Abstract
Rats with unilateral striatal kainic acid (KA) lesions showed ipsilateral rotation to subcutaneous apomorphine, contralateral rotation to intranigral muscimol and reductions in striatal glutamic acid decarboxylase (GAD) activity and nigral γ-aminobutyric acid (GABA) concentration. Rotational responses to apomorphine were highly correlated with nigral GABA depletions, and were a sensitive index of the functional integrity of striatonigral GABA neurons. Rotational responses to muscimol were also correlated with nigral GABA depletions, consistent with supersensitivity of denervated nigral GABA receptors. Striatal GAD was not correlated with either behavioural measure or with nigral GABA, and was a poor index of striatonigral function. These results are discussed in terms of (i) the functional role and adaptive capacity of striatonigral GABA neurons in linking the striatum with its effector mechanisms, (ii) parallels between parameters in GABA-dependent and DA-dependent rotational models and (iii) the status of the striatal KA lesion as a model for Huntington's disease and other extrapyramidal movement disorders.
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