A Model of Information Carried over a Neuron Soma

Quantal secretion at nerve terminals in mature muscles depends on the number of terminal branches and the size of release sites (sect. VB4). The physical length of SBL determines the length of terminal branch that can be laid down in a reinnervation experiment (sect. IVA4). A limit is set on the total length of terminal branches formed by a motoneuron; this limit is determined by the amount of TF (sect. IVB) made available from the neuron soma to the peripheral branches of the neuron (sect. VC). As a result of this limit, not all SBL needs to be occupied at a site by terminal branches. The SBL eventually disappears if it is not occupied by terminal branches (sect. IVA2). If a muscle is relatively inactive, it synthesizes and releases at synaptic sites additional amounts of NGF, which stimulates the growth of additional terminal branches. These may secrete sufficient amounts of AF to induce the formation of new SRs with associated SBL. In these circumstances a new synaptic site is formed or an extension of an existing site is created. If the size of a motor unit is decreased, the enhanced release of TF at the remaining terminals ensures that each occupies all the SBL at the synaptic site. Furthermore the enhanced release of AF per terminal induces more SBL, allowing additional terminal branches on the muscle cells to be established. Neither of these changes occurs unless the threshold amount of NGF is available from the muscle to stabilize the terminals. If this condition is met, an increase in quantal release per terminal occurs after reducing the size of a motor unit (sect. VC). An increase in quantal release per terminal also occurs after inactivation of a muscle. Such inactivation leads to an enhanced release of NGF per synaptic site (sect. VA4). Extra terminals may then form if sufficient TF is available; these may innervate existing but empty synaptic sites. In rare circumstances the extra terminal may induce SBL and innervate these new sites if sufficient AF is available. In both cases the quantal release per terminal increases. During development the secretory capacity of the axon terminal depends on the muscle cells with which it synapses. This secretory capacity can be enhanced either by increasing the number of terminal branch pairs or by increasing the secretory capacity of individual release sites. If two terminals innervate a synaptic site, their individual secretory capacity is reduced--in these circumstances the terminal's secretory capacity depends on the amount of NGF available to the terminal; two terminals must share their NGF.

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Evidence That Long-Term Hyperexcitability of the Sensory Neuron Soma Induced by Nerve Injury in Aplysia Is Adaptive

Journal of Neurophysiology ◽

10.1152/jn.00169.2005 ◽

2005 ◽

Vol 94 (3) ◽

pp. 2218-2230 ◽

Cited By ~ 9

Author(s):

Xavier Gasull ◽

Xiaogang Liao ◽

Michael F. Dulin ◽

Cynthia Phelps ◽

Edgar T. Walters

Keyword(s):

Sensory Neuron ◽

Sensory Input ◽

Aplysia Californica ◽

Afferent Pathway ◽

Sensory Deficits ◽

Diverse Species ◽

Peripheral Injury ◽

Adaptive Consequences ◽

Neuron Soma

Peripheral axotomy induces long-term hyperexcitability (LTH) of centrally located sensory neuron (SN) somata in diverse species. In mammals this LTH can promote spontaneous activity of pain-related SNs, and such activity may contribute to neuropathic pain and hyperalgesia. However, few axotomized SN somata begin to fire spontaneously in any species, and why so many SNs display soma LTH after axotomy remains a mystery. Is soma LTH a side effect of injury with pathological but no adaptive consequences, or was this response selected during evolution for particular functions? A hypothesis for one function of soma LTH in nociceptive SNs in Aplysia californica is proposed: after peripheral injury that produces partial axotomy of some SNs, compensation for sensory deficits and protective sensitization are achieved by facilitating afterdischarge near the soma, which amplifies sensory input from injured peripheral fields. Four predictions of this hypothesis were confirmed in SNs that innervate the tail. First, LTH of SN somata was induced by a relatively natural axotomizing event—a small cut across part of the tail in the absence of anesthesia. Second, soma LTH was selectively expressed in SNs having axons in cut or crushed nerves rather than nearby, uninjured nerves. Third, after several weeks soma LTH began to reverse when functional recovery of the interrupted afferent pathway was shown by reestablishment of a centrally mediated siphon reflex. Fourth, axotomized SNs developed central afterdischarge that amplified sensory discharge coming from the periphery, and the afterdepolarization underlying this afterdischarge was enhanced by previous axotomy.

