Loss of Cav1.2 channels impairs hippocampal theta burst stimulation-induced long-term potentiation

CACNA1 C, which codes for the Ca(v)1.2 isoform of L-type Ca(2+) channels (LTCCs), is a prominent risk gene in neuropsychiatric and neurodegenerative conditions. A role forLTCCs, and Ca(v)1.2 in particular, in transcription-dependent late long-term potentiation (LTP) has long been known. Here, we rep...

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Detalles Bibliográficos
Autores principales: Sridharan, Preethy S., Lu, Yuan, Rice, Richard C, Pieper, Andrew A., Rajadhyaksha, Anjali M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2020
Materias:
Brief Report
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7515572/
https://www.ncbi.nlm.nih.gov/pubmed/32799605
http://dx.doi.org/10.1080/19336950.2020.1807851
Descripción
Sumario:CACNA1 C, which codes for the Ca(v)1.2 isoform of L-type Ca(2+) channels (LTCCs), is a prominent risk gene in neuropsychiatric and neurodegenerative conditions. A role forLTCCs, and Ca(v)1.2 in particular, in transcription-dependent late long-term potentiation (LTP) has long been known. Here, we report that elimination of Ca(v)1.2 channels in glutamatergic neurons also impairs theta burst stimulation (TBS)-induced LTP in the hippocampus, known to be transcription-independent and dependent on N-methyl D-aspartate receptors (NMDARs) and local protein synthesis at synapses. Our expansion of the established role of Ca(v)1.2channels in LTP broadens understanding of synaptic plasticity and identifies a new cellular phenotype for exploring treatment strategies for cognitive dysfunction.

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