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In vivo transgenic expression of collybistin in neurons of the rat cerebral cortex
Author(s) -
Fekete Christopher D.,
Goz Roman U.,
Dinallo Sean,
Miralles Celia P.,
Chiou TzuTing,
Bear John,
Fiondella Christopher G.,
LoTurco Joseph J.,
De Blas Angel L.
Publication year - 2017
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.24137
Subject(s) - gephyrin , biology , glycine receptor , neuroscience , gabaergic , hippocampal formation , inhibitory postsynaptic potential , postsynaptic potential , cerebral cortex , in vivo , gabaa receptor , microbiology and biotechnology , receptor , glycine , amino acid , biochemistry , genetics
Collybistin (CB) is a guanine nucleotide exchange factor selectively localized to γ‐aminobutyric acid (GABA)ergic and glycinergic postsynapses. Active CB interacts with gephyrin, inducing the submembranous clustering and the postsynaptic accumulation of gephyrin, which is a scaffold protein that recruits GABA A receptors (GABA A Rs) at the postsynapse. CB is expressed with or without a src homology 3 (SH3) domain. We have previously reported the effects on GABAergic synapses of the acute overexpression of CB SH3− or CB SH3+ in cultured hippocampal (HP) neurons. In the present communication, we are studying the effects on GABAergic synapses after chronic in vivo transgenic expression of CB2 SH3− or CB2 SH3+ in neurons of the adult rat cerebral cortex. The embryonic precursors of these cortical neurons were in utero electroporated with CB SH3− or CB SH3+ DNAs, migrated to the appropriate cortical layer, and became integrated in cortical circuits. The results show that: 1) the strength of inhibitory synapses in vivo can be enhanced by increasing the expression of CB in neurons; and 2) there are significant differences in the results between in vivo and in culture studies. J. Comp. Neurol. 525:1291–1311, 2017. © 2016 Wiley Periodicals, Inc.