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The Ca_V1.2 G406R mutation decreases synaptic inhibition and alters L-type Ca²⁺ channel-dependent LTP at hippocampal synapses in a mouse model of Timothy Syndrome.

ABSTRACT: Genetic alterations in autism spectrum disorders (ASD) frequently disrupt balance between synaptic excitation and inhibition and alter plasticity in the hippocampal CA1 region. Individuals with Timothy Syndrome (TS), a genetic disorder caused by Ca_V1.2 L-type Ca²⁺ channel (LTCC) gain-of function mutations, such as G406R, exhibit social deficits, repetitive behaviors, and cognitive impairments characteristic of ASD that are phenocopied in TS2-neo mice expressing G406R. Here, we characterized hippocampal CA1 synaptic function in male TS2-neo mice and found basal excitatory transmission was slightly increased and inhibitory transmission strongly decreased. We also found distinct impacts on two LTCC-dependent forms of long-term potentiation (LTP) synaptic plasticity that

SUBMITTER: Sanderson JL

PROVIDER: S-EPMC9644825 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature

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The Ca_V1.2 G406R mutation decreases synaptic inhibition and alters L-type Ca²⁺ channel-dependent LTP at hippocampal synapses in a mouse model of Timothy Syndrome.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

The CaV1.2 G406R mutation decreases synaptic inhibition and alters L-type Ca2+ channel-dependent LTP at hippocampal synapses in a mouse model of Timothy Syndrome.

OmicsDI is part of the ELIXIR infrastructure

Tweets

The Ca_V1.2 G406R mutation decreases synaptic inhibition and alters L-type Ca²⁺ channel-dependent LTP at hippocampal synapses in a mouse model of Timothy Syndrome.