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Differential Distribution of Ca(2+) Channel Subtypes at Retinofugal Synapses

Retinofugal synapses serve as models for understanding how sensory signals from the periphery are relayed to the brain. Past studies have focused primarily on understanding the postsynaptic glutamatergic receptor subtypes involved in signal transmission, but the mechanisms underlying glutamate relea...

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Detalles Bibliográficos
Autores principales: Govindaiah, Gubbi, Campbell, Peter W., Guido, William
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Society for Neuroscience 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7768275/
https://www.ncbi.nlm.nih.gov/pubmed/33097488
http://dx.doi.org/10.1523/ENEURO.0293-20.2020
Descripción
Sumario:Retinofugal synapses serve as models for understanding how sensory signals from the periphery are relayed to the brain. Past studies have focused primarily on understanding the postsynaptic glutamatergic receptor subtypes involved in signal transmission, but the mechanisms underlying glutamate release at presynaptic retinal terminals remains largely unknown. Here we explored how different calcium (Ca(2+)) channel subtypes regulate glutamatergic excitatory synaptic transmission in two principal retinorecipient targets, the dorsal lateral geniculate nucleus (dLGN) and superior colliculus (SC) of the mouse. We used an in vitro slice preparation to record the synaptic responses of dLGN and SC neurons evoked by the electrical stimulation of optic tract (OT) fibers before and during the application of selective Ca(2+) channel blockers. We found that synaptic responses to paired or repetitive OT stimulation were highly sensitive to extracellular levels of Ca(2+) and to selective antagonists of voltage gated Ca(2+) channels, indicating that these channels regulate the presynaptic release of glutamate at retinal synapses in both dLGN and SC. Bath application of selective Ca(2+) channel blockers revealed that P/Q-type Ca(2+) channels primarily operate to regulate glutamate release at retinal synapses in dLGN, while N-type Ca(2+) channels dominate release in the SC.