Differential Actions of Serotonin, Mediated by 5-HT1Band 5-HT2C Receptors, on GABA-Mediated Synaptic Input to Rat Substantia Nigra Pars Reticulata Neurons In Vitro

摘要: The ability of serotonin to modulate GABA-mediated synaptic input substantia nigra pars reticulata (SNr) neurons was investigated with the use whole-cell patch-clamp recording from slices rat midbrain. Fast evoked GABAA receptor-mediated currents (IPSCs) were attenuated reversibly ∼60% by serotonin, which also caused an inward current reversal potential −25 mV. This blocked 5-HT2 receptor antagonist ritanserin, whereas IPSC depression 5-HT1B pindolol. amplitude ratio pairs (50 msec interpulse interval) enhanced (in ritanserin) and GABAB agonist baclofen (which depressed IPSC), consistent a presynaptic site action in both cases. In contrast, spontaneous tetrodotoxin-sensitive (sIPSCs) increased frequency (an that sensitive but not pindolol) reduced baclofen. SNr therefore receive inhibitory mediated receptors at least two distinct sources. One, probably originating striatum, may be via receptors. second is likely arise axon collaterals themselves facilitated increase firing postsynaptic, somatodendritic 5-HT2C activation, it activation. Thus, can depolarize disinhibit receptors, respectively, excitation limited GABA released collaterals.