Chronic cobalt-induced epilepsy: noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex.
Several studies indicate that brain noradrenaline (NA) depletion facilitates the occurrence of epileptogenic syndromes in various animal models. In cobalt-induced epilepsy in the rat activity is associated with a cortical NA denervation. In order to search for cortical adrenoceptor modifications, inonophoretic studies and adrenoceptor binding assays were performed. At the period of maximal seizure activity, there was a significant supersensitivity of cortical neurons to the ionophoretic application of NA. An increase in the density of beta-adrenoceptor binding sites was observed. No modification in alpha 1- and alpha 2-adrenoceptor binding sites was found. This suggests that in cobalt-induced epilepsy there is a denervation supersensitivity which rests on a selective involvement of beta-adrenoceptors.
D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D002908:Chronic Disease; D003000:Clonidine / Q000378:metabolism; D003035:Cobalt; D004082:Dihydroalprenolol / Q000378:metabolism; D004827:Epilepsy / Q000139:chemically induced / Q000378:metabolism*; D007478:Iontophoresis; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D011224:Prazosin / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011941:Receptors, Adrenergic / Q000378:metabolism*
D011941:Receptors, Adrenergic; D003035:Cobalt; D004082:Dihydroalprenolol; D003000:Clonidine; D009638:Norepinephrine; D011224:Prazosin