Abstract
An attempt has been made to obtain direct histological evidence for a neurotoxic effect of p-chloroamphetamine (PCA) on serotonergic (5-HT) neurones using the silver-staining method of Fink and Heimer. In order to validate this procedure, 5-HT axon pathways were traced at various survival times after electrolytic lesions of the dorsal and medial raphe nuclei. The high affinity uptake of monoamines in small nuclear areas was also studied to provide a guide to the selectivity of the lesions and to the time course of degeneration of 5-HT cells. Degenerating 5-HT axons were traced from the lesion through the median forebrain bundle in a pattern similar to that found with histofluorescence. Serotonergic axon terminals were not demonstrable, however, in the suprachiasmatic or ventrolateral geniculate nuclei, areas known to have a dense 5-HT terminal input. After the injection of 10 mg/kg of PCA. no degeneration of 5-HT axons or axon terminals was seen. This suggested that PCA was not toxic to 5-HT axons, but it did not rule out the possibility that 5-HT axon terminals might be selectively damaged. This hypothesis was tested by measuring levels of 5-HT in axons vs axon terminals of the spinal cord. p-Chloroamphetamine caused a decrease in terminal-5-HT while simultaneously increasing axonal 5-HT levels, suggesting that PCA is primarily toxic to 5-HT nerve terminals in the CNS.
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