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Enhanced long-term potentiation and impaired learning in mice lacking alternative exon 33 of Ca_V1.2 calcium channel.

ABSTRACT: The CACNA1C (calcium voltage-gated channel subunit alpha 1 C) gene that encodes the Ca_V1.2 channel is a prominent risk gene for neuropsychiatric and neurodegenerative disorders with cognitive and social impairments like schizophrenia, bipolar disorders, depression and autistic spectrum disorders (ASD). We have shown previously that mice with exon 33 deleted from Ca_V1.2 channel (Ca_V1.2-exon 33^-/-) displayed increased Ca_V1.2 current density and single channel open probability in cardiomyocytes, and were prone to develop arrhythmia. As Ca²⁺ entry through Ca_V1.2 channels activates gene transcription in response to synaptic activity, we were intrigued to explore the possible role of Cav1.2_Δ₃₃ chan

SUBMITTER: Navakkode S

PROVIDER: S-EPMC8748671 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature

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Enhanced long-term potentiation and impaired learning in mice lacking alternative exon 33 of Ca_V1.2 calcium channel.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Enhanced long-term potentiation and impaired learning in mice lacking alternative exon 33 of CaV1.2 calcium channel.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Enhanced long-term potentiation and impaired learning in mice lacking alternative exon 33 of Ca_V1.2 calcium channel.