show that intrinsic membrane properties of respiratory neurons are integrated with network properties of the CRPG at three hierarchical levels: at the cellular level to provide the specific firing patterns of respiratory neurons (e.g., ramp firing patterns); at the network level to provide switching between the respiratory phases; and at the systems level to control the duration of inspiration and expiration under different conditions (e.g., lack of PSR feedback).
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Weng, Minrui, Xiaoji Xie, Chao Liu, Kah-Leong Lim, Cheng-wu Zhang, and Lin Li. "The Sources of Reactive Oxygen Species and Its Possible Role in the Pathogenesis of Parkinson’s Disease." Parkinson's Disease 2018 (September 2, 2018): 1–9. http://dx.doi.org/10.1155/2018/9163040.
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Parkinson’s disease (PD) is the second most common neurodegenerative disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra. The precise mechanism underlying pathogenesis of PD is not fully understood, but it has been widely accepted that excessive reactive oxygen species (ROS) are the key mediator of PD pathogenesis. The causative factors of PD such as gene mutation, neuroinflammation, and iron accumulation all could induce ROS generation, and the later would mediate the dopaminergic neuron death by causing oxidation protein, lipids, and other macromolecules in the cells. Obviously, it is of mechanistic and therapeutic significance to understand where ROS are derived and how ROS induce dopaminergic neuron damage. In the present review, we try to summarize and discuss the main source of ROS in PD and the key pathways through which ROS mediate DA neuron death.
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Kwag, Jeehyun, Hyun Jae Jang, Mincheol Kim, and Sujeong Lee. "M-type potassium conductance controls the emergence of neural phase codes: a combined experimental and neuron modelling study." Journal of The Royal Society Interface 11, no. 99 (October 6, 2014): 20140604. http://dx.doi.org/10.1098/rsif.2014.0604.
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Rate and phase codes are believed to be important in neural information processing. Hippocampal place cells provide a good example where both coding schemes coexist during spatial information processing. Spike rate increases in the place field, whereas spike phase precesses relative to the ongoing theta oscillation. However, what intrinsic mechanism allows for a single neuron to generate spike output patterns that contain both neural codes is unknown. Using dynamic clamp, we simulate an in vivo -like subthreshold dynamics of place cells to in vitro CA1 pyramidal neurons to establish an in vitro model of spike phase precession. Using this in vitro model, we show that membrane potential oscillation (MPO) dynamics is important in the emergence of spike phase codes: blocking the slowly activating, non-inactivating K + current ( I M ), which is known to control subthreshold MPO, disrupts MPO and abolishes spike phase precession. We verify the importance of adaptive I M in the generation of phase codes using both an adaptive integrate-and-fire and a Hodgkin–Huxley (HH) neuron model. Especially, using the HH model, we further show that it is the perisomatically located I M with slow activation kinetics that is crucial for the generation of phase codes. These results suggest an important functional role of I M in single neuron computation, where I M serves as an intrinsic mechanism allowing for dual rate and phase coding in single neurons.
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Sorribas, Helga, Celestino Padeste, and Louis Tiefenauer. "Photolithographic generation of protein micropatterns for neuron culture applications." Biomaterials 23, no. 3 (February 2002): 893–900. http://dx.doi.org/10.1016/s0142-9612(01)00199-5.
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Su, Hong-Lin, Keiko Muguruma, Mami Matsuo-Takasaki, Mineko Kengaku, Kiichi Watanabe, and Yoshiki Sasai. "Generation of cerebellar neuron precursors from embryonic stem cells." Developmental Biology 290, no. 2 (February 2006): 287–96. http://dx.doi.org/10.1016/j.ydbio.2005.11.010.
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Arifuzzaman, Md, Akira Ito, Kazushi Ikeda, Yoshinori Kawabe, and Masamichi Kamihira. "Fabricating Muscle–Neuron Constructs with Improved Contractile Force Generation." Tissue Engineering Part A 25, no. 7-8 (April 2019): 563–74. http://dx.doi.org/10.1089/ten.tea.2018.0165.
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Bogason, G. "Generation of a neuron transfer function and its derivatives." Electronics Letters 29, no. 21 (1993): 1867. http://dx.doi.org/10.1049/el:19931243.
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Siegenthaler, Julie A., Amir M. Ashique, Konstantinos Zarbalis, Katelin P. Patterson, Jonathan H. Hecht, Maureen A. Kane, Alexandra E. Folias, et al. "Retinoic Acid from the Meninges Regulates Cortical Neuron Generation." Cell 139, no. 3 (October 2009): 597–609. http://dx.doi.org/10.1016/j.cell.2009.10.004.
