Abstract
To assess the nature and extent of ultrastructural damage due to low unilateral intracerebroventricular doses of kainic acid, treated rats were killed at survival times from 8 h to 14 weeks. Degenerative changes in field CA1 of the hippocampus included dark profiles (often presynaptic), lucent areas enveloping axonic or dendritic elements, damaged myelin sheaths, and enlarged glial profiles. The effect of kainic acid ipsilaterally was maximal at three days but also apparent up to 14 weeks. Contralateral CA1 showed similar though less extensive abnormalities. These observations suggest that, despite rapid synaptic replacement (Nadler et al., Brain Res. 191, 387–403, 1980), long-term electrophysiological abnormalities (Cornish and Wheal, Neuroscience 28, 563–571, 1989) may stem not only from inappropriate reactive synaptogenesis but also from a continuing state of neuronal degeneration.
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