IL-2 induces vasopressin release from the hypothalamus and the amygdala: Role of nitric oxide-mediated signaling

Jacob Raber, Floyd E. Bloom

Research output: Contribution to journalArticle

93 Citations (Scopus)

Abstract

The neuropeptide arginine vasopressin (AVP) can replace the cytokine interleukin 2 (IL-2) as a T-cell mitogen for the induction of interferon γ (IFN γ) expression in splenic cultures. IL-2-like and IL-2 receptor immunoreactivity have been reported in different brain regions, under normal and pathophysiological conditions. Regulatory functions for IL-2 in the CNS have been suggested. In addition to the spleen, AVP might also mediate some IL-2 effects centrally. In the present study, we evaluated the effect of IL- 2 on the in vitro release of AVP from the hypothalamus and amygdala. In addition, we used these release systems to study the possible involvement of NO-mediated signaling in AVP release, based on the reported detection of nitric oxide synthase (NOS) in the hypothalamus and amygdala. IL-2 rapidly stimulates AVP release in both regions, in a calcium- and dose-dependent manner. In addition, nitroprusside also induces AVP release. Norepinephrine also induces AVP release from both the hypothalamus, as well as the amygdala. The norepinephrine-induced AVP release is antagonized by phentolamine, but not by propanolol, suggesting an α-adrenergic receptor-mediated AVP response in both brain regions. The IL-2- and acetylcholine-induced AVP release is antagonized by N(g)-methyl-L-arginine, indicating a role for NO in this AVP release. N(g)-methyl-L-arginine does not affect the norepinephrine-induced AVP release. A stimulatory effect of IL-2 on hypothalamic CRF release and plasma ACTH has already been reported. Our results suggest that in addition to CRF, AVP may also mediate the IL-2 stimulation of ACTH secretion. These data further suggest that in addition to the hypothalamus, the amygdala may also play a role in the bidirectional communication between neuroendocrine and immune systems. Understanding the mode of interaction between IL-2 with AVP could clarify the pathophysiologic or toxic effects of high brain levels of IL-2.

Original languageEnglish (US)
Pages (from-to)6187-6195
Number of pages9
JournalJournal of Neuroscience
Volume14
Issue number10
StatePublished - Oct 1994
Externally publishedYes

Fingerprint

Arginine Vasopressin
Amygdala
Vasopressins
Hypothalamus
Interleukin-2
Nitric Oxide
Norepinephrine
Adrenocorticotropic Hormone
Arginine
Brain
Neurosecretory Systems
Phentolamine
Interleukin-2 Receptors
Poisons
Nitroprusside
Neuropeptides
Mitogens
Propranolol
Nitric Oxide Synthase
Adrenergic Receptors

Keywords

  • acetylcholine
  • amygdala
  • hypothalamus
  • interleuki n-2
  • nitric oxide
  • norepinephrine
  • rat
  • vasopressin

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

IL-2 induces vasopressin release from the hypothalamus and the amygdala : Role of nitric oxide-mediated signaling. / Raber, Jacob; Bloom, Floyd E.

In: Journal of Neuroscience, Vol. 14, No. 10, 10.1994, p. 6187-6195.

Research output: Contribution to journalArticle

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N2 - The neuropeptide arginine vasopressin (AVP) can replace the cytokine interleukin 2 (IL-2) as a T-cell mitogen for the induction of interferon γ (IFN γ) expression in splenic cultures. IL-2-like and IL-2 receptor immunoreactivity have been reported in different brain regions, under normal and pathophysiological conditions. Regulatory functions for IL-2 in the CNS have been suggested. In addition to the spleen, AVP might also mediate some IL-2 effects centrally. In the present study, we evaluated the effect of IL- 2 on the in vitro release of AVP from the hypothalamus and amygdala. In addition, we used these release systems to study the possible involvement of NO-mediated signaling in AVP release, based on the reported detection of nitric oxide synthase (NOS) in the hypothalamus and amygdala. IL-2 rapidly stimulates AVP release in both regions, in a calcium- and dose-dependent manner. In addition, nitroprusside also induces AVP release. Norepinephrine also induces AVP release from both the hypothalamus, as well as the amygdala. The norepinephrine-induced AVP release is antagonized by phentolamine, but not by propanolol, suggesting an α-adrenergic receptor-mediated AVP response in both brain regions. The IL-2- and acetylcholine-induced AVP release is antagonized by N(g)-methyl-L-arginine, indicating a role for NO in this AVP release. N(g)-methyl-L-arginine does not affect the norepinephrine-induced AVP release. A stimulatory effect of IL-2 on hypothalamic CRF release and plasma ACTH has already been reported. Our results suggest that in addition to CRF, AVP may also mediate the IL-2 stimulation of ACTH secretion. These data further suggest that in addition to the hypothalamus, the amygdala may also play a role in the bidirectional communication between neuroendocrine and immune systems. Understanding the mode of interaction between IL-2 with AVP could clarify the pathophysiologic or toxic effects of high brain levels of IL-2.

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