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Article

Synaptic plasticity deficits in a mouse model of Timothy syndrome: LTP saturation and its pharmacological rescue by nifedipine.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie - 1 Mar 2025

Lado Wudu, Wu Xiaoping, Choi Sejoon, Dong Yuxin, Yang Guang, Arancio Ottavio, Tempia Filippo, Miniaci Maria Concetta, Sulzer David, Mosharov Eugene, Tang Guomei

Abstract excerpt

Timothy syndrome (TS) is a multisystem disorder characterized by cardiovascular abnormalities and a spectrum of neuropsychiatric symptoms, including language impairment, seizure, cognitive disability and autism. TS is caused by gain of function mutations in the CACNA1C gene that encodes the CaV1.2 L-type calcium channel. TS mutations have been reported to disrupt hippocampal long-term potentiation (LTP), a...

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Identifiers

PMID: 39938350
DOI: 10.1016/j.biopha.2025.117896
PMCID: PMC12744305

Genes

CACNA1C

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 25 Oct 2026.

Related research

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Research trail→

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Synaptic plasticity deficits in a mouse model of Timothy syndrome: LTP saturation and its pharmacological rescue by nifedipine.PMID 39938350Read ↗

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.Semantic proximity Read ↗

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Aberrant calcium channel splicing drives defects in cortical differentiation in Timothy syndrome.Semantic proximity Read ↗

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Disruptions in Primary Visual Cortex Physiology and Function in a Mouse Model of Timothy SyndromeSemantic proximity Read ↗

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Calcium sensor regulation of the CaV2.1 Ca2+ channel contributes to long-term potentiation and spatial learning.Semantic proximity Read ↗

CACNA1C TS-II variants alter single-cell dynamics in computational models of cortical pyramidal cellsSemantic proximity Read ↗

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The Timothy syndrome mutation differentially affects voltage- and calcium-dependent inactivation of CaV1.2 L-type calcium channels.Semantic proximity Read ↗

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