Neurochemical Mediators of Anxiety have Inconsistent Effects on Hypothalamic Self‐Stimulation in Rats

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Abstract
We studied effects of anxiogenic and anxiolytic compounds on the electric self-stimulation of the medial forebrain bundle in male rats to find out if there is a link between reward and anxiety-related behaviours. The cholecystokinin agonist, caerulein (25-100 μg/kg) and the 5-HT agonist 1-(3-chlorophenyl)piperazine (0.2-1 mg/kg) dose-dependently inhibited the electric self-stimulation. The 5-HT2A antagonist, ketanserin, at 2.5 mg/kg, increased the self-stimulation at high currents but not at threshold current. The 5-HT3 antagonist ondansetron (10 and 100 μg/kg). The α1-adrenergic antagonist, prazosin (0.125 and 0.5 mg/kg), the β-adrenergic antagonist, propranolol (5 and 10 mg/kg) and the α2-adrenoreceptor antagonist, atipamezole (4 mg/kg), did not affect the self-stimulation. Nor did the benzodiazepine agonist, di-azepam (5-15 mg/kg), a benzodiazepine receptor antagonist flumazenil (at 10 and 25 mg/kg) or the inverse agonist of benzodiazepine receptors, N-methyl-β-carboline-3-carboxamide (10 and 20 mg/kg), cause any substantial changes of the self-stimulation. We conclude that only two anxiolytic drugs (caerulein and l-(3-chlorophenyl)piperazine) suppress the electric self-stimulation. These findings indicate that anxiogenicity as such is not able to weaken the hypothalamic electric self-stimulation. Anxiety and reward are apparently mediated through separate neural pathways.