The tuberoinfundibular system of the rat as demonstrated by immunohistochemical localization of retrogradely transported wheat germ agglutinin (WGA) from the median eminence

Lechan, Ronald M.; Nestler, Jeffrey L.; Jacobson, Stanley

doi:10.1016/0006-8993(82)90334-1

Cited by 148 publications

(35 citation statements)

References 57 publications

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“…In agreement with previous reports of the localization of tuberoinfundibular neurons by mapping with retrogradely transported morphologic markers (18,19), we observed labeled neurons restricted to the supraoptic, paraventricular, arcuate, and ventromedial nuclei, where the few retrogradely labeled neurons were concentrated in the posterior ventrolateral subdivision (20) (Fig. 7).…”

Section: Resultssupporting

confidence: 93%

“…Labeled (18,19). Indeed, tuberoinfundibular neurons appear to have the capacity to take up and concentrate other circulating proteins and polypeptides (18,19). This capacity has been cited in support of a theory that would account for the presence of adrenocorticotropin and related peptides in arcuate hypothalamic neurons on the basis of direct uptake from the portal blood (1,(5)(6)(7).…”

Section: Resultsmentioning

confidence: 96%

“…Labeled (18,19). Indeed, tuberoinfundibular neurons appear to have the capacity to take up and concentrate other circulating proteins and polypeptides (18,19).…”

Section: Resultsmentioning

confidence: 99%

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NH2-terminal specificity and axonal localization of adrenocorticotropin binding sites in rat median eminence.

Houten¹,

Khan²,

Walsh³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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Adrenocorticotropin binding sites in the rat median eminence have been localized in vivo. These binding sites occur in the basalar zone, which is rich in axonal endings. Using competitive binding and quantitative light-microscope radioautography, we found that the median-eminence binding site, in contradistinction to the adrenal receptor, binds specifically the residue 4-10 region of the adrenocorticotropin molecule. Using quantitative electron-microscope radioautography and median-eminence deafferentation, we localized the binding sites to axon terminals in this region. In time-delayed uptake studies using light-microscope radioautography, we failed to observe concentration of radiolabel in neurons of the medial basal hypothalamus after the direct injection of radioiodinated adrenocorticotropin(1-24) into the median eminence.Binding sites for blood-borne adrenocorticotropin (ACTH) have been localized to the rat median eminence by quantitative radioautography (1). The median eminence is one of the four circumventricular organs of the brain, which are targets for direct interaction with a variety of circulating peptide hormones (2). Of these four regions, the median eminence is the only brain region in which specific binding sites for blood-borne adrenocorticotropin have been demonstrated (1). In view of the various purportedly direct effects of blood-borne adrenocorticotropin and related peptides on brain function (3, 4), we have attempted to determine the cellular location and binding specificity of adrenocorticotropin binding sites in the rat median eminence by using quantitative light-and electron-microscope radioautography. In addition, we report the results of pilot radioautographic investigations of brain uptake of circulating adrenocorticotropin (5-8). METHODSSynthetic ACTH1-24 (Cortrosyn), a gift from Organon, was iodinated using lactoperoxidase under mild conditions for 30 sec, as described by McIlhinney and Schulster (8). Monoiodinated hormone prepared by this method has been shown to retain its steroidogenic properties and capacity to bind receptors isolated from rat adrenocortical cells (8). lodinated peptide was purified by the silicic acid adsorption method of Rees et al. (9) with minor modifications, as follows. Ten milligrams of silicic acid (Bio-Sil A, mesh 200-325, Bio-Rad), which had been suspended in 2 ml of 50 mM sodium phosphate buffer, pH 7.4, containing 1.5% (wt/vol) bovine serum albumin, was added to the iodination mixture to terminate the iodination reaction. After 30 min at room temperature, the pellet was washed three times with 2 ml of cold distilled water and once with 1 M HCl. The adsorbed hormone was eluted in 2 ml of acetone/water/acetic acid (40:59:1, vol/vol) and concentrated by evaporation under a stream of N2. The purified 125I-labeled ACTH1-24 (125I-ACTH1-24) had a specific activity of 124 ,uCi/,g (1 Ci = 37 GBq). After purification, >98% of the radioactivity could be adsorbed by silicic acid and >95% could be precipitated by 10% (wt/vol) trichloroacetic acid. The l...

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Section: Resultssupporting

confidence: 93%

Section: Resultsmentioning

confidence: 96%

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NH2-terminal specificity and axonal localization of adrenocorticotropin binding sites in rat median eminence.

Houten¹,

Khan²,

Walsh³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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“…Injection of HRP or wheat germ agglutinin into the pituitary in rats resulted in retrograde labeling in SOR, SON, magnocellular PVN and accessory magnocellular neurosecretory cell groups in the basal forebrain [7, 38, 39]. However, injection of these tracers into the median eminence in rats resulted in uptake in the OVLT, periventricular and preoptic areas, parvicellular PVN and ARC without any noticeable labeling in the magnocellular neurons in the SON, SOR, PVN and the accessory magnocellular structures [40, 41]. Thus the pattern of retrograde labeling following systemic tracer administration appears to be the equivalent of combined pituitary and median eminence tracer injections.…”

Section: Discussionmentioning

confidence: 99%

Galanin Immunoreactivity in Mouse Basal Forebrain: Sex Differences and Discrete Projections of Galanin-Containing Cells beyond the Blood-Brain Barrier

Rajendren

Levenkova²,

Gibson³

2000

Neuroendocrinology

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The distribution of galanin-immunoreactive (GAL-IR) cell bodies in the basal forebrain of mice was investigated. The overall pattern of staining for GAL in the area of brain analyzed was similar to that reported in other species with noticeable variations. Distinctive groups of GAL-IR cells were present in the bed nucleus of stria terminalis (BNST), supraoptic nucleus, retrochiasmatic supraoptic nucleus (SOR), magnocellular paraventricular nucleus, arcuate nucleus (ARC) and the nucleus circularis which is one of the cell groups belonging to the accessory magnocellular system. Comparison of the number of GAL-IR cells between the sexes indicated sexual dimorphism in the BNST, SOR and the ARC. As compared with female mice, the mean number of GAL-IR cells/section in the BNST and the SOR was higher and that in the ARC was lower in the males. Unlike in rats, the preoptic area contained mostly scattered GAL-IR cell bodies. Intraperitoneal injection of the retrograde tracer fluoro-gold in male mice resulted in uptake of fluoro-gold by selective GAL-IR cell groups in the basal forebrain suggesting that only some of these cell groups may project outside the blood-brain barrier whereas others may be involved in intracerebral neural transmission.

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“…Based on the correspondence of their distribution with that of neurons that are known from retrograde transport studies to project to the median eminence (23,24), these cells must certainly correspond to the heretofor unidentified population that delivers vasopressin to the hypophysial portal system. The co-occurrence of vasopressin and CRF in single neurons has important implications for understanding the interaction of these two peptides in the control of ACTH secretion and suggests the existence of a plasticity in the expression of biologically active peptides by neuroendocrine neurons as a function of physiological state.…”

Section: Discussionmentioning

confidence: 99%

Co-expression of corticotropin-releasing factor and vasopressin immunoreactivity in parvocellular neurosecretory neurons of the adrenalectomized rat.

Sawchenko¹,

Swanson²,

Vale³

1984

Proc. Natl. Acad. Sci. U.S.A.

435

198

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To clarify the anatomical organization that allows for the synergy of vasopressin and oxytocin with corticotropin-releasing factor (CRF) in promoting adrenocorticotropic hormone secretion from the anterior pituitary, immunohistochemical double staining methods were used to compare the distribution of these peptides in the hypothalamic paraventricular nucleus of normal, colchicine-treated, and adrenalectomized male rats. In untreated animals, a few CRFstained cells were found in the parvocellular division of the paraventricular nucleus, while brightly stained oxytocin-and vasopressin-immunoreactive cells were centered in the magnocellular division. In animals treated with colchicine, an inhibitor of axonal transport, large numbers of CRF-stained cells were found in the parvocellular division of the nucleus, and 1-2% of these also stained with antivasopressin. As reported previously, a substantial number of oxytocin-stained cells, centered in a discrete anterior part of the magnocellular division, also expressed CRF immunoreactivity. In contrast, after adrenalectomy, CRF immunostaining of cells in the parvocellular division was enhanced selectively and >70% of these cells also stained positively for vasopressin. The distribution of oxytocin-stained cells was not influenced by adrenalectomy. The unusual localization of vasopressin immunoreactivity in parvocellular neurosecretory neurons in the adrenalectomized rat suggests that a single population of cells can produce CRF and vasopressin, both of which are potent promoters of adrenocorticotropic hormone secretion. These findings indicate that there is a state-dependent plasticity in the expression of biologically active peptides by individual neuroendocrine neurons.The isolation and characterization of a peptide that has potent corticotropin-releasing activity (1) has effectively ended a longstanding controversy as to whether the posterior pituitary hormone vasopressin might serve an additional role as the principal corticotropin-releasing factor (CRF) of the hypothalamus (2). Nevertheless, it is clear that both vasopressin and the related nonapeptide, oxytocin, can potentiate the effects of CRF on the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary (3-5). The anatomical organization of neurons that might allow for this kind of synergy is unclear.Physiological (6) and anatomical (7-10) studies indicate that neurons delivering CRF to hypophysial portal vessels in the median eminence are concentrated in a discrete zone of the parvocellular division of the paraventricular nucleus of the hypothalamus (PVH). In contrast, most oxytocinergic and vasopressinergic neurons in the PVH of the normal rat are concentrated in an anatomically distinct magnocellular division that projects to the posterior pituitary (11,12), though a few cells of each type are scattered throughout the The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 ...

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The tuberoinfundibular system of the rat as demonstrated by immunohistochemical localization of retrogradely transported wheat germ agglutinin (WGA) from the median eminence

Cited by 148 publications

References 57 publications

NH2-terminal specificity and axonal localization of adrenocorticotropin binding sites in rat median eminence.

NH2-terminal specificity and axonal localization of adrenocorticotropin binding sites in rat median eminence.

Galanin Immunoreactivity in Mouse Basal Forebrain: Sex Differences and Discrete Projections of Galanin-Containing Cells beyond the Blood-Brain Barrier

Co-expression of corticotropin-releasing factor and vasopressin immunoreactivity in parvocellular neurosecretory neurons of the adrenalectomized rat.

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