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On the presynaptic action of baclofen at inhibitory synapses between cultured rat hippocampal neurones.
Author(s) -
Harrison N L
Publication year - 1990
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.1990.sp017993
Subject(s) - baclofen , inhibitory postsynaptic potential , postsynaptic potential , gabab receptor , neurotransmission , neuroscience , chemistry , hippocampal formation , gabaergic , postsynaptic current , pharmacology , excitatory postsynaptic potential , biology , gabaa receptor , receptor , agonist , biochemistry
1. (‐)Baclofen reduces inhibitory postsynaptic potentials (IPSPs) and the associated synaptic currents (IPSCs) at inhibitory GABAergic synapses between cultured rat hippocampal neurones. The reversal potential for the IPSC is unaltered. 2. The effect of (‐)baclofen is concentration dependent; the EC50 for (‐)baclofen is approximately 5 microM. 3. Statistical analyses of the amplitude fluctuations of the IPSC in the presence of (‐)baclofen suggested a presynaptic location for the depression of synaptic transmission by (‐)baclofen. In control experiments, lowering extracellular Ca2+ produced similar effects. (‐)Baclofen has no detectable postsynaptic actions in these cultured neurones. 4. Phaclofen (0.2‐0.5 mM) increases IPSC amplitude but does not significantly block the depressant effect of (‐)baclofen on synaptic transmission. 5. The effect of (‐)baclofen is not blocked by pertussis toxin pre‐treatment. 6. It is concluded that (‐)baclofen acts presynaptically to reduce the release of GABA. The mechanism by which release is reduced may involve a phaclofen‐insensitive GABAB receptor.