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

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

Channels (Austin, Tex.) (2020-08-18)
Preethy S Sridharan, Yuan Lu, Richard C Rice, Andrew A Pieper, Anjali M Rajadhyaksha
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.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-NR2B Antibody, Upstate®, from rabbit
Sigma-Aldrich
Anti-NMDAR1 Antibody, rabbit monoclonal, culture supernatant, clone 1.17.2.6, Chemicon®