Action of Ca2+ agonists/antagonists in mammalian peripheral neurons

NG2-glia, also called Oligodendrocyte Precursor Cells (OPCs), account for approximately 5%-10% of the cells in the developing and adult brain and constitute the fifth major cell population in the central nervous system. NG2-glia express receptors and ion channels involved in rapid modulation of neuronal activities and signaling with neuronal synapses, which have functional significance in both physiological and pathological states. NG2-glia participate in quick signaling with peripheral neurons via direct synaptic touches in the developing and mature central nervous system. These distinctive glia perform the unique function of proliferating and differentiating into oligodendrocytes in the early developing brain, which is critical for axon myelin formation. In response to injury, NG2-glia can proliferate, migrate to the lesions, and differentiate into oligodendrocytes to form new myelin sheaths, which wrap around damaged axons and result in functional recovery. The capacity of NG2-glia to regulate their behavior and dynamics in response to neuronal activity and disease indicate their critical role in myelin preservation and remodeling in the physiological state and in repair in the pathological state. In this review, we provide a detailed summary of the characteristics of NG2-glia, including their heterogeneity, the regulators of their proliferation, and the modulators of their differentiation into oligodendrocytes.

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C-terminal domain small phosphatase 1 (CTDSP1) regulates growth factor expression and axonal regeneration in peripheral nerve tissue

Scientific Reports ◽

10.1038/s41598-021-92822-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Noreen M. Gervasi ◽

Alexander Dimtchev ◽

Desraj M. Clark ◽

Marvin Dingle ◽

Alexander V. Pisarchik ◽

...

Keyword(s):

Chronic Pain ◽

Peripheral Nerve ◽

Neurotrophic Factor ◽

Axon Growth ◽

Nerve Tissue ◽

Mesenchymal Progenitor Cells ◽

Drg Neurons ◽

Peripheral Neurons ◽

Terminal Domain ◽

Factor Expression

AbstractPeripheral Nerve Injury (PNI) represents a major clinical and economic burden. Despite the ability of peripheral neurons to regenerate their axons after an injury, patients are often left with motor and/or sensory disability and may develop chronic pain. Successful regeneration and target organ reinnervation require comprehensive transcriptional changes in both injured neurons and support cells located at the site of injury. The expression of most of the genes required for axon growth and guidance and for synapsis formation is repressed by a single master transcriptional regulator, the Repressor Element 1 Silencing Transcription factor (REST). Sustained increase of REST levels after injury inhibits axon regeneration and leads to chronic pain. As targeting of transcription factors is challenging, we tested whether modulation of REST activity could be achieved through knockdown of carboxy-terminal domain small phosphatase 1 (CTDSP1), the enzyme that stabilizes REST by preventing its targeting to the proteasome. To test whether knockdown of CTDSP1 promotes neurotrophic factor expression in both support cells located at the site of injury and in peripheral neurons, we transfected mesenchymal progenitor cells (MPCs), a type of support cells that are present at high concentrations at the site of injury, and dorsal root ganglion (DRG) neurons with REST or CTDSP1 specific siRNA. We quantified neurotrophic factor expression by RT-qPCR and Western blot, and brain-derived neurotrophic factor (BDNF) release in the cell culture medium by ELISA, and we measured neurite outgrowth of DRG neurons in culture. Our results show that CTDSP1 knockdown promotes neurotrophic factor expression in both DRG neurons and the support cells MPCs, and promotes DRG neuron regeneration. Therapeutics targeting CTDSP1 activity may, therefore, represent a novel epigenetic strategy to promote peripheral nerve regeneration after PNI by promoting the regenerative program repressed by injury-induced increased levels of REST in both neurons and support cells.

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Novel Insights on the Role of Nitric Oxide in the Ovary: A Review of the Literature

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph18030980 ◽

2021 ◽

Vol 18 (3) ◽

pp. 980

Author(s):

Maria Cristina Budani ◽

Gian Mario Tiboni

Keyword(s):

Nitric Oxide ◽

In Vivo Studies ◽

Published Data ◽

Vitro Fertilization ◽

Peripheral Neurons ◽

Relevant Role ◽

Oocyte Meiotic Maturation

Nitric oxide (NO) is formed during the oxidation of L-arginine to L-citrulline by the action of multiple isoenzymes of NO synthase (NOS): neuronal NOS (nNOS), endotelial NOS (eNOS), and inducible NOS (iNOS). NO plays a relevant role in the vascular endothelium, in central and peripheral neurons, and in immunity and inflammatory systems. In addition, several authors showed a consistent contribution of NO to different aspects of the reproductive physiology. The aim of the present review is to analyse the published data on the role of NO within the ovary. It has been demonstrated that the multiple isoenzymes of NOS are expressed and localized in the ovary of different species. More to the point, a consistent role was ascribed to NO in the processes of steroidogenesis, folliculogenesis, and oocyte meiotic maturation in in vitro and in vivo studies using animal models. Unfortunately, there are few nitric oxide data for humans; there are preliminary data on the implication of nitric oxide for oocyte/embryo quality and in-vitro fertilization/embryo transfer (IVF/ET) parameters. NO plays a remarkable role in the ovary, but more investigation is needed, in particular in the context of human ovarian physiology.

