Partial lesions were made with kainic acid in the interpeduncular nucleus of the ventral midbrain of the rat. Compared with sham-operated controls, lesions significantly (p < 0.25) blunted the early (< 60 min) free-field locomotor hypoactivity caused by nicotine (0.5 mg kg-1, i.m.), enhanced the later (60-120 min) nicotine-induced hyperactivity, and raised spontaneous nocturnal activity. Lesions reduced the extent of immunohistological staining for choline acetyltransferase in the interpeduncular nucleus (p < 0.025), but not for tyrosine hydroxylase in the surrounding catecholaminergic A10 region.. We conclude that the interpeduncular nicotinic depression of locomotor nicotinic arousal mechanisms located elsewhere in the brain.
- Kainic acid
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