Gaseous Transmitters and Neuroendocrine Regulation

Darrell W Brann, Ganapathy K. Bhat, Charisee A. Lamar, Virendra B. Mahesh

Research output: Contribution to journalArticle

132 Citations (Scopus)

Abstract

Recent work has demonstrated that the brain has the capacity to synthesize impressive amounts of the gases nitric oxide (NO) and carbon monoxide (CO). There is growing evidence that these gaseous molecules function as novel neural messengers in the brain. This article reviews the pertinent literature concerning the putative role of NO and CO as critical neurotransmitters and biological mediators of the neuroendocrine axis. Abundant evidence is presented which suggests that NO has an important role in the control of reproduction due to its ability to control GnRH secretion from the hypothalamus. NO potently stimulates GnRH secretion and also appears to mediate the action of one of the major transmitters controlling GnRH secretion, glutamate. Evidence is presented which suggests that NO stimulates GnRH release due to its ability to modulate the heme-containing enzyme, guanylate cyclase, which leads to enhanced production of the second messenger molecule, cGMP. A physiological role for NO in the preovulatory LH surge was also evidenced by findings that inhibitors and antisense oligonucleotides to nitric oxide synthase (NOS) attenuate the steroid-induced and preovulatory LH surge. CO may also play a role in stimulating GnRH secretion as heme molecules stimulate GnRH release in vitro, an effect which requires heme oxygenase activity and is blocked by the gaseous scavenger molecule, hemoglobin. Evidence is also reviewed which suggests that NO acts to restrain the hypothalamic-pituitary-adrenal (HPA) axis, as it inhibits HPA stimulation by various stimulants such as interleukin-1β, vasopressin, and inflammation. This effect fits a proinflammatory role of NO as it leads to suppression of the release of the anti-inflammatory corticosteroids from the adrenal. Although not as intensely studied as NO, CO has been shown to suppress stimulated CRH release and may also function to restrain the HPA axis. Evidence implicating NO in the control of prolactin and growth hormone secretion is also reviewed and discussed, as is the possible role of NO acting directly at the anterior pituitary. Taken as a whole, the current data suggest that the diffusible gases, NO and CO, act as novel transmitters in the neuroendocrine axis and mediate a variety of important neuroendocrine functions.

Original languageEnglish (US)
Pages (from-to)385-395
Number of pages11
JournalNeuroendocrinology
Volume65
Issue number6
DOIs
StatePublished - Jan 1 1997

Fingerprint

Nitric Oxide
Gonadotropin-Releasing Hormone
Carbon Monoxide
Heme
Gases
Heme Oxygenase (Decyclizing)
Antisense Oligonucleotides
Guanylate Cyclase
Brain
Second Messenger Systems
Vasopressins
Interleukin-1
Nitric Oxide Synthase
Prolactin
Growth Hormone
Hypothalamus
Reproduction
Neurotransmitter Agents
Glutamic Acid
Adrenal Cortex Hormones

Keywords

  • Carbon monoxide
  • Corticotropin
  • Corticotropin-releasing hormone
  • Folliculo-stellate cells
  • Gonadotropes
  • Gonadotropin-releasing hormone
  • Gonadotropins
  • Growth hormone
  • Growth hormone-releasing hormone
  • Neuroimmune interactions
  • Nitric oxide
  • Prolactin

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

Cite this

Gaseous Transmitters and Neuroendocrine Regulation. / Brann, Darrell W; Bhat, Ganapathy K.; Lamar, Charisee A.; Mahesh, Virendra B.

In: Neuroendocrinology, Vol. 65, No. 6, 01.01.1997, p. 385-395.

Research output: Contribution to journalArticle

Brann, DW, Bhat, GK, Lamar, CA & Mahesh, VB 1997, 'Gaseous Transmitters and Neuroendocrine Regulation', Neuroendocrinology, vol. 65, no. 6, pp. 385-395. https://doi.org/10.1159/000127201
Brann, Darrell W ; Bhat, Ganapathy K. ; Lamar, Charisee A. ; Mahesh, Virendra B. / Gaseous Transmitters and Neuroendocrine Regulation. In: Neuroendocrinology. 1997 ; Vol. 65, No. 6. pp. 385-395.
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