Evidence for a cholinergic influence on catecholaminergic pathways terminating in the anterior and medial basal hypothalamus.

Adult male Sprague-Dawley rats were given hourly injections of physostigmine for 1--4 h, and the effect of this treatment on dopamine (DA) and noradrenaline (NA) content or on DA and NA was estimated by measuring the decline in these amines produced following the inhibition of tyrosine hydroxylase with alpha-methyl-p-tyrosine (alpha MPT). In later experiments oxotremorine was administered instead of physostigmine at hourly intervals for 2 h. Physostigmine administration resulted in a highly significant increase in the depletion of NA produced by alpha MPT indicating that the turnover of NA was increased by this drug. This effect was observed in the medial basal hypothalamus and anterior hypothalamus but not in the telencephalon-thalamus. Oxotremorine also produced an increase in NA turnover, but this drug was effective in all three brain areas. Atropine pretreatment blocked the effect of both physostigmine and oxotremorine on NA turnover. However, in the case of physostigmine, atropine was only effective if it was given 30 min before each injection of physostigmine. Mecamylamine, a nicotine blocker, did not reverse the effect of physostigmine on NA turnover. These results suggest that there is a cholinergic input via muscarinic receptors which influences the activity of noradrenergic pathways terminating in the anterior or medial basal hypothalamus.