5-HT1A RECEPTOR-MEDIATED INHIBITION OF NUCLEUS-ACCUMBENS NEURONS ACTIVATED BY STIMULATION OF PARAFASCICULAR NUCLEUS OF THALAMUS

Electrophysiological studies using chloral hydrate-anesthetized rats w ere performed to elucidate the role of serotonin(1A) (5-WT1A) receptor s in the regulation of neuronal activity of nucleus accumbens (Acc) ne urons receiving input from the parafascicular nucleus of the thalamus (Pf). Extracellular neuronal activities were recorded in Ace using a g lass microelectrode attached along a seven-barreled micropipette. each barrel of which was filled with dopamine, 5-HT, 8-hydroxy-2-(di-n-pro pylamino)tetralin (8-OH-DPAT: 5-HT1A agonist) hydrobromide, thoxypheny l)-4-[4-(2-phthalimido)butyl]-piperazine (NAN-190: 5-HT1A antagonist) hydrobromide, glutamate and 2 M NaCl. These drugs were microiontophore tically applied to the immediate vicinity of the target neuron. Spikes elicited by Pf stimulation were inhibited by iontophoretically applie d dopamine, 5-HT and 8-OH-DPAT in a dose-dependent manner. In these ne urons, firing induced by iontophoretic application of glutamate was al so suppressed by dopamine: 5-HT and 8-OH-DPAT. The 5-HT or 8-OH-DPAT-i nduced inhibitions of the glutamate-induced firing were antagonized by concomitant application of NAN-190. These findings suggest that the d opamine-sensitive Ace neurons receiving input from Pf are inhibited by 5-HT via 5-HT1A receptors located on postsynaptic Ace neurons.