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Baclofen blocks postsynaptic inhibition but not the effect of muscimol in the olfactory cortex
Author(s) -
Scholfield C.N.
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb09365.x
Subject(s) - inhibitory postsynaptic potential , excitatory postsynaptic potential , baclofen , postsynaptic potential , chemistry , neuroscience , muscimol , biophysics , pharmacology , gabaa receptor , biology , agonist , biochemistry , receptor
1 The olfactory cortex slice preparation from the guinea‐pig brain was used to study the effects of baclofen on inhibition using intracellular recording. Stimulation of the lateral olfactory tract activates sequentially excitatory and inhibitory pathways. Inhibition is manifest as a period of increased membrane conductance (termed postsynaptic inhibitory conductance, IPSC). 2 Bath application of baclofen (0.2–500 μ m ) reversibly blocked the IPSC. Baclofen also produced a secondary increase in the amplitude and duration of the initial excitatory postsynaptic potential. 3 Baclofen (0.5–500 μ m ) slightly augmented the ability of bath‐applied muscimol to increase the resting membrane conductance. Baclofen had no effect on cell excitability and membrane potential and no effect on the action of γ‐aminobutyric acid (GABA), noradrenaline, glycine, taurine or 5‐hydroxytrypamine. 4 These results confirm previous suggestions that baclofen at low concentrations acts outside the GABA receptor mediating the IPSC perhaps by reducing the release of the excitatory transmitter activating the inhibitory interneurones.