scholarly journals Characterization of Mice with Targeted Deletion of Glycine Receptor Alpha 2

2006 ◽  
Vol 26 (15) ◽  
pp. 5728-5734 ◽  
Author(s):  
T. L. Young-Pearse ◽  
L. Ivic ◽  
A. R. Kriegstein ◽  
C. L. Cepko
Keyword(s):  
Nervous System ◽  
Chloride Channels ◽  
Neuronal Development ◽  
Glycine Receptor ◽  
Receptor Activity ◽  
Rod Photoreceptor ◽  
Targeted Deletion ◽  
Receptor Alpha ◽  
Molecular Alterations ◽  
Electrophysiological Responses

ABSTRACT Glycine receptors are ligand-gated chloride channels that mediate inhibitory neurotransmission in the adult nervous system. During development, glycine receptor alpha 2 (GlyRα2) is expressed in the retina, in the spinal cord, and throughout the brain. Within the cortex, GlyRα2 is expressed in immature cells and these receptors have been shown to be active and excitatory. In the developing retina, inhibition of glycine receptor activity prevents proper rod photoreceptor development. These data suggest that GlyRα2, the developmentally expressed glycine receptor, may play an important role in neuronal development. We have generated mice with a targeted deletion of glycine receptor alpha 2 (Glra2). Although these mice lack expression of GlyRα2, no gross morphological or molecular alterations were observed in the nervous system. In addition, the cerebral cortex does not appear to require glycine receptor activity for proper development, as Glra2 knockout mice did not show any electrophysiological responses to glycine.

scholarly journals Rgs4 is a regulator of mTOR activity required for motoneuron axon outgrowth and neuronal development in zebrafish

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Aya Mikdache ◽  
Marie-José Boueid ◽  
Lorijn van der Spek ◽  
Emilie Lesport ◽  
Brigitte Delespierre ◽  
...  
Keyword(s):  
Nervous System ◽  
G Protein ◽  
Neural Development ◽  
Neuronal Development ◽  
Axon Outgrowth ◽  
Rgs Proteins ◽  
Protein Signaling ◽  
Loss Of Function ◽  
G Protein Coupled

AbstractThe Regulator of G protein signaling 4 (Rgs4) is a member of the RGS proteins superfamily that modulates the activity of G-protein coupled receptors. It is mainly expressed in the nervous system and is linked to several neuronal signaling pathways; however, its role in neural development in vivo remains inconclusive. Here, we generated and characterized a rgs4 loss of function model (MZrgs4) in zebrafish. MZrgs4 embryos showed motility defects and presented reduced head and eye sizes, reflecting defective motoneurons axon outgrowth and a significant decrease in the number of neurons in the central and peripheral nervous system. Forcing the expression of Rgs4 specifically within motoneurons rescued their early defective outgrowth in MZrgs4 embryos, indicating an autonomous role for Rgs4 in motoneurons. We also analyzed the role of Akt, Erk and mechanistic target of rapamycin (mTOR) signaling cascades and showed a requirement for these pathways in motoneurons axon outgrowth and neuronal development. Drawing on pharmacological and rescue experiments in MZrgs4, we provide evidence that Rgs4 facilitates signaling mediated by Akt, Erk and mTOR in order to drive axon outgrowth in motoneurons and regulate neuronal numbers.

scholarly journals KBP interacts with SCG10, linking Goldberg–Shprintzen syndrome to microtubule dynamics and neuronal differentiation

2010 ◽  
Vol 19 (18) ◽  
pp. 3642-3651 ◽  
Author(s):  
Maria M. Alves ◽  
Grzegorz Burzynski ◽  
Jean-Marie Delalande ◽  
Jan Osinga ◽  
Annemieke van der Goot ◽  
...  
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Neuronal Differentiation ◽  
Cortical Neurons ◽  
Neuronal Development ◽  
Direct Interaction ◽  
Clinical Disorder ◽  
Neurite Development

Abstract Goldberg–Shprintzen syndrome (GOSHS) is a rare clinical disorder characterized by central and enteric nervous system defects. This syndrome is caused by inactivating mutations in the Kinesin Binding Protein (KBP) gene, which encodes a protein of which the precise function is largely unclear. We show that KBP expression is up-regulated during neuronal development in mouse cortical neurons. Moreover, KBP-depleted PC12 cells were defective in nerve growth factor-induced differentiation and neurite outgrowth, suggesting that KBP is required for cell differentiation and neurite development. To identify KBP interacting proteins, we performed a yeast two-hybrid screen and found that KBP binds almost exclusively to microtubule associated or related proteins, specifically SCG10 and several kinesins. We confirmed these results by validating KBP interaction with one of these proteins: SCG10, a microtubule destabilizing protein. Zebrafish studies further demonstrated an epistatic interaction between KBP and SCG10 in vivo . To investigate the possibility of direct interaction between KBP and microtubules, we undertook co-localization and in vitro binding assays, but found no evidence of direct binding. Thus, our data indicate that KBP is involved in neuronal differentiation and that the central and enteric nervous system defects seen in GOSHS are likely caused by microtubule-related defects.

