Lack of induction of substance P gene expression by hypoxia and absence of neurokinin 1-receptor mRNAs in the rat carotid body

Research output: Contribution to journalArticle

Abstract

Peripheral chemoreceptors are commonly thought to respond to hypoxia by releasing neurotransmitters from the type 1 cells of the carotid body; these molecules then bind to post-synaptic receptors on the carotid sinus nerve. The tachykinin substance P (SP) may act as an important neurotransmitter/neuromodulator in hypoxic chemotransmission in peripheral arterial chemoreceptors. In order to elucