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GABAB receptor‐mediated inhibition of spontaneous inhibitory synaptic currents in rat midbrain culture.
Author(s) -
Rohrbacher J,
Jarolimek W,
Lewen A,
Misgeld U
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1997.sp022055
Subject(s) - gabab receptor , inhibitory postsynaptic potential , excitatory postsynaptic potential , baclofen , tetrodotoxin , postsynaptic potential , chemistry , neuroscience , pharmacology , biology , agonist , biophysics , receptor , biochemistry
1. Tight‐seal, whole‐cell recording was used to study GABAB receptor‐mediated inhibition of spontaneous inhibitory synaptic currents in cultured rat midbrain neurones. 2. Spontaneous miniature inhibitory postsynaptic currents (mIPSCs) were recorded in tetrodotoxin (TTX), Cd2+ and Ba2+. (R)‐(‐)‐baclofen reduced the frequency of mIPSCs through a presynaptic mechanism. The EC50 for this effect was 7 microM. It was antagonized by the GABAB receptor antagonist CGP55845A (0.5 microM). 3. In pertussis toxin (PTX)‐treated cultures, some GABAB receptor‐mediated reduction of the frequency of mIPSCs persisted. In contrast, PTX treatment totally abolished inhibition of miniature excitatory postsynaptic currents (mEPSCs). 4. In PTX‐treated cultures, a saturating concentration of (R)‐(‐)‐baclofen inhibited action potential‐generated IPSCs but no EPSCs. 5. PTX treatment abolished the (R)‐(‐)‐baclofen‐mediated inhibition of high voltage‐activated somatic Ca2+ currents and of spontaneous IPSCs depending on presynaptic Ca2+ entry. 6. We conclude that cellular mechanisms underlying GABAB receptor‐mediated inhibition of mIPSCs contribute to auto‐inhibition of GABA release.