The pharmacological effects of acute and chronic clenbuterol treatments after lesions of central noradrenergic nerve terminals.
Acute administration of clenbuterol, a lipophilic beta-adrenergic agonist, decreases motor activity and antagonizes the reserpine-induced hypothermia in mice. After chronic administration of clenbuterol, the acute effect on motor activity disappears (tachyphylaxis) and the acute effect on reserpine hypothermia is potentiated (facilitation). These effects of clenbuterol (either acute or chronic + acute treatments) are not abolished after specific lesions of the noradrenergic system by the neurotoxin DSP-4 which reduces the cerebral levels of norepinephrine to 30% of controls. Although it cannot be excluded that a 70% lesion may be insufficient, another explanation is that beta-adrenergic receptors involved in hypomotility and in reserpine-induced hypothermia may not be located on noradrenergic neurons or may be different from the post-synaptic beta-adrenergic receptors which become hypersensitive after DSP-4 denervation.
D000818:Animals; D001596:Benzylamines / Q000633:toxicity; D001831:Body Temperature / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects; D002976:Clenbuterol / Q000494:pharmacology*; D004983:Ethanolamines / Q000494:pharmacology*; D008297:Male; D051379:Mice; D009043:Motor Activity / Q000187:drug effects; D009411:Nerve Endings / Q000187:drug effects*; D009498:Neurotoxins / Q000633:toxicity; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology*; D013618:Tachyphylaxis / Q000187:drug effects
D001596:Benzylamines; D004983:Ethanolamines; D009498:Neurotoxins; C012102:DSP 4; D009638:Norepinephrine; D002976:Clenbuterol