Effect of β-adrenoceptors on the behaviour induced by the neuropeptide glutamic acid isoleucine amide

Excessive grooming behaviour is induced by intracerebroventricular injections of the neuropeptide glutamic acid isoleucine amide (neuropeptide-EI), via the activation of A-10 dopaminergic neurons and the noradrenergic system. Our object was to study the latter system involved in these behaviours, using male Wistar rats weighing 250–300 g with i.c.v. implants. The results show that all the adrenoceptor antagonists “per se” do not affect excessive grooming behaviour or motor activity. Intracerebroventricular administration of propranolol, a general β-adrenoceptor antagonist, before neuropeptide-EI, inhibited the induced excessive grooming behaviour in a dose dependent manner. Metoprolol, a β1-adrenoceptor antagonist, also blocked this behaviour. However, intracerebroventricular injections of phentolamine, an α-adrenoceptor antagonist, and ((±)-1-[2,3-(Dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol), a β2-adrenoceptor antagonist, had no effect on the behaviour induced by neuropeptide-EI induced behaviour for any of the doses tested. On the other hand, isoproterenol, a general β-adrenoceptor agonist and dobutamine, a β1-adrenoceptor agonist, both elicited similar behaviours as those induced by neuropeptide-EI. These results support the hypothesis that a relationship exists between neuropeptide-EI and β-adrenoceptors, more specifically the β1-adrenoceptor, as found with other similar endogenous peptides such as neurotensin, cholecystin, substance P and α-melanocyte stimulating hormone. Hence, neuropeptide-EI could probably be exerting a neuromodulating effect on the central nervous system.