Antidepressants induce regeneration of catecholaminergic axon terminals in the rat cerebral cortex.
Although repeated but not single administration of antidepressants exerts therapeutic effect on clinical depression, the mechanism of the clinical efficacy of antidepressants remains unknown. This report shows a novel action of antidepressants which can explain the delayed onset of clinical action of the drugs. Continuous infusion of the antidepressants maprotiline or desipramine into the rat cerebral cortex pretreated with the catecholamine neurotoxin 6-hydroxydopamine induced regeneration of noradrenergic axon terminals. This finding provides evidence that antidepressants possess the ability to cause axonal sprouting of central noradrenergic (and possibly dopaminergic) neurons in the mature brain.
Nakamura
S
S
Department of Physiology, Faculty of Medicine, Kanazawa University, Japan.
D000818:Animals; D000928:Antidepressive Agents / Q000494:pharmacology*; D002395:Catecholamines / Q000378:metabolism*; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006892:Hydroxydopamines; D007260:Infusion Pumps; D009411:Nerve Endings / Q000502:physiology; D009416:Nerve Regeneration / Q000187:drug effects*; D009498:Neurotoxins / Q000494:pharmacology; D016627:Oxidopamine; D051381:Rats; D011919:Rats, Inbred Strains
D000928:Antidepressive Agents; D002395:Catecholamines; D006892:Hydroxydopamines; D009498:Neurotoxins; D016627:Oxidopamine