IL-1β potentiates the acetylcholine induced release of vasopressin from the hypothalamus in vitro, but not from the amygdala

Jacob Raber, E. M. Pich, G. F. Koob, F. E. Bloom

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

In addition to the magnocellular hypothalamic nuclei, arginine vasopressin (AVP)-containing neurons have also been identified in limbic structures, including the hippocampus and amygdala. In the present study, we compared the qualitative properties of the in vitro release of AVP from the dissected hypothalamus with the in vitro release from the dissected amygdala and used these release systems to evaluate the interactions with neurotransmitters and cytokines. The areas of the paraventricular nucleus and supraoptic nucleus that contain the AVP neurons and that receive cholinergic innervation are also interleukin (IL)-1β immunoreactive. Acetylcholine or high KCl (60 mM) induces AVP release in both regions, and the AVP release is calcium dependent. Acetylcholine-induced AVP release is antagonized by atropine or mecamylamine, indicating that both muscarinic and nicotinic receptors are mediating the cholinergic effect in these brain regions. IL-1β (100 U/ml) had no effect on the basal AVP release from the hypothalamus, but significantly potentiated the acetylcholine-induced AVP release, lowering the threshold from 500 to 100 nM. This effect was completely blocked in the presence of neutralizing antibodies to IL-1β, atropine (10 μM) or mecamylamine (10 μM). IL-6, like IL-1β, also potentiated acetylcholine-induced AVP release, but to a lesser extent. Neither tumor necrosis factor-α nor interferon-γ had any effect on the basal or acetylcholine-induced AVP release from the hypothalamus. None of the cytokines tested had any effect on the basal or acetylcholine-induced AVP release from the amygdala. Our results suggest a hypothalamic site of action of IL-1β and IL-6 on the acetylcholine-induced AVP release. The stimulatory effects of IL-1 and IL-6 on adrenocorticotropin release have been ascribed to an increased release of corticotropin-releasing factor (CRF). These data further suggest that, in addition to CRF, AVP plays a role in the bidirectional communication between neuroendocrine and immune systems. Understanding the mode of interaction between IL-1β and IL-6 with AVP could clarify pathophysiologic or toxic effects of high brain levels of these cytokines.

Original languageEnglish (US)
Pages (from-to)208-217
Number of pages10
JournalNeuroendocrinology
Volume59
Issue number3
StatePublished - 1994
Externally publishedYes

Fingerprint

Arginine Vasopressin
Amygdala
Vasopressins
Interleukin-1
Hypothalamus
Acetylcholine
Interleukin-6
Mecamylamine
Corticotropin-Releasing Hormone
Cytokines
In Vitro Techniques
Atropine
Supraoptic Nucleus
Neurosecretory Systems
Cholinergic Neurons
Paraventricular Hypothalamic Nucleus
Poisons
Brain
Nicotinic Receptors
Muscarinic Receptors

Keywords

  • Acetylcholine
  • Amygdala
  • Hypothalamus
  • Interleukin-1
  • Interleukin-6
  • Rat
  • Vasopressin

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)

Cite this

IL-1β potentiates the acetylcholine induced release of vasopressin from the hypothalamus in vitro, but not from the amygdala. / Raber, Jacob; Pich, E. M.; Koob, G. F.; Bloom, F. E.

In: Neuroendocrinology, Vol. 59, No. 3, 1994, p. 208-217.

Research output: Contribution to journalArticle

@article{5fb8e8392c074c22a2d65749b0e2388c,
title = "IL-1β potentiates the acetylcholine induced release of vasopressin from the hypothalamus in vitro, but not from the amygdala",
abstract = "In addition to the magnocellular hypothalamic nuclei, arginine vasopressin (AVP)-containing neurons have also been identified in limbic structures, including the hippocampus and amygdala. In the present study, we compared the qualitative properties of the in vitro release of AVP from the dissected hypothalamus with the in vitro release from the dissected amygdala and used these release systems to evaluate the interactions with neurotransmitters and cytokines. The areas of the paraventricular nucleus and supraoptic nucleus that contain the AVP neurons and that receive cholinergic innervation are also interleukin (IL)-1β immunoreactive. Acetylcholine or high KCl (60 mM) induces AVP release in both regions, and the AVP release is calcium dependent. Acetylcholine-induced AVP release is antagonized by atropine or mecamylamine, indicating that both muscarinic and nicotinic receptors are mediating the cholinergic effect in these brain regions. IL-1β (100 U/ml) had no effect on the basal AVP release from the hypothalamus, but significantly potentiated the acetylcholine-induced AVP release, lowering the threshold from 500 to 100 nM. This effect was completely blocked in the presence of neutralizing antibodies to IL-1β, atropine (10 μM) or mecamylamine (10 μM). IL-6, like IL-1β, also potentiated acetylcholine-induced AVP release, but to a lesser extent. Neither tumor necrosis factor-α nor interferon-γ had any effect on the basal or acetylcholine-induced AVP release from the hypothalamus. None of the cytokines tested had any effect on the basal or acetylcholine-induced AVP release from the amygdala. Our results suggest a hypothalamic site of action of IL-1β and IL-6 on the acetylcholine-induced AVP release. The stimulatory effects of IL-1 and IL-6 on adrenocorticotropin release have been ascribed to an increased release of corticotropin-releasing factor (CRF). These data further suggest that, in addition to CRF, AVP plays a role in the bidirectional communication between neuroendocrine and immune systems. Understanding the mode of interaction between IL-1β and IL-6 with AVP could clarify pathophysiologic or toxic effects of high brain levels of these cytokines.",
keywords = "Acetylcholine, Amygdala, Hypothalamus, Interleukin-1, Interleukin-6, Rat, Vasopressin",
author = "Jacob Raber and Pich, {E. M.} and Koob, {G. F.} and Bloom, {F. E.}",
year = "1994",
language = "English (US)",
volume = "59",
pages = "208--217",
journal = "Neuroendocrinology",
issn = "0028-3835",
publisher = "S. Karger AG",
number = "3",

