Vasopressin and Corticotropin‐releasing Factor: An Axonal Pathway to Portal Capillaries in the Zona Externa of the Median Eminence Containing Vasopressin and Its Interaction With Adrenal Corticoids*

Zimmerman, Earl A.; Stillman, Margaret A.; Recht, Larry; Antunes, J L; Carmel, Peter W.; Goldsmith, Paul C.

doi:10.1111/j.1749-6632.1977.tb41872.x

Cited by 108 publications

(32 citation statements)

References 41 publications

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“…A less dense plexus of VP-immunoreactive fibers is visible in the external zone of the ME. Consequently, the pattern of distribution of VP-containing nerve endings in the jerboa ME is similar to the one of the rat [42, 43]. Such a pattern suggests an eventual hypophysiotropic effect of VP in jerboas.…”

Section: Discussionmentioning

confidence: 56%

Vasopressin-Containing Neurons of the Hypothalamic Parvocellular Paraventricular Nucleus of the Jerboa: Plasticity Related to Immobilization Stress

Barakat

Pape²,

Boutahricht

et al. 2006

Neuroendocrinology

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The corticotropin-releasing hormone (CRH) neurons of the hypothalamic parvocellular paraventricular nucleus (PVN) have a high potential for phenotypical plasticity, allowing them to rapidly modify their neuroendocrine output, depending upon the type of stressors. Indeed, these neurons coexpress other neuropeptides, such as cholecystokinin (CCK), vasopressin (VP), and neurotensin, subserving an eventual complementary function to CRH in the regulation of the pituitary. Unlike in rats, our previous data showed that in jerboas, CCK is not coexpressed within CRH neurons in control as well as stressed animals. The present study explored an eventual VP participation in the phenotypic plasticity of CRH neurons in the jerboa. We analyzed the VP expression within the PVN by immunocytochemistry in male jerboas submitted to acute stress. Our results showed that, contrary to CRH and CCK, no significant change concerned the number of VP-immunoreactive neurons following a 30-min immobilization. The VP/CRH coexpression within PVN and median eminence was investigated by double immunocytochemistry. In control as well as stressed animals, the CRH-immunopositive neurons coexpressed VP within cell bodies and terminals. No significant difference in the number of VP/CRH double-labeled cells was found between both groups. However, such coexpression was quantitatively more important into the posterior PVN as compared with the anterior PVN. This suggests an eventual autocrine/paracrine or endocrine role for jerboa parvocellular VP which is not correlated with acute immobilization stress. VP-immunoreactive neurons also coexpressed CCK within PVN and median eminence of control and stressed jerboas. Such coexpression was more important into the anterior PVN as compared with the posterior PVN. These results showed the occurrence of at least two VP neuronal populations within the jerboa PVN. In addition, the VP expression did not depend upon acute immobilization stress. These data highlight differences in the neuroendocrine regulatory mechanisms of the stress response involving CRH/CCK or VP. They also underline that adaptative physiological mechanisms to stress might vary from one mammal species to another.

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Section: Discussionmentioning

confidence: 56%

Vasopressin-Containing Neurons of the Hypothalamic Parvocellular Paraventricular Nucleus of the Jerboa: Plasticity Related to Immobilization Stress

Barakat

Pape²,

Boutahricht

et al. 2006

Neuroendocrinology

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“…While it appears established that ADX increases the delivery as well as the storage of AVP in the external zone of the ME [22,32], the actual size of these changes has not been deter mined, due to the presence of two distinct pools (internal zone and external zone fibers) of AVP in the ME. In con trast, about 95% of the CRF is found in the external zone fibers, and the changes of its release can be related to the alterations in ME content.…”

Section: Discussionmentioning

confidence: 99%

Predominant Release of Vasopressin vs. Corticotropin-Releasing Factor from the Isolated Median Eminence after Adrenalectomy

et al. 1986

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In an in vitro system, we have demonstrated concomitant release of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) from the median eminence (ME) of normal and adrenalectomized rats. The ME were incubated in a Krebs-Ringer bicarbonate medium, CRF and AVP released into the medium were measured by radioimmunoassay. The release of both neuropeptides was stimulated by increasing concentrations of potassium (28–56 µM) in the incubation medium, or by addition of veratridine (5–20 µM). In both cases the release process was dependent on the presence of calcium in the incubation medium. Interestingly, potassium-induced release was found to be relatively insensitive to calcium channel antagonists that are potent inhibitors in smooth and cardiac muscle. The sodium channel antagonist, tetrodotoxin (1 µM), completely blocked the effect of veratridine, while no change was seen in the response to potassium. Adrenalectomy increased the ratio of AVP:CRF release from 2:1 in ME removed from sham-operated rats to 8:1 in ME from the adrenalectomized group. We suggest that this ratio of AVP:CRF release may also pertain in vivo, and that AVP could be the predominant corticotropic stimulus in adrenalectomized rats.

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“…Zimmerman et al (1977) suggested that AVP neurons which project from PVN to ME have an important role in releasing ACTH from the pituitary. However, we reported that CRF and AVP were not identical, although AVP was responsible for 20-40% of CRF activity in crude hypothalamic extract (Hashimoto et al, 1981 b) and that CRF and AVP in the hypothalamic nuclei showed different changes after adrenalectomy, dexamethasone or estradiol treatment (Hashimoto et al, 1981 a, c).…”

mentioning

confidence: 99%

“…We also examined the effect of the compound on plasma and hypothalamic AVP content, because a close relationship has been reported between CRF and AVP (Zimmerman et al 1977;Gillies et al, 1978;Dornhost et al, 1981 (Fig. 4).…”

mentioning

confidence: 99%

The effect of serotonin agonist 1-(trifluoromethylphenly)-piperazine on corticotropin releasing factor and arginine vasopressin in rat hypothalamic nuclei.

et al. 1982

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Effects of 1-(m-trifluoromethylphenyl)-piperazine, a serotonin agonist, were examined on rat plasma levels of adrenocorticotropin (ACTH) and arginine vasopressin (AVP), and on hypothalamic contents of corticotropin releasing factor (CRF) and AVP, to investigate the role of brain serotonin in ACTH regulation.Both plasma ACTH and AVP levels increased markedly 30 min after injection of the compound and were still elevated at 80 min. CRF and AVP contents in the median eminence decreased 30 min after injection but returned to the basal levels by 80 min. The AVP content in the supraoptic nucleus was elevated 80 min after injection.The CRF and AVP content did not significantly change in the paraventricular, suprachiasmatic and arcuate nuclei. Serotonin or 1-(m-trifluoromethylphenyl)-piperazine did not stimulate the release of ACTH in pituitary cell cultures. These results suggest that both CRF and AVP were secreted into the portal vessels by 1-(mtrifluoromethylphenyl)-piperazine to release ACTH from the anterior pituitary and that both the ACTH and AVP release were stimulated via the brain serotonergic mechanism.

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Vasopressin and Corticotropin‐releasing Factor: An Axonal Pathway to Portal Capillaries in the Zona Externa of the Median Eminence Containing Vasopressin and Its Interaction With Adrenal Corticoids*

Cited by 108 publications

References 41 publications

Vasopressin-Containing Neurons of the Hypothalamic Parvocellular Paraventricular Nucleus of the Jerboa: Plasticity Related to Immobilization Stress

Vasopressin-Containing Neurons of the Hypothalamic Parvocellular Paraventricular Nucleus of the Jerboa: Plasticity Related to Immobilization Stress

Predominant Release of Vasopressin vs. Corticotropin-Releasing Factor from the Isolated Median Eminence after Adrenalectomy

The effect of serotonin agonist 1-(trifluoromethylphenly)-piperazine on corticotropin releasing factor and arginine vasopressin in rat hypothalamic nuclei.

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