Modulation of Nicotinic Receptor Activity in the Central Nervous System

2001 ◽  
Vol 15 ◽  
pp. S19-S25 ◽  
Author(s):  
E. X. Albuquerque ◽  
M. D. Santos ◽  
M. Alkondon ◽  
E. F. R. Pereira ◽  
A. Maelicke
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nicotinic Receptor ◽  
Receptor Activity ◽  
The Central Nervous System

scholarly journals Patch Clamp: A Powerful Technique for Studying the Mechanism of Acupuncture

2012 ◽  
Vol 2012 ◽  
pp. 1-7
Author(s):  
D. Zhang
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Patch Clamp ◽  
Powerful Method ◽  
Patch Clamp Technique ◽  
Powerful Technique ◽  
Molecular Events ◽  
Electrophysiological Responses ◽  
The Central Nervous System ◽  
Patch Clamp Method

Cellular and molecular events can be investigated using electrophysiological techniques. In particular, the patch-clamp method provides detailed information. In addition, the patch-clamp technique has become a powerful method for investigating the mechanisms underlying the effects of acupuncture. In this paper, recent researches on how acupuncture might modulate electrophysiological responses in the central nervous system (CNS) and affect peripheral structures are reviewed.

Investigating the Tissue Specific Expression Patterns of Murine Semaphorins 3C, 4D, 4G, 6A and 7A in Primary Lymphoid Tissues

2001 ◽  
Vol 7 (S2) ◽  
pp. 76-77
Author(s):  
Sreedevi Chalasani ◽  
David Matthes
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Cell Survival ◽  
Neuronal Development ◽  
Expression Patterns ◽  
Human Neutrophils ◽  
Lymphoid Tissues ◽  
Specific Expression ◽  
Est Analysis

Semaphorins are primarily known for the important role they play in the guidance of growth cones during neuronal development. There is evidence, however, that semaphorins are expressed outside the nervous system as well, suggesting a wider scope for semaphorin function. The overall objective of our study is to identify the functions of semaphorins outside central nervous system especially in T cell development. Some of the 20 semaphorins have been shown to have extra-neural functions that include (for different semaphorins) bone differentiation, promotion of B-cell survival and aggregation, and activation of T-cells. Apart from central nervous system statement of most semaphorins, one semaphorin (CD 100) has transcripts in T cells, B cells, neutrophils, monocytes and granulocytes. EST analysis suggests that other semaphorins are expressed in lymphoid tissues such as thymus, spleen, tonsil, and the interfollicular areas and germinal centers of lymph nodes.Semaphorins have been related to several cell survival mechanisms, immunosuppression and promotion of cell death resistance. in preliminary studies our lab found that viral semaphorins inhibit the migration of human T cells and human SEMA3A can inhibit migration of human neutrophils.

scholarly journals Diabetic db/db mice exhibit central nervous system and peripheral molecular alterations as seen in neurological disorders

2013 ◽  
Vol 3 (5) ◽  
pp. e263-e263 ◽  
Author(s):  
A Ernst ◽  
A N Sharma ◽  
K M Elased ◽  
P C Guest ◽  
H Rahmoune ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Disorders ◽  
Molecular Alterations

scholarly journals Distribution of Receptor Activity Modifying Protein (RAMP) mRNAS in the Rat Central Nervous System

2001 ◽  
Vol 1 ◽  
pp. 45-45
Author(s):  
K. R. Oliver ◽  
A. M. Kinsey ◽  
N. Keyvan-Fouladi ◽  
R. Heavens ◽  
A. Wainwright
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Receptor Activity

scholarly journals Drosophila Glia: Models for Human Neurodevelopmental and Neurodegenerative Disorders

2020 ◽  
Vol 21 (14) ◽  
pp. 4859
Author(s):  
Taejoon Kim ◽  
Bokyeong Song ◽  
Im-Soon Lee
Keyword(s):  
Nervous System ◽  
Neurodegenerative Disorders ◽  
Brain Function ◽  
Cell Biology ◽  
Disease Susceptibility ◽  
Neuronal Development ◽  
In Vivo Model ◽  
Health And Disease ◽  
Drosophila Models

Glial cells are key players in the proper formation and maintenance of the nervous system, thus contributing to neuronal health and disease in humans. However, little is known about the molecular pathways that govern glia–neuron communications in the diseased brain. Drosophila provides a useful in vivo model to explore the conserved molecular details of glial cell biology and their contributions to brain function and disease susceptibility. Herein, we review recent studies that explore glial functions in normal neuronal development, along with Drosophila models that seek to identify the pathological implications of glial defects in the context of various central nervous system disorders.

scholarly journals Niacin in the Central Nervous System: An Update of Biological Aspects and Clinical Applications

2019 ◽  
Vol 20 (4) ◽  
pp. 974 ◽  
Author(s):  
Valeria Gasperi ◽  
Matteo Sibilano ◽  
Isabella Savini ◽  
Maria Catani
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nicotinamide Adenine Dinucleotide ◽  
Cell Cycle Progression ◽  
Neuronal Development ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Vitamin B3 ◽  
Traumatic Injuries ◽  
The Central Nervous System

Niacin (also known as “vitamin B3” or “vitamin PP”) includes two vitamers (nicotinic acid and nicotinamide) giving rise to the coenzymatic forms nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). The two coenzymes are required for oxidative reactions crucial for energy production, but they are also substrates for enzymes involved in non-redox signaling pathways, thus regulating biological functions, including gene expression, cell cycle progression, DNA repair and cell death. In the central nervous system, vitamin B3 has long been recognized as a key mediator of neuronal development and survival. Here, we will overview available literature data on the neuroprotective role of niacin and its derivatives, especially focusing especially on its involvement in neurodegenerative diseases (Alzheimer’s, Parkinson’s, and Huntington’s diseases), as well as in other neuropathological conditions (ischemic and traumatic injuries, headache and psychiatric disorders).

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