Ontogenetic patterns of thyrotropin-releasing hormone-like material in rat hypothalamus, pancreas, and retina: selective effect of light deprivation.

Abstract

ABSTRACr Recent observations have shown the presence of thyrotropin-releasing hormone-like material (TRH-LM) in rat pancreatic islets and in retina. Its immunological and biological properties are identical to those of synthetic thyrotropin-releasing hormone (thyroliberin) This communication deals with the ontogenesis of TRH-LM in rat pancreas and retina as compared to that of rat hypothalamus. Effects of sex and exposure to constant dark were also studied. Results show that asynchronous changes in the concentration of TRH-LM occur during the postnatal maturation of these tissues, presumably mediated by organ-specific control mechanisms-e.g., light affects only the accumulation of TRH-LM in the retina. TRH-LM may act as neurotransmitter in the regulation of pancreatic islet cell function and in the development of photoreception in the retina. Increases in hypothalamic TRH-LM seem to parallel the development of the pituitary-thyroid secretory activity, but the function of extrahypothalamic TRH-LM remains speculative.Thyrotropin-releasing hormone (TRH, thyroliberin) is a tripeptide that was isolated from mammalian hypothalami and characterized as pyroglutamylhistidylproline amide (1, 2). As evidenced by its name, TRH was initially considered to play a specific role in the regulation of pituitary thyrotropin secretion. Subsequently, it has been shown that TRH also stimulates pituitary prolactin and growth hormone secretion (3-5). Effects unrelated to the control of adenohypophyseal function have also been reported. These include: potentiation of behavioral excitation (6), mood elevation (7-9), stimulation of muscular activity of the intestine (10), induction of hypothermia (11), enhancement of cerebral noradrenaline turnover (12), inhibition of the electrical activity of some brain neurones (13), and potentiation of the excitatory action of acetylcholine (14). Thus, it is not surprising that significant amounts of TRH-like material (TRH-LM) have been found in areas of the central nervous system other than the hypothalamus (15)(16)(17)(18). The presence of immunoreactive (IR) and bioreactive TRH-LM has also been reported outside the central nervous system in human placenta (19,20), rat retina (21-23), frog skin (22), and rat gastrointestinal tract, including the pancreas (24-26). In the latter, the main source of TRH appears to be the islets of Langerhans (26).Although it has been speculated that TRH may act as neurotransmitter or modulator of synaptic function, its function in extrahypothalamic tissues remains unknown, as is the precise cell of origin. Because there appears to be a good correlation between the postnatal changes in hypothalamic IR-TRH content and in pituitary and serum thyrotropin concentrations (27) and because exposure to dark has been shown to reduce the METHODSAll rats were of the CD strain obtained from Charles River Breeding Laboratories. They were housed in individual cages in a temperature-controlled (19-210C) and artifically illuminated (light from 0700 to 1900) room and allowed free acces...

Thyrotropin-releasing Hormone in the Pancreas and Brain of the Rat Is Regulated by Central Noradrenergic and Dopaminergic Pathways

“…This work was presented in part at the 63rd Annual Meeting of the Endocrine Society, [17][18][19] June 1981, Cincinnati, Ohio.…”

Pancreatic pattern of expression of thyrotropin-releasing hormone during rat embryonic development

“…Its pattern of expression is tightly controlled in a temporal and cell-type-specific manner. Indeed, in the pancreas, TRH is found at high levels specifically in insulin-expressing cells at around the time of birth, the TRH levels decreasing very rapidly during the first days of postnatal life (Martino et al 1980, Leduque et al 1987, Scharfmann et al 1988. Such data were mainly obtained at the protein level.…”

“…Its expression is also tightly regulated temporally. Indeed, a large number of studies have demonstrated that the levels of TRH are high in pancreatic beta cells during the neonatal period (Martino et al 1980, Aratan-Spire et al 1984 and decrease rapidly, when postnatal development progresses (Martino et al 1980, Aratan-Spire et al 1984, Scharfmann et al 1988. To the best of our knowledge, the prenatal pattern of pancreatic TRH expression remains poorly studied.…”

Glucose stimulates and insulin inhibits release of pancreatic TRH in vitro

“…Immunoreactive TRH was later detected in the rat pancreas (3,4) where its concentration, as well as the levels of its messenger RNA, are highest during the neonatal period (5)(6)(7)(8). Within the pancreas, TRH is localized in the insulin-producing B-cells of the islets of Langerhans (9)(10)(11).…”