The role of voltage‐gated calcium channels in neurotransmitter phenotype specification: Coexpression and functional analysis inXenopus laevis

Autor: Lauren E. Miller, Wendy A. Herbst, Brittany B. Lewis, Margaret S. Saha
Rok vydání: 2014
Předmět:
Vesicular Inhibitory Amino Acid Transport Proteins
Xenopus
embryo
Action Potentials
Glutamic Acid
chemistry.chemical_element
glutamate
Xenopus Proteins
Calcium
calcium activity
Inhibitory postsynaptic potential
Retina
GABA
Xenopus laevis
03 medical and health sciences
Glutamatergic
Calcium Channels
N-Type
0302 clinical medicine
Animals
GABAergic Neurons
development
Research Articles
Cells
Cultured
In Situ Hybridization
Fluorescence
gamma-Aminobutyric Acid
030304 developmental biology
Neurons
Neurotransmitter Agents
0303 health sciences
biology
Voltage-dependent calcium channel
General Neuroscience
Cranial Nerves
T-type calcium channel
Glutamate receptor
Brain
biology.organism_classification
Spinal Cord
chemistry
Vesicular Glutamate Transport Protein 1
Excitatory postsynaptic potential
Calcium Channels
Neuroscience
030217 neurology & neurosurgery
Zdroj: The Journal of Comparative Neurology
ISSN: 1096-9861
0021-9967
Popis: Calcium activity has been implicated in many neurodevelopmental events, including the specification of neurotransmitter phenotypes. Higher levels of calcium activity lead to an increased number of inhibitory neural phenotypes, whereas lower levels of calcium activity lead to excitatory neural phenotypes. Voltage-gated calcium channels (VGCCs) allow for rapid calcium entry and are expressed during early neural stages, making them likely regulators of activity-dependent neurotransmitter phenotype specification. To test this hypothesis, multiplex fluorescent in situ hybridization was used to characterize the coexpression of eight VGCC α1 subunits with the excitatory and inhibitory neural markers xVGlut1 and xVIAAT in Xenopus laevis embryos. VGCC coexpression was higher with xVGlut1 than xVIAAT, especially in the hindbrain, spinal cord, and cranial nerves. Calcium activity was also analyzed on a single-cell level, and spike frequency was correlated with the expression of VGCC α1 subunits in cell culture. Cells expressing Cav2.1 and Cav2.2 displayed increased calcium spiking compared with cells not expressing this marker. The VGCC antagonist diltiazem and agonist (−)BayK 8644 were used to manipulate calcium activity. Diltiazem exposure increased the number of glutamatergic cells and decreased the number of γ-aminobutyric acid (GABA)ergic cells, whereas (−)BayK 8644 exposure decreased the number of glutamatergic cells without having an effect on the number of GABAergic cells. Given that the expression and functional manipulation of VGCCs are correlated with neurotransmitter phenotype in some, but not all, experiments, VGCCs likely act in combination with a variety of other signaling factors to determine neuronal phenotype specification. J. Comp. Neurol. 522:2518–2531, 2014.
Databáze: OpenAIRE
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