1 In the present study the mechanisms were examined by which the neuropeptide galanin modulates the extracellular concentrations of striatal acetylcholine (ACh) in en¯urane anaesthetized and in freely moving male rats by use of in vivo microdialysis and high performance liquid chromatography. 2 The perfusion of galanin through the microdialysis probe (0.3 nmol ml 71 ,¯ow rate: 2 ml min 71 ) caused a statistically signi®cant increase in the basal striatal ACh levels in anaesthetized but a decrease in awake animals. No signi®cant eect was revealed after a low dose (0.1 nmol ml 71 ,¯ow rate: 2 ml min 71 ) of galanin perfusion. Both the stimulating and inhibitory eects of galanin on basal ACh release were reversible. 3 The muscarinic antagonist scopolamine (0.1 mg kg 71 , subcutaneously (s.c.)) caused a signi®cant increase in ACh release in both anaesthetized and awake animals. 4 The combination of galanin plus scopolamine attenuated the stimulant eect on ACh release caused by scopolamine alone in awake animals. 5 The putative galanin receptor antagonist M35 at 0.3 nmol ml 71 but not at 0.1 nmol ml 71 caused a signi®cant reduction (20%) in ACh release, supporting the view that M35 at higher concentrations behaves as a partial agonist at the galanin receptor. When M35 (0.1 nmol ml 71 ) was co-infused with galanin (0.3 nmol ml 71) the galanin-evoked decrease in ACh release was completely blocked. 6 Taken together, these results indicate that galanin aects basal ACh release via stimulation of galanin receptors within the striatum. The mechanism involved is dependent on the anaesthesia procedure which may act via enhancement of g-aminobutyric acid A (GABA A ) mediated transmission within striatal and/or output neurones. In addition, anaesthesia may also decrease the activity of glutamatergic striatal aerents. The results with M35 indicate that the role of galanin perfused in striatum is permissive in the normal rat. Furthermore, galanin is a potent inhibitory modulator of basal ACh release also in the striatum, as recently was shown in the ventral hippocampus in awake animals.
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