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

Channels (Austin). 2020 Dec;14(1):287-293. doi: 10.1080/19336950.2020.1807851.

Abstract

CACNA1 C, which codes for the Cav1.2 isoform of L-type Ca2+ channels (LTCCs), is a prominent risk gene in neuropsychiatric and neurodegenerative conditions. A role forLTCCs, and Cav1.2 in particular, in transcription-dependent late long-term potentiation (LTP) has long been known. Here, we report that elimination of Cav1.2 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 Cav1.2channels in LTP broadens understanding of synaptic plasticity and identifies a new cellular phenotype for exploring treatment strategies for cognitive dysfunction.

Keywords: Calcium; Cav1.2; long-term potentiation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium Channels, L-Type / metabolism*
  • Electrophysiology
  • Hippocampus / metabolism*
  • Hippocampus / physiology*
  • In Vitro Techniques
  • Long-Term Potentiation / physiology*
  • Male
  • Mice
  • Transcranial Magnetic Stimulation*

Substances

  • Calcium Channels, L-Type
  • L-type calcium channel alpha(1C)