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 |
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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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