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Migrating into Genomics with the Neural Crest

Advances in Biology ◽

10.1155/2014/264069 ◽

2014 ◽

Vol 2014 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

Marianne E. Bronner

Keyword(s):

Neural Crest ◽

Gene Regulatory Network ◽

Regulatory Network ◽

Neural Crest Cells ◽

Embryonic Cell ◽

Putative Gene ◽

Peripheral Neurons ◽

Neural Plate Border ◽

The Central Nervous System ◽

Gene Regulatory

Neural crest cells are a fascinating embryonic cell type, unique to vertebrates, which arise within the central nervous system but emigrate soon after its formation and migrate to numerous and sometimes distant locations in the periphery. Following their migratory phase, they differentiate into diverse derivatives ranging from peripheral neurons and glia to skin melanocytes and craniofacial cartilage and bone. The molecular underpinnings underlying initial induction of prospective neural crest cells at the neural plate border to their migration and differentiation have been modeled in the form of a putative gene regulatory network. This review describes experiments performed in my laboratory in the past few years aimed to test and elaborate this gene regulatory network from both an embryonic and evolutionary perspective. The rapid advances in genomic technology in the last decade have greatly expanded our knowledge of important transcriptional inputs and epigenetic influences on neural crest development. The results reveal new players and new connections in the neural crest gene regulatory network and suggest that it has an ancient origin at the base of the vertebrate tree.

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Characterization of Tusc5, an adipocyte gene co-expressed in peripheral neurons

Molecular and Cellular Endocrinology ◽

10.1016/j.mce.2007.06.005 ◽

2007 ◽

Vol 276 (1-2) ◽

pp. 24-35 ◽

Cited By ~ 34

Author(s):

Pieter J. Oort ◽

Craig H. Warden ◽

Thomas K. Baumann ◽

Trina A. Knotts ◽

Sean H. Adams

Keyword(s):

Peripheral Neurons

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Cellular studies of peripheral neurons in siphon skin of Aplysia californica

Journal of Neurophysiology ◽

10.1152/jn.1979.42.2.530 ◽

1979 ◽

Vol 42 (2) ◽

pp. 530-557 ◽

Cited By ~ 33

Author(s):

C. H. Bailey ◽

V. F. Castellucci ◽

J. Koester ◽

E. R. Kandel

Keyword(s):

Motor Neurons ◽

Synaptic Input ◽

Firing Pattern ◽

White Cell ◽

Type I ◽

Type Ii ◽

Peripheral Neurons ◽

Peripheral Neuron ◽

Type I Neuron ◽

Kinetics Of

1. To account for the similarity in the kinetics of habituation between the central and peripheral components of siphon withdrawal, we have tested the idea (52) that each centrally located mechanoreceptor sensory neuron sends two branches to siphon motor neurons; one to centrally located siphon motor neurons and a collateral branch that remains in the periphery and innervates the peripheral siphon motor neurons. 2. We have found a group of peripheral siphon motor neurons and tested the connection onto these cells by central mechanoreceptors. In addition, we have defined by various electrophysiological and morphological criteria two general classes of peripheral neurons that lie along the course of the siphon nerve. 3. One class (type I) consists of only a single cell in each animal. This peripheral neuron typically has the largest cell body found lying along the siphon nerve and is the only peripheral nerve cell that appears white when viewed under epi-illumination. The type I neuron often has a highly regular firing pattern, which occurs in the absence of spontaneous synaptic input. The three-dimensional morphology of this neuron suggests a paucity of fine processes, most of which do not arborize and may terminate in the connective tissue sheath. Fine structural observations of the peripheral white cell have revealed the presence of large densecore granules. The peripheral type I neuron is similar in most of its electrophysiological and morphological properties to central neurons postulated to be neurosecretory. The peripheral white cell is, at present, the only peripheral neuron we can identify with certainty as a unique individual. 4. The second class (type II) of peripheral neurons are siphon motor neurons for the peripheral component of the siphon-withdrawal reflex. In contrast to the type I neurons, members of the second class of peripheral neurons possess smaller, more spherical cell bodies that have varying amounts of orange pigmentation and which give rise to a relatively well-developed and arborized dendritic tree. Type II neurons feature an irregular spontaneous firing pattern that is occasionally modulated by a rich spontaneous synaptic input. Peripheral siphon motor neurons have restricted motor fields that produce contraction of the mantle floor and the base of the siphon. Most of the type II neurons were found to be electrically coupled to one another. 5. The peripheral siphon motor neurons resemble the central siphon motor neurons in that they receive a collateral synapse from centrally located mechanoreceptor sensory neurons. This peripheral sensory-to-motor synapse exhibits the same kinetics of decrement as its central counterpart, both of which parallel behavioral habituation. 6. The rich mechanoreceptor input onto the relatively isolated dendritic trees of the peripheral siphon motor neurons provide a uniquely restricted neuropil to study the sensory-to-motor synapse. The peripheral motor neurons may, therefore, be a useful simple preparation for the cellular study of behavioral plasticity.

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