CORTICAL REGULATION OF STRIATAL NEUROPEPTIDE-Y (NPY)-CONTAINING NEURONS IN THE RAT - PUTATIVE MODULATORY INFLUENCE ON STRIATAL DOPAMINE NPY RELATIONSHIPS

This study examined the functional relationships established by nigral, cortical, and thalamic striatal afferent pathways with neuropeptide Y (NPY)‐containing neurons in the rat rostral striatum by coupling selective deafferentation procedures and NPY immunohistochemistry. Previous experiments have shown that after unilateral 6‐hydroxydopamine (6‐OHDA)‐induced degeneration of nigrostriatal dopaminergic neurons, the mean number of NPY‐immunoreactive (lr) neurons per frontal section was increased in the striatum ipsilateral to the lesion side and unaltered in the contralateral striatum. The present topographical analysis of the 6‐OHDA lesion effects led us to state that the increase in NPY‐lr neuron density occurs in restricted ventral and medial zones of the ipsilateral striatum. Unilateral ablation of the frontoparietal cerebral cortex by thermocoagulation was moreover shown to elicit, 20–30 days later, a significant bilateral increase in the number of striatal NPY‐lr cells. The increase was more marked in the striatum ipsilateral to the hemidecortication where it was similar in amplitude to that induced by the 6‐OHDA lesion. The topographical analysis of the cortical lesion effects also revealed an uneven striatal response, but, in contrast to that observed for the 6‐OHDA lesion, changes were restricted to dorsolateral areas of the striatum in both brain sides, revealing an apparent complementarity of nigral dopaminergic and cortical influences over striatal NPY neuronal system. Combined unilateral nigral and cortical lesions surprisingly counteracted in a survival time dependent manner the effects of each lesion considered separately. In that condition topographical changes related to the 6‐OHDA lesion totally disappeared and those related to the cortical lesion were attenuated but still present. These results suggest that expression of striatal dopamine—NPY interaction is dependent on corticostriatal transmission. Interestingly lesion of thalamic areas projecting to the striatum did not significantly modify the mean number of NPY‐lr neurons determined per section from the whole striatal surface, but selectively increased the NPY neuron density in the mediodorsal region of the striatum, suggesting that the striatal NPY‐containing neuronal system is also influenced by thalamostriatal projections. Copyright © 1990, Wiley Blackwell. All rights reserved