}

TY - JOUR

T1 - IL-1β potentiates the acetylcholine induced release of vasopressin from the hypothalamus in vitro, but not from the amygdala

AU - Raber, Jacob

AU - Pich, E. M.

AU - Koob, G. F.

AU - Bloom, F. E.

PY - 1994

Y1 - 1994

N2 - In addition to the magnocellular hypothalamic nuclei, arginine vasopressin (AVP)-containing neurons have also been identified in limbic structures, including the hippocampus and amygdala. In the present study, we compared the qualitative properties of the in vitro release of AVP from the dissected hypothalamus with the in vitro release from the dissected amygdala and used these release systems to evaluate the interactions with neurotransmitters and cytokines. The areas of the paraventricular nucleus and supraoptic nucleus that contain the AVP neurons and that receive cholinergic innervation are also interleukin (IL)-1β immunoreactive. Acetylcholine or high KCl (60 mM) induces AVP release in both regions, and the AVP release is calcium dependent. Acetylcholine-induced AVP release is antagonized by atropine or mecamylamine, indicating that both muscarinic and nicotinic receptors are mediating the cholinergic effect in these brain regions. IL-1β (100 U/ml) had no effect on the basal AVP release from the hypothalamus, but significantly potentiated the acetylcholine-induced AVP release, lowering the threshold from 500 to 100 nM. This effect was completely blocked in the presence of neutralizing antibodies to IL-1β, atropine (10 μM) or mecamylamine (10 μM). IL-6, like IL-1β, also potentiated acetylcholine-induced AVP release, but to a lesser extent. Neither tumor necrosis factor-α nor interferon-γ had any effect on the basal or acetylcholine-induced AVP release from the hypothalamus. None of the cytokines tested had any effect on the basal or acetylcholine-induced AVP release from the amygdala. Our results suggest a hypothalamic site of action of IL-1β and IL-6 on the acetylcholine-induced AVP release. The stimulatory effects of IL-1 and IL-6 on adrenocorticotropin release have been ascribed to an increased release of corticotropin-releasing factor (CRF). These data further suggest that, in addition to CRF, AVP plays a role in the bidirectional communication between neuroendocrine and immune systems. Understanding the mode of interaction between IL-1β and IL-6 with AVP could clarify pathophysiologic or toxic effects of high brain levels of these cytokines.

AB - In addition to the magnocellular hypothalamic nuclei, arginine vasopressin (AVP)-containing neurons have also been identified in limbic structures, including the hippocampus and amygdala. In the present study, we compared the qualitative properties of the in vitro release of AVP from the dissected hypothalamus with the in vitro release from the dissected amygdala and used these release systems to evaluate the interactions with neurotransmitters and cytokines. The areas of the paraventricular nucleus and supraoptic nucleus that contain the AVP neurons and that receive cholinergic innervation are also interleukin (IL)-1β immunoreactive. Acetylcholine or high KCl (60 mM) induces AVP release in both regions, and the AVP release is calcium dependent. Acetylcholine-induced AVP release is antagonized by atropine or mecamylamine, indicating that both muscarinic and nicotinic receptors are mediating the cholinergic effect in these brain regions. IL-1β (100 U/ml) had no effect on the basal AVP release from the hypothalamus, but significantly potentiated the acetylcholine-induced AVP release, lowering the threshold from 500 to 100 nM. This effect was completely blocked in the presence of neutralizing antibodies to IL-1β, atropine (10 μM) or mecamylamine (10 μM). IL-6, like IL-1β, also potentiated acetylcholine-induced AVP release, but to a lesser extent. Neither tumor necrosis factor-α nor interferon-γ had any effect on the basal or acetylcholine-induced AVP release from the hypothalamus. None of the cytokines tested had any effect on the basal or acetylcholine-induced AVP release from the amygdala. Our results suggest a hypothalamic site of action of IL-1β and IL-6 on the acetylcholine-induced AVP release. The stimulatory effects of IL-1 and IL-6 on adrenocorticotropin release have been ascribed to an increased release of corticotropin-releasing factor (CRF). These data further suggest that, in addition to CRF, AVP plays a role in the bidirectional communication between neuroendocrine and immune systems. Understanding the mode of interaction between IL-1β and IL-6 with AVP could clarify pathophysiologic or toxic effects of high brain levels of these cytokines.

KW - Acetylcholine

KW - Amygdala

KW - Hypothalamus

KW - Interleukin-1

KW - Interleukin-6

KW - Rat

KW - Vasopressin

UR - http://www.scopus.com/inward/record.url?scp=0028176588&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028176588&partnerID=8YFLogxK

M3 - Article

VL - 59

SP - 208

EP - 217

JO - Neuroendocrinology

JF - Neuroendocrinology

SN - 0028-3835

IS - 3

ER -