Experimentally-induced neuron loss in the locus coeruleus of adult rats.
Systemic administration of the noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) to adult rats causes widespread degeneration of locus coeruleus (LC) axon terminals. The present study was conducted to determine the effects of DSP-4-induced LC axon lesions on LC cell bodies. Six months after DSP-4 treatment, quantitative analysis of Nissl-stained sections revealed a profound loss of LC perikarya, ranging from 20 to 73% of control. The remaining LC neurons appeared shrunken, but stained strongly with dopamine beta-hydroxylase immunohistochemistry. These findings support the conclusion that DSP-4-induced LC axon lesions cause retrograde degeneration of LC neurons. DSP-4 may serve as a useful tool in studies of the mechanisms of LC neuron degeneration.
Fritschy
J M
JM
Johns Hopkins University School of Medicine, Department of Neuroscience, Baltimore, Maryland 21205.
Grzanna
R
R
D000818:Animals; D001596:Benzylamines / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects; D008125:Locus Coeruleus / Q000254:growth & development* / Q000648:ultrastructure; D008297:Male; D009474:Neurons / Q000502:physiology* / Q000648:ultrastructure; D009498:Neurotoxins / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013566:Sympathomimetics / Q000494:pharmacology
D001596:Benzylamines; D009498:Neurotoxins; D013566:Sympathomimetics; C012102:DSP 4