Neurochemical correlates of the Klüver-Bucy syndrome by in vivo microdialysis in monkey.
The Klüver-Bucy syndrome is a well known consequence of lesions of the temporal lobe, but the neural mechanisms remain obscure. To elucidate the neurochemical changes in this syndrome, we utilized in vivo microdialysis of amygdala and hypothalamus in two Cebus monkeys (C. apella) before and after bilateral lesions of the temporal pole (TP). Both subjects were housed and observed in a social group when not being dialyzed. Behavioral changes consequent to the TP lesion included early postoperative anorexia, adipsia, hunched posture, tameness, and lethargy. Subsequently loss of fear, hyperorality, loss of social rank, and social withdrawal were observed. Neurochemical changes in amygdala included fall in DA metabolites, increase in NE, and fall in 5-HIAA. The amino acids glutamate and aspartate were both lower postoperatively but more so in the subject with the greatest behavioral changes. Similar changes were noted in hypothalamus except for DA metabolites which remained unchanged. The Klüver-Bucy syndrome consequent to ablation of the temporal pole appears related to a partial deafferentation of excitatory projections to amygdala, along with a lowering of DA and 5-HIAA and an increase in NE.[1]References
- Neurochemical correlates of the Klüver-Bucy syndrome by in vivo microdialysis in monkey. Kling, A.S., Tachiki, K., Lloyd, R. Behav. Brain Res. (1993) [Pubmed]
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