Dopamine-dependent modulation of rat globus pallidus excitation by nicotine acetylcholine receptors.

The globus pallidus (GP) coordinates information processing in the basal ganglia nuclei. The contribution of nicotinic cholinergic receptors (nAChRs) to the spiking activity of GP neurons is largely unknown. Several studies have reported that the effect of nAChRs in other nuclei depends on dopaminergic input. Via in vivo single unit extracellular recordings and intranuclear drug infusions, we analyzed the effects of local activation and blockade of nAChRs in neurons of both sham and 6-hydroxydopamine (6-OHDA)-lesioned rats. In sham rats, the local application of nicotine and edrophonium (an acetylcholinesterase inhibitor) increases GP neurons spiking rate. Local application of mecamylamine, a neuronal nicotinic cholinergic antagonist, diminishes pallidal neurons spiking rate, an effect not produced by d-tubocurarine, a peripheral nicotinic cholinergic antagonist. Moreover, mecamylamine blocks the excitatory effect evoked by nicotine and edrophonium. In 6-OHDA-lesioned rats, local infusion of nicotine does not change pallidal neurons firing rate. Our results show that there is a tonic cholinergic input to the GP that increases their spiking rate through the activation of nAChRs and that this effect depends on functional dopaminergic pathways.

Dopaminergic denervation of the globus pallidus produces short-memory impairment in rats.

Rats with low-level globus pallidus (GP) dopaminergic denervation can develop anxiety without any motor alterations. The aim of this study was to evaluate the effect of low-level 6-OHDA-induced unilateral and bilateral GP lesions in male Wistar rats (n = 8/group) on recognition memory, motor activity, and the number of TH+ neurons in the SNc. For unilateral- and bilateral-lesioned animals, there was a significant decrease in the number of TH+ neurons (27% and 42%, respectively) and in the object, location, and temporal order discrimination indexes of recognition memory tests. Motor activity was unaffected. Thus, GP dopamine denervation was detrimental to short-memory.

6-Hydroxydopamine lesion in thalamic reticular nucleus reduces anxiety behaviour in the rat.

We have studied the effect of the lesion of the dopaminergic innervation of the thalamic reticular nucleus (TRn) on anxiety and motor behaviour. The lesion of the dopamine innervation was produced by the injection of 6-hydroxydopamine into the dorsal part of the thalamic reticular nucleus. The lesion decreased the number of TH (+) cells of the pars compacta of substantia nigra by 33%, without modifying the number of TH (+) cells in ventral tegmental area. The lesion increased the time spent by the rats on the open arms of the elevated plus maze and decreased the duration of burying in the shock-probe test. Both results suggest reduced anxiety. The loss of the dopamine innervation to the TRn decreased the number of rearings but did not significantly affect total motor activity, gait or motor coordination, as evidenced by rotarod performance. These findings suggest that dopamine in the TRn plays a role in fear-related behaviour.