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Different GABA B ‐Mediated Effects on Protein Kinase C Activity and Immunoreactivity in Neonatal and Adult Rat Hippocampal Slices
Author(s) -
Tremblay E.,
BenAri Y.,
Roisin M. P.
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.65020863.x
Subject(s) - hippocampal formation , neuroscience , protein kinase a , chemistry , kinase , hippocampus , endocrinology , medicine , biology , biochemistry
The effects of GABA on protein kinase C (PKC) were investigated in rat hippocampal slices at various postnatal ages [postnatal day (P) 1‐P60]. At P4, GABA (300 µ M ) induced a rapid (in 1–2 min) 40–50% increase of PKC activity in the membrane fraction and a decrease in the cytosol. These effects were mediated by GABA B receptors because (a) they were neither blocked by 10 µ M bicuculline nor reproduced by 10 µ M isoguvacine and (b) they were mimicked by the GABA B agonist baclofen (3–30 µ M ), an effect fully antagonized by the GABA B antagonist 2‐hydroxysaclofen (10 µ M ). A baclofen‐induced increased PKC activity in the membrane fraction was only present during the early postnatal period (P1–P14); it was associated with a translocation from the cytosol to the membrane of the immunoreactivity of some PKC isoforms (α‐, β‐, and ε‐PKCs). In contrast, after P21, PKC activity and α‐, β‐, ε‐, and γ‐PKC immunoreactivities were decreased by baclofen in the membrane fraction and increased in the cytosol. These results suggest that the stimulation of GABA B receptors differentially modulates PKC activity via distinct second messenger pathways in developing and mature hippocampi.