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The effect of morphine, administered intrapallidally, on extracellular concentrations of DA, DOPAC, and HVA in the nucleus accumbens and striatum was studied in the behaving rat using the in vivo microdialysis technique. Unilateral application of morphine hydrochloride was performed through microdialysis probes into the rat ventral pallidum (10 microliters of 0, 2.6, 4.0, 13.0, and 26.0 mM) or globus pallidus (10 microliters of 0 and 26.0 mM). The levels of DA, DOPAC, and HVA were measured using the HPLC with EC detection in dialysates collected from the nucleus accumbens, anteromedial, and anterolateral striatum. Samples were taken every 45 min over 3 h before and over 5 h after morphine or vehicle administration. Administration of morphine into the ventral pallidum resulted in increased DOPAC and HVA concentrations in the nucleus accumbens. Pretreatment with naloxone (1 mg/kg, SC) abolished this effect of morphine. Administration of morphine into the globus pallidus resulted in increased DA, DOPAC, and HVA concentrations in the nucleus accumbens and DA in the anteromedial striatum. The levels of DA and metabolites in anterolateral striatum remained rather unchanged following morphine administered into the ventral pallidum or the globus pallidus. The changes in DA neurotransmission into the nucleus accumbens induced by morphine application into the ventral pallidum and globus pallidus are reminiscent of a phasic and tonic release of DA respectively. The results show that intrapallidal morphine increases DA neurotransmission in nucleus accumbens and suggest that the effect of morphine is mediated by ventral pallidum/mesolimbic and globus pallidus/thalamocortical pathways, depending on the site of injection.

Amphetamine hyperactivity, apomorphine stereotypy and haloperidol catalepsy were studied in rats following selective damage to cell bodies within the globus pallidus (GP). Ibotenic acid-induced bilateral lesions of GP attenuated the spontaneous locomotion of rats, but they did not influence the locomotor response to amphetamine. Apomorphine-induced gnawing and licking but not sniffing were attenuated in rats with GP lesions. The effect of haloperidol on catalepsy was enhanced following the GP lesion. It is concluded that the normal expression of some dopamine-related functions depends to a great degree on the integrity of cells within the GP region.

Rats with kainic acid-induced lesions of the ventromedial thalamic (VMt) nucleus were compared with sham-operated controls on two behavioural tasks. The kainic acid injection resulted in loss of local neurons in the VMt nuclei with no appreciable damage to other thalamic nuclei or to other distant brain areas. VMt nuclei lesion animals learned to run in an L-maze for food reinforcement and to avoid electric foot-shock in the two way active avoidance shuttle-box procedure. Extinction of the food reinforced response was not altered by the lesion. One week retention of the acquired two-way active avoidance response was almost abolished on the animals with the lesion. Open field locomotion or escape latencies were not influenced by the lesion. It is concluded that VMt nuclei of rats are involved in the retention of aversively reinforced behaviours.