DSP-4 lesioning prevents the enhancement of dopamine and 5-hydroxytryptamine mediated behavioural changes by repeated electroconvulsive shock.
DSP-4 (N-(2-chloroethyl)-ethyl-2-bromobenzylamine) a novel neurotoxin which destroys central noradrenaline neurones after peripheral injection was administered to rats (50 mg/kg X 2). This procedure did not alter activity responses to quipazine (7.5 mg/kg) or apomorphine (0.2 mg/kg) but prevented their enhancement by repeated electroconvulsive shocks (ECS X 10). This confirms that intact noradrenergic function is required for ECS-induced enhancement of 5-HT and dopamine mediated responses. Furthermore, DSP-4 is shown to provide a simple, effective alternative to centrally injected 6-hydroxydopamine for noradrenergic lesioning.
D000588:Amines / Q000494:pharmacology*; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001522:Behavior, Animal / Q000187:drug effects*; D001596:Benzylamines / Q000494:pharmacology*; D001923:Brain Chemistry / Q000187:drug effects; D004597:Electroshock; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D011814:Quipazine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects*; D011985:Receptors, Serotonin / Q000187:drug effects*
D000588:Amines; D001596:Benzylamines; D011954:Receptors, Dopamine; D011985:Receptors, Serotonin; D011814:Quipazine; D001058:Apomorphine; C012102:DSP 4; D009638:Norepinephrine