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Siegenthaler, Julie A., Amir M. Ashique, Konstantinos Zarbalis, Katelin P. Patterson, Jonathan H. Hecht, Maureen A. Kane, Alexandra E. Folias, et al. "Retinoic Acid from the Meninges Regulates Cortical Neuron Generation." Cell 146, no. 3 (August 2011): 486. http://dx.doi.org/10.1016/j.cell.2011.07.011.
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Kosuge, Yasuhiro, Hiroshi Nango, Hiroki Kasai, Takuya Yanagi, Takayuki Mawatari, Kenta Nishiyama, Hiroko Miyagishi, Kumiko Ishige, and Yoshihisa Ito. "Generation of Cellular Reactive Oxygen Species by Activation of the EP2 Receptor Contributes to Prostaglandin E2-Induced Cytotoxicity in Motor Neuron-Like NSC-34 Cells." Oxidative Medicine and Cellular Longevity 2020 (January 11, 2020): 1–14. http://dx.doi.org/10.1155/2020/6101838.
Full textAbstract:
Amyotrophic lateral sclerosis (ALS) is a devastating motor neuron disease characterized by progressive degeneration of motor neurons in the central nervous system. Prostaglandin E2 (PGE2) plays a pivotal role in the degeneration of motor neurons in human and transgenic models of ALS. We have shown previously that PGE2 directly induces neuronal death through activation of the E-prostanoid (EP) 2 receptor in differentiated NSC-34 cells, a motor neuron-like cell line. In the present study, to clarify the mechanisms underlying PGE2-induced neurotoxicity, we focused on generation of intracellular reactive oxygen species (ROS) and examined the effects of N-acetylcysteine (NAC), a cell-permeable antioxidant, on PGE2-induced cell death in differentiated NSC-34 cells. Dichlorofluorescein (DCF) fluorescence analysis of PGE2-treated cells showed that intracellular ROS levels increased markedly with time, and that this effect was antagonized by a selective EP2 antagonist (PF-04418948) but not a selective EP3 antagonist (L-798,106). Although an EP2-selective agonist, butaprost, mimicked the effect of PGE2, an EP1/EP3 agonist, sulprostone, transiently but significantly decreased the level of intracellular ROS in these cells. MTT reduction assay and lactate dehydrogenase release assay revealed that PGE2- and butaprost-induced cell death were each suppressed by pretreatment with NAC in a concentration-dependent manner. Western blot analysis revealed that the active form of caspase-3 was markedly increased in the PGE2- and butaprost-treated cells. These increases in caspase-3 protein expression were suppressed by pretreatment with NAC. Moreover, dibutyryl-cAMP treatment of differentiated NSC-34 cells caused intracellular ROS generation and cell death. Our data reveal the existence of a PGE2-EP2 signaling-dependent intracellular ROS generation pathway, with subsequent activation of the caspase-3 cascade, in differentiated NSC-34 cells, suggesting that PGE2 is likely a key molecule linking inflammation to oxidative stress in motor neuron-like NSC-34 cells.
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Gelenbe, Erol, and Jean-Michel Fourneau. "Random Neural Networks with Multiple Classes of Signals." Neural Computation 11, no. 4 (May 1, 1999): 953–63. http://dx.doi.org/10.1162/089976699300016520.
Full textAbstract:
By extending the pulsed recurrent random neural network (RNN) discussed in Gelenbe (1989, 1990, 1991), we propose a recurrent random neural network model in which each neuron processes several distinctly characterized streams of “signals” or data. The idea that neurons may be able to distinguish between the pulses they receive and use them in a distinct manner is biologically plausible. In engineering applications, the need to process different streams of information simultaneously is commonplace (e.g., in image processing, sensor fusion, or parallel processing systems). In the model we propose, each distinct stream is a class of signals in the form of spikes. Signals may arrive to a neuron from either the outside world (exogenous signals) or other neurons (endogenous signals). As a function of the signals it has received, a neuron can fire and then send signals of some class to another neuron or to the outside world. We show that the multiple signal class random model with exponential interfiring times, Poisson external signal arrivals, and Markovian signal movements between neurons has product form; this implies that the distribution of its state (i.e., the probability that each neuron of the network is excited) can be computed simply from the solution of a system of 2Cn simultaneous nonlinear equations where C is the number of signal classes and n is the number of neurons. Here we derive the stationary solution for the multiple class model and establish necessary and sufficient conditions for the existence of the stationary solution. The recurrent random neural network model with multiple classes has already been successfully applied to image texture generation (Atalay & Gelenbe, 1992), where multiple signal classes are used to model different colors in the image.