Involvement of catecholamines in kindled amygdaloid convulsions in the rat.

The seizure state induced by amygdaloid kindling in the rat was accompanied by a significant depletion of norepinephrine (NE) in the hippocampus, midbrain, limbic lobes and frontal cortex. In contrast, there was no change in NE levels of the hypothalamus, brain stem or basal ganglia, nor were the levels of dopamine affected in any of these brain regions. Drugs which impair central noradrenergic mechanisms, including α-methyl-p-tyrosine, disulfiram and propranolol, enhanced the rate of development of kindled seizures; disulfiram and propranolol also increased the duration of after discharges accompanying the seizures. In contrast, drugs affecting dopaminergic mechanisms, including pimozide and apomorphine, as well as drugs acting on α-adrenergic receptors, phenoxybenzamine and clonidine, had no influence on the seizure state. It appears that central noradrenergic mechanisms, particularly those involving β-adrenergic receptors, may be involved in the pathogenesis of amygdaloid kindled seizures.