Ultradian oscillation in somatostatin binding in the arcuate nucleus of adult male rats.

The ultradian rhythm of GH secretion in the male rat is generated by the reciprocal cyclic release of somatostatin (SRIF) and GH-releasing factor (GRF) from the hypothalamus. We recently demonstrated the presence of high affinity [125I]SRIF-binding sites on a subpopulation of GRF-containing arcuate neurons in rat hypothalamus. In the present study, we tested the hypothesis that these binding sites undergo rhythmic fluctuations in parallel with those of GH. Adult male rats were killed at times associated with either a peak (1100 h) or trough (1300 h) period of the GH rhythm. The hypothalamus was serially sectioned from the retrochiasmatic nucleus, rostrally, to the mammillary recess of the third ventricle, caudally, and [125I]SRIF-binding sites were labeled in vitro using high resolution autoradiography. [125I]SRIF-labeled neuronal perikarya were counted at eight cross-sectional levels across the arcuate nucleus, and binding densities were quantitated over each of these cross-sectional surfaces using computer-assisted microdensitometry. Both the number of labeled cells and the density of [125I]SRIF binding varied as a function of the time of death. The average number of [125I]SRIF-labeled cells per 10-microns thick section was 2- to 3-fold higher in rats killed at 1100 h than in those killed at 1300 h. In addition, overall binding density levels were 65% higher in animals killed at the onset of a GH peak than in those killed at the time of a GH trough. Both of these effects were apparent throughout the rostrocaudal extent of the arcuate nucleus. In contrast, [125I]SRIF binding density in the cerebral cortex did not vary between 1100 and 1300 h. These results demonstrate an ultradian variation in SRIF binding to arcuate neurons in relation to the peaks and troughs of the GH rhythm. Such rhythmicity in SRIF receptors might underlie a temporal responsiveness of arcuate GRF neurons to endogenous SRIF and may be an important mechanism by which SRIF modulates the rhythmic release of hypothalamic GRF in generation of the ultradian rhythm of GH secretion.