Impaired GABA_B-mediated presynaptic inhibition increases excitatory strength and alters short-term plasticity in synapsin knockout mice.

ABSTRACT: Synapsins are a family of synaptic vesicle phosphoproteins regulating synaptic transmission and plasticity. SYN1/2 genes are major epilepsy susceptibility genes in humans. Consistently, synapsin I/II/III triple knockout (TKO) mice are epileptic and exhibit severe impairments in phasic and tonic GABAergic inhibition that precede the appearance of the epileptic phenotype. These changes are associated with an increased strength of excitatory transmission that has never been mechanistically investigated. Here, we observed that an identical effect in excitatory transmission could be induced in wild-type (WT) Schaffer collateral-CA1 pyramidal cell synapses by blockade of GABA_B receptors (GABA_BRs). The same treatment was virtually ineffective in TKO slices, suggesting

SUBMITTER: Valente P 

PROVIDER: S-EPMC5685732 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature