Effects of neurotransmitters on the release of corticotropin releasing hormone (CRH) by rat hypothalamic tissue in vitro

Fehm, Horst L.; Voigt, Kai‐Ingo; Lang, R.; Pfeiffer, E. F.

doi:10.1007/bf00237553

Cited by 64 publications

(26 citation statements)

References 33 publications

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“…The reason for the difference in results is not clear; however, the stimulatory action of NE on CRF release observed in this study is in agreement with a previous report (19) that showed that NE induces a dose-related stimulation of CRF release. Our results are also in agreement with another study (21) in which CRF released into the incubation medium was measured by bioassay. The stimulatory effect of NE on CRF release was confirmed by an in vivo investigation (22) in which intracerebroventricular administration of NE induced a dose-related elevation of CRF in portal plasma.…”

Section: Discussionsupporting

confidence: 93%

Role of nitric oxide in interleukin 2-induced corticotropin-releasing factor release from incubated hypothalami.

Karanth

Lysoń

McCann

1993

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

171

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Stimulation of corticotropin-releasing factor (CRF) release from the hypothalamus by interleukin 2 (IL-2) was recently demonstrated. Cytokines induce nitric oxide synthase (NOS), an enzyme that converts L-arginine into L-citrulline and nitric oxide (NO). NO is believed to be responsible for the cytotoxic action of these agents. The constitutive form of NOS occurs in neurons in the central nervous system and NO appears to play a neurotransmitter role in cerebeilar and hippocampal function. We explored the probability that IL-2 and synaptic transmitters might release CRF via NO. The effects of L-arginine, the substrate for NOS, and NG_ monomethyl-L-arginine (NMMA), a competitive inhibitor of NOS, on IL-2-induced CRF release were studied using mediobasal hypothalami (MBHs) incubated in vitro in KrebsRinger bicarbonate buffer. L-Argoinue did not alter basal and IL-2-induced CRF release after 30 min of incubation but significantly elevated both basal and IL-2-induced CRF release when MBHs were incubated 30 min longer, presumably because the endogenous substrate had been depleted after the initial 30-min incubation period. In 30-min incubations, both carbachol, an acetylcholineomimetic drug, and norepinephrine stimulated CRF release. There was an additive effect of incubation of the MBHs in the presence of carbachol (10-7 M) and IL-2 (10-13 M). On the other hand, coincubation of MBHs with norepinephrine (10-6 M) and IL-2 (10-13 M) did not produce any additive effect. Addition of NMMA, an inhibitor of NOS, at 1 or 3 x 10-4 M completely suppressed IL-2-induced release of CRF as well as that caused by IL-2 plus carbachol. In contrast, the release of CRF induced by norepinephrine was not blocked by 3 x 10-4 M NMMA. The data indicate that IL-2 can activate constitutive NOS leading to increased NO release, which activates CRF release. It appears that NO is also involved in the release of CRF induced by carbachol but not by norepinephrine.Recent reports have demonstrated a stimulatory action of interleukin 2 (IL-2) on corticotropin-releasing factor (CRF) release using~ptoerfused hypothalami (1) or after static incubation with mediobasal hypothalami (MBHs) (unpublished data). In peripheral tissues, cytokines have been found to induce nitric oxide synthase (NOS), an enzyme that converts L-arginine (L-Arg) into L-citrulline and a reactive gas, nitric oxide (NO) (3, 4). The NO can induce cell death. It takes a number of hours for a cytokine to induce NOS. Consequently, this form of the enzyme has been termed the inducible NOS. A second type of NOS exists in a number of cells throughout the body, for example, in vascular endothelium, and it is termed the constitutive form of the enzyme (3, 4). In contrast to the inducible form, the constitutive form requires activation by an increase in intracellular calcium and its interaction with calmodulin. Both forms of NOS require L-Arg as the substrate (3, 4) and are inhibited by L-Arg analogues, such as NG-monomethyl-L-arginine (NMMA) (3, 4).The constitutive form of the enzyme ...

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Section: Discussionsupporting

confidence: 93%

Role of nitric oxide in interleukin 2-induced corticotropin-releasing factor release from incubated hypothalami.

Karanth

Lysoń

McCann

1993

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

171

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“…However, as there are reports of a negative effect of HA on the hypothalamic CRF level [6,7], histaminergic effect on the circadian rhythms of ACTH and CS may occur at the level of the hypophysis or by downward mechanisms. Moreover, as vaso pressin and oxytocin possess potent ACTH-releasing activities that mimic the CRF property [1,2], it is also possible that HA modulates the plasma CS level indirectly through these two neurohormones secreted from the neurohypophysis, as HA is also reported to be interrelated with vasopressin and oxytocin [3,20).…”

Section: Discussionmentioning

confidence: 99%

Effect of Histamine Depletion on Circadian Variations of Corticotropin and Corticosterone in Rats

Itowi¹,

Yamatodani²,

Cacabelos

et al. 1989

Neuroendocrinology

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The effects of cerebral histamine depletion induced by α-fluoromethylhistidine (FMH) on corticotropin (ACTH) and corticosterone secretions were examined. Neither acute nor chronic FMH treatment altered the corticoadrenal responses to three types of stress: transposition, immobilization and water immersion. And exposure to stress did not affect the hypothalamic content of histamine. However, chronic intracerebral treatment with FMH had a significant effect on the circadian rhythm of the plasma corticosterone (CS) level in rats. Namely, it caused a marked attenuation of the amplitude of the peaks of the CS level resulting in an almost arrythmic state. The maximum differences between FMH treated and untreated groups were seen at 8.00 and 20.00 h, the times when the illumination condition changed (light onset 8.00 h). This treatment with FMH also had a similar effect on the plasma ACTH concentration; namely the plasma ACTH level in the saline-treated group was lower than that of the FMH-treated group at light onset and higher than the latter at dark onset, but was similar to the latter at other sampling points. These results indicate the histaminergic modulation of the circadian rhythm of hormonal secretion of the adrenal cortex and show that this phenomenon is mediated through the central nervous system by an influence on the rhythm of hypophyseal ACTH secretion possibly through alteration in the concentration of corticotropin-releasing factor.

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“…Although HA and the Hr and H 2-receptor agonists stimulate POMC mRNA in the AL, the effect of the com pounds seems to be indirect, exerted at a hypothalamic level, since HA may have no effect on hormone secretion from pituitary glands in vitro [16,17]. It is likely that the effect of HA is caused by activation of CRH-and AVPcontaining neurons in the hypothalamus, since specific CRH or AVP antisera or receptor antagonists inhibited the ACTH and (3-END response to HA [18], since activa tion of H i and H2 receptors increased the concentration of CRH in pituitary portal blood [31], and since HA in creased c-Jos expression and slightly increased CRH and AVP mRNA in CRH and AVP neurons in the paraven tricular and supraoptic nuclei [19,32], CRH and AVP released by HA may subsequently stimulate the AL directly.…”

Section: Discussionmentioning

confidence: 99%

“…HA has been shown to stimulate the secretion of ACTH, [3-LPH, p-END and a-MSH from the AL and IL [14,15]. This effect of HA, which is mainly indirect [16,17], is exerted by activation of postsynaptic Hi and/or H2 recep tors, since specific agonists to these receptors increased hormone secretion and since H 1 and H2 receptor antago nists inhibited the ACTH, p-END and a-MSH responses to HA.…”

Section: Introductionmentioning

confidence: 99%

Effect of Histamine on Gene Expression and Release of Proopiomelanocortin-Derived Peptides from the Anterior and Intermediate Pituitary Lobes in Conscious Male Rats

Knigge

Kjær²,

Larsen³

et al. 1995

Neuroendocrinology

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Via activation of H₁ or H₂ receptors histamine (HA) stimulates the secretion of proopiomelanocortin (POMC)-derived peptides from the anterior (AL) and intermediate (IL) pituitary lobes of male rats. During selective inhibition of the AL or IL by pretreatment with dexamethasone (Dx) or bromocriptine (Br), respectively, we studied the effect of equipotent doses of intracerebroventricularly infused HA, the H₁-receptor agonist 2-thiazolylethylamine (2TEA) or the H₂-receptor agonist 4-methylHA (4MeHA) on the release of ACTH, β-endor-phin (β-END) immunoreactivity (ir) and α-melanocyte-stimulating hormone (α-MSH) in conscious male rats. Dx blocked the ACTH responses whereas Br prevented the α-MSH responses. Dx and Br equally inhibited the response of β-ENDir to HA and 4MeHA (80 and 70%, respectively). In contrast, the β-ENDir response to 2TEA was totally blocked by Dx but only inhibited 50% by Br. The inhibitory effect of Dx on the β-ENDir response to 2TEA was significantly stronger than the effect on the responses to HA and 4MeHA. POMC mRNA in the AL but not in the IL was increased almost 45% by HA and 2TEA and 20% by 4MeHA. Since all three histaminergic compounds in the doses used stimulated the release of β-ENDir equipotently, the results indicate that H₁-receptor activation predominantly affects the release and synthesis of β-ENDir from the AL while H₁-receptor activation affects the release of β-ENDir equally from the two lobes and only to some extent increases the synthesis in the AL. Thus, the findings suggest a differential involvement of H₁ and H₂ receptors in the mediation of the HA-induced effect on POMC-derived peptides in the AL and IL.

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Effects of neurotransmitters on the release of corticotropin releasing hormone (CRH) by rat hypothalamic tissue in vitro

Cited by 64 publications

References 33 publications

Role of nitric oxide in interleukin 2-induced corticotropin-releasing factor release from incubated hypothalami.

Role of nitric oxide in interleukin 2-induced corticotropin-releasing factor release from incubated hypothalami.

Effect of Histamine Depletion on Circadian Variations of Corticotropin and Corticosterone in Rats

Effect of Histamine on Gene Expression and Release of Proopiomelanocortin-Derived Peptides from the Anterior and Intermediate Pituitary Lobes in Conscious Male Rats

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