Intracellular recordings were made from presumed dopamine-containing neurons in slices cut from the midbrain of the rat. Focal electrical stimulation produced a hyperpolarizing synaptic potential that was reduced by 75-95% by the GABA(B)-receptor antagonist 2-hydroxysaclofen (300 μM). 5-HT (3-100 μM) reduced the amplitude of the GABA(B) synaptic potential by 20- 74%, with a 50% reduction at 10 μM, but did not reduce the amplitude of synaptic potentials mediated by GABA(A) receptors. 5-HT acted presynaptically because hyperpolarizations produced by exogenously administered GABA (1 mM) in picrotoxin (100 μM) were not affected by 5-HT (30 μM). (±)- Cyanopindolol (100 nM), a 5-HT(1B) antagonist, blocked the effect of 5-HT (10 μM); spiperone (1 μM), which is an antagonist at 5-HT(1A) and 5-HT2 receptors, had no effect. The amplitude of the GABA(B) synaptic potential was reduced by the 5-HT(1B) receptor agonists 1-[3-(trifluoromethyl)-phenyl]- piperazine (300 nM) and 7-trifluoromethyl-4-(4-methyl-1-piperazinyl)- pyrrolo[1,2-a]quinoxaline (1 μM), but not by the 5-HT(1A) agonist N,N- dipropyl-5-carboxamidotryptamine (1 μM) or the 5-HT2 agonist (±)-1-(2,5- dimethoxy-4-iodophenyl)-2-amino-propane (10 μM). We conclude that 5-HT activates presynaptic 5-HT(1B) receptors that inhibit the release of GABA onto GABA(B) but not GABA(A) receptors.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Neuroscience|
|State||Published - 1992|
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