Pre- and Postnatal Developmental Changes in Hypothalamic and Pituitary Content of α-Melanocyte-Stimulating Hormone and Somatostatin in the Rat

Abstract

The developmental pattern of hypothalamic and pituitary somatostatin and α-melanocyte-stimulating hormone (α-MSH) was studied in the rat by radioimmunoassay (RIA). Prenatally hypothalamic somatostatin was low and the first increase in content occurred on day 5 of the postnatal period. Pituitary somatostatin was undetectable prenatally and was first detected on day 6 postnatally. Pituitary somatostatin showed the same development pattern as hypothalamic somatostatin. Whole pituitaries were analyzed from the fetuses and neonates. Analysis of anterior and posterior lobes from adults revealed that all the somatostatin was in the posterior lobe. Therefore, it is believed that the somatostatin found in the glands of the younger animals was in the neural lobe. α-MSH was detected in the fetal hypothalamus as early as day 16, with a marked increase occurring on day 19 prenatally and a further increase on day 10 postnatally. Pituitary α-MSH content, readily detectable on the first day examined, i.e. day 16 of the fetal period, increased throughout development. The effect of α-MSH on the release of growth hormone in vitro from pituitaries of rats of various ages was tested. α-MSH had no effect on growth hormone release.

Pituitary mRNA Expression of the Growth Hormone Axis in the 1‐Year‐Old Intrauterine Growth Restricted Rat

“…Indeed, several studies have demonstrated increased somatostatin during fasting (48–50), which is thought to reduce serum GH levels in the food deprived postnatal rat. However, because the perinatal pituitary is relatively resistant to somatostatin (51–53), probably due to low levels of sst2 and sst5 mRNA expression (54), it fails to inhibit GH secretion directly after ligation in the fetal IUGR rat.…”

“…During this very narrow time window of GH‐axis‐development, the fasting induced adaptations are (re)programmed and several of these adjustments are still present postnatally although food is freely available. After birth, when somatostatin receptors are fully matured and functioning, which is around day 5–6 (51, 53), the increased somatostatin level inhibits GH secretion and thereby normalises serum GH.…”

“…The pituitary GH-axis after IUGR in the rat 615 (48)(49)(50), which is thought to reduce serum GH levels in the food deprived postnatal rat. However, because the perinatal pituitary is relatively resistant to somatostatin (51)(52)(53), probably due to low levels of sst2 and sst5 mRNA expression (54), it fails to inhibit GH secretion directly after ligation in the fetal IUGR rat. Taken together, our fetal IUGR pups have increased GH, GHRH-R and somatostatin mRNA expression levels, increased pituitary GH content and increased GH serum levels, whereas somatostatin receptors are unaffected.…”

Ontogeny of Somatostatin Gene Expression in Rat Diencephalon

“…This tech nique provides anatomic detail of the structures in volved. ISH afford enhanced sensitivity compared with radioimmunoassay of the peptide [10], as well as avoid ing issues of antibody specificity to the somatostatin-14 and somatostatin-28 forms. While northern blot analysis allows pooling of several animals, and can thus prove more sensitive, it does not share the anatomical detail provided by ISH [9,[11][12][13], Our results show the onset of SS-mRNA synthesis as early as the 14th fetal day.…”

“…The ontogeny of immunoreactive somatostatin in the rat brain has been described in cortical neurons [7] as well as in the hippocampus and hypothalamus [8][9][10], Somatostatin messenger RNA (SS-mRNA) has been de tected as early as the 7th fetal day in whole rat brain [11]. Using northern blot analysis, SS-mRNA was detected on the 14th and 16th fetal days in rat diencephalon and hypothalamus, respectively [12,13].…”