Heterogeneous Immunocytochemical Reactivities of oCRF-41-Like Material in the Human Hypothalamus, Pituitary and Gastrointestinal Tract

Abstract

Tissue specimens of human hypothalami, pituitaries and gastrointestinal tract were studied with an indirect immunoperoxidase technique using 6 different rabbit ovine corticotrophin-releasing factor (oCRF-41) antisera. All these antisera detected oCRF-41-like immunoreactivity in parvocellular neurones of the paraventricular nucleus of the hypothalamus and their nerve terminals adjacent to portal capillaries in the infundibular stem and posterior pituitary. 1 antiserum recognised oCRF-41-like immunoreactivity in the growth hormone cells of the anterior pituitary. 3 other antisera recognised oCRF-41-like immunoreactivity in mucosal cells of the gastric antrum. Pre-treatment of the antisera with sauvagine did not affect the immunostaining of the hypothalamic and gastric cells, but quenched the immunostaining of growth hormone cells in the anterior pituitary. It is concluded that (1) in human hypothalami a CRF is synthesized that is structurally very similar to oCRF-41; (2) in growth hormone cells of the anterior pituitary oCRF-41-like immunoreactive material can be detected which shares antigenic determinants with sauvagine; (3) in mucosal cells of the gastric antrum oCRF-41-like immunoreactivity is present that is comparable but probably not identical to hypothalamic CRF and is not sauvagine-like.

Corticotropin‐releasing hormone neurons in hypertensive patients are activated in the hypothalamus but not in the brainstem

“…Note that in hypertensive patients the area of CRH-immunoreactive fibers within the SCh is almost three times higher than it is in the normotensive group centrated solely in the hypothalamic paraventricular nucleus (Pa). In the control group some individual variability was present in the density of the CRH immunoreactivity, but generally the distribution was consistent with descriptions by Pelletier et al (1983), Mouri et al (1984), Nieuwenhuyzen Kruseman et al (1984), Takahashi et al (1989), and Raadsheer et al (1993). However, the density of CRH immunoreactivity was much lower than that reported by Mihaly et al (2002).…”

Rat Corticotropin-Releasing Hormone Gene: Sequence and Tissue-Specific Expression*

“…The presence of CRH mRNA in the spinal cord and adrenal gland correlates well with the reported presence of CRH immunoreactivity in these tissues (9)(10)(11)(12). Additionally, previous reports have demonstrated CRH-like immunoreactivity in the rat and human anterior pituitary, although the cell types containing CRH immunoreactivity differed in these reports (14,15). In contrast, the presence of CRH mRNA in the testis appears to describe a novel region of synthesis.…”

“…Numerous groups have used immunocytochemical methods to show that CRH peptides are present in widespread regions of the brain as well as some nonbrain tissues (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). In order to determine whether this material is synthesized at these sites or transported to these sites from other regions of synthesis, RNA blot analysis was used to detect the presence of CRH mRNA in a variety of tissues (Figs.…”

“…The portal blood subsequently flows through the anterior pituitary where CRH can influence the secretion of ACTH. CRH has also been immunocytochemically localized in other regions of the brain and in various peripheral tissues (4)(5)(6)(8)(9)(10)(11)(12)(13)(14)(15) where it may mediate other aspects of the mammalian stress response.…”

Food‐induced Cortisol Secretion Is Mediated by Central Alpha‐1 Adrenoceptor Modulation of Pituitary Acth Secretion

“…Slag et al (1981) found a small rise of plasma ACTH following food ingestion but their findings could not be confirmed by Fehm et al (1983). The human stomach and pancreas contain immunoreactive C R F (Nieuwenhuijzen Kruseman et al, 1982Petrusz et al, 1983;Suda et al, 1984), but there is no detectable rise in immunoreactive C R F in plasma following lunch ingestion in normal human subjects (Cunnah et al, 1986). The inability of the earlier study to demonstrate an ACTH increment may be related to inadequate assay sensitivity.…”