Salin P, Kerkerian-Le Goff L, Heidet V, Epelbaum J, Nieoullon A
Unité de Neurochimie, C.N.R.S., Marseille, France.
Brain Res. 1990 Jun 25;521(1-2):23-32. doi: 10.1016/0006-8993(90)91520-q.
The present study examined the effects of the impairment of corticostriatal and nigrostriatal dopaminergic transmission on the mean number and the topographical distribution of somatostatin-containing neurons in frontal sections of the rat rostral striatum. These neurons, visualized by an immunohistochemical method using a specific anti-somatostatin(28) antibody were shown to be unevenly distributed; the number of immunoreactive perikarya being consistently lower in the dorsolateral and higher in the middle areas of striatal sections than in the remaining parts of the structure. Such a distribution and number were not altered either by unilateral 6-hydroxydopamine (6-OHDA)-induced lesion of the nigrostriatal dopaminergic neurons after 2- to 3-week survival periods, or by alpha-methylparatyrosine-induced dopamine depletion. In animals with similar 6-OHDA-induced lesions, no change in the striatal concentration of somatostatin measured by radioimmunoassay was observed. These results suggest that somatostatin levels in striatal neurons are not under a dopaminergic influence in contrast to that previously described for neuropeptide Y, although both peptides are thought to coexist extensively in the same striatal neuron population. On the contrary, extensive unilateral frontoparietal ablation of the cerebral cortex elicited, 2-3 weeks later, a significant increase in the mean number of somatostatin-immunoreactive cells per section in the ipsilateral striatum preferentially localized to the dorsolateral zone of the structure with no change in the contralateral side. Data from immunohistochemical studies were further discussed in comparison with results obtained by radioimmunoassay showing that similar cortical lesion induced no change in somatostatin endogenous levels in the ipsilateral striatum and a 30% decreased concentration of the peptide in the contralateral striatum. These data suggest that the corticostriatal pathway influences the expression of somatostatin at either a translational, processing or metabolic level in a topographically restricted population of striatal somatostatin-containing neurons.