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Axonal spike generation near the giant neuron soma computed by the Hodgkin-Huxley equation

Neurophysiology ◽

10.1007/bf01063247 ◽

1976 ◽

Vol 7 (4) ◽

pp. 328-332

Author(s):

I. Z. Zamekhovskii ◽

A. N. Degtyarenko

Keyword(s):

Spike Generation ◽

Giant Neuron ◽

Huxley Equation ◽

Neuron Soma

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Measurement of neuron soma size by fluorescent Nissl stain

Protocol Exchange ◽

10.1038/protex.2012.022 ◽

2012 ◽

Author(s):

James Cronk ◽

Noel Derecki ◽

Jonathan Kipnis

Keyword(s):

Soma Size ◽

Nissl Stain ◽

Neuron Soma

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A Model of Neuropeptide Transport in Various Types of Nerve Terminals Containing En Passant Boutons: The Effect of the Rate of Neuropeptide Production in the Neuron Soma

Volume 3: Biomedical and Biotechnology Engineering ◽

10.1115/imece2015-50439 ◽

2015 ◽

Author(s):

I. A. Kuznetsov ◽

A. V. Kuznetsov

Keyword(s):

Mathematical Model ◽

Production Rate ◽

Retrograde Transport ◽

Dense Core ◽

Experimental Results ◽

Nerve Terminals ◽

Dense Core Vesicles ◽

Type Iii ◽

Neuropeptide Release ◽

Neuron Soma

After being synthesized in the soma, neuropeptides are packaged in dense core vesicles (DCVs) and transported toward nerve terminals. It is known, from published experimental results, that in terminals with type Ib boutons DCVs circulate in the terminal, undergoing repeated anterograde and retrograde transport, while in type III terminals DCVs do not circulate in the terminal. Our goal here is to investigate whether the increased DCV production in the soma can lead to the appearance of DCV circulation in type III boutons. For this purpose we developed a mathematical model that simulates DCV transport in various terminals. Our model reproduces some important experimental results, such as those concerning DCV circulation in type Ib and type III terminals. We used the developed model to make testable predictions. The model predicts that an increased DCV production rate in the soma leads to increased DCV circulation in type Ib boutons and to the appearance of DCV circulation in type III boutons. The model also predicts that there are different stages in the development of DCV circulation in the terminals after they were depleted of DCVs due to neuropeptide release.

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EphrinB2-EphB2 signaling for dendrite protection after neuronal ischemia in vivo and oxygen-glucose deprivation in vitro

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x20973119 ◽

2020 ◽

pp. 0271678X2097311

Author(s):

Zhanyang Yu ◽

Wenlu Li ◽

Jing Lan ◽

Kazuhide Hayakawa ◽

Xunming Ji ◽

...

Keyword(s):

Cerebral Ischemia ◽

Mouse Model ◽

Therapeutic Potential ◽

Focal Cerebral Ischemia ◽

Ischemic Injury ◽

Glucose Deprivation ◽

Oxygen Glucose Deprivation ◽

Neuron Soma

In order to rescue neuronal function, neuroprotection should be required not only for the neuron soma but also the dendrites. Here, we propose the hypothesis that ephrin-B2-EphB2 signaling may be involved in dendritic degeneration after ischemic injury. A mouse model of focal cerebral ischemia with middle cerebral artery occlusion (MCAO) method was used for EphB2 signaling test in vivo. Primary cortical neuron culture and oxygen-glucose deprivation were used to assess EphB2 signaling in vitro. siRNA and soluble ephrin-B2 ectodomain were used to block ephrin-B2-Ephb2 signaling. In the mouse model of focal cerebral ischemia and in neurons subjected to oxygen-glucose deprivation, clustering of ephrin-B2 with its receptor EphB2 was detected. Phosphorylation of EphB2 suggested activation of this signaling pathway. RNA silencing of EphB2 prevented neuronal death and preserved dendritic length. To assess therapeutic potential, we compared the soluble EphB2 ectodomain with the NMDA antagonist MK801 in neurons after oxygen-glucose deprivation. Both agents equally reduced lactate dehydrogenase release as a general marker of neurotoxicity. However, only soluble EphB2 ectodomain protected the dendrites. These findings provide a proof of concept that ephrin-B2-EphB2 signaling may represent a novel therapeutic target to protect both the neuron soma as well as dendrites against ischemic injury.

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Simulating a Neuron Soma

The Book of GENESIS ◽

10.1007/978-1-4684-0189-9_12 ◽

1995 ◽

pp. 203-213

Author(s):

David Beeman

Keyword(s):

Neuron Soma

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NMDA Receptor Subunits Change after Synaptic Plasticity Induction and Learning and Memory Acquisition

Neural Plasticity ◽

10.1155/2018/5093048 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11 ◽

Cited By ~ 27

Author(s):

María Verónica Baez ◽

Magalí Cecilia Cercato ◽

Diana Alicia Jerusalinsky

Keyword(s):

Synaptic Plasticity ◽

Learning And Memory ◽

De Novo ◽

Physiological Profile ◽

Regulatory Subunits ◽

Neuronal Soma ◽

Synaptic Changes ◽

Memory Acquisition ◽

Activity Dependent ◽

Neuron Soma

NMDA ionotropic glutamate receptors (NMDARs) are crucial in activity-dependent synaptic changes and in learning and memory. NMDARs are composed of two GluN1 essential subunits and two regulatory subunits which define their pharmacological and physiological profile. In CNS structures involved in cognitive functions as the hippocampus and prefrontal cortex, GluN2A and GluN2B are major regulatory subunits; their expression is dynamic and tightly regulated, but little is known about specific changes after plasticity induction or memory acquisition. Data strongly suggest that following appropriate stimulation, there is a rapid increase in surface GluN2A-NMDAR at the postsynapses, attributed to lateral receptor mobilization from adjacent locations. Whenever synaptic plasticity is induced or memory is consolidated, more GluN2A-NMDARs are assembled likely using GluN2A from a local translation and GluN1 from local ER. Later on, NMDARs are mobilized from other pools, and there are de novo syntheses at the neuron soma. Changes in GluN1 or NMDAR levels induced by synaptic plasticity and by spatial memory formation seem to occur in different waves of NMDAR transport/expression/degradation, with a net increase at the postsynaptic side and a rise in expression at both the spine and neuronal soma. This review aims to put together that information and the proposed hypotheses.

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The morphology and distribution of ‘Kolmer–Agduhr cells’, a class of cerebrospinal-fluid-contacting neurons revealed in the frog embryo spinal cord by GABA immunocytochemistry

Proceedings of the Royal Society of London Series B Biological Sciences ◽

10.1098/rspb.1987.0068 ◽

1987 ◽

Vol 232 (1267) ◽

pp. 193-203 ◽

Cited By ~ 68

Keyword(s):

Spinal Cord ◽

Cerebrospinal Fluid ◽

Central Canal ◽

Ventral Part ◽

Fixed Tissue ◽

Frog Embryo ◽

Axonal Projections ◽

Embryonic Origin ◽

Immunocytochemical Method ◽

Neuron Soma

An immunocytochemical method that localizes GABA in glutaraldehyde- fixed tissue has been applied to the study of the Xenopus embryo spinal cord. This procedure stained an anatomical class of neuron, which had somata forming two more or less continuous rows, one on either side of the central canal, in the ventral part of the spinal cord. The total number of stained neurons in the stage 37–38 embryo spinal cord was about 300. The medial surface of the soma protruded into the central canal and had a brush border which electron microscope studies showed to consist of many microvilli or stereocilia and one or two cilia. The external end of the neuron soma had an ipsilateral ascending axon. The axon of many of these neurons had a growth cone which was also clearly stained. We propose calling these neurons ‘Kolmer–Agduhr cells’ after W. Kolmer and E. Agduhr who described them in the spinal cords of many vertebrate classes. Their early embryonic origin, GABA-like immunoreactivity, axonal projections and distribution as a whole population have not previously been known.

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