125I-somatostatin-labeled cells in the anterior arcuate nucleus mediate somatostatin effects on growth hormone but not prolactin secretion.

Abstract

The regional brain distribution of 125I-somatostatin (SRIH) binding sites was determined by quantitative radioautography in neonatally monosodium glutamate (MSG) treated adult male rats, a procedure which selectively destroys most neurons of the arcuate nucleus. Neonatal MSG treatment did not modify the extrahypothalamic distribution of 125I-SRIH-binding sites. In contrast, the number of 125I-SRIH-labeled cells in the ventrolateral part of the arcuate nucleus was strongly reduced in MSG-treated animals. The effect was selective for the anterior part of the arcuate nucleus and was not found in its posterior part or in the cells located more dorsally, beneath the ependymal zone of the periventricular nucleus. Intracerebroventricular SRIH injections, which increased growth hormone levels in control rats, were totally ineffective in MSG-treated animals. In contrast, the prolactin levels were equally stimulated by intracerebroventricular injections in control and MSG-treated animals. These results demonstrate that extrahypothalamic SRIH-binding sites are not located on neurons originating in the anterior arcuate nucleus neurons. In addition, 125I-SRIH-labeled cells in the ventrolateral part of the arcuate nucleus are necessary for the paradoxical stimulation of growth hormone secretion induced by intracerebroventricular SRIH injection, but do not seem to be essential for the increased prolactin secretion observed under these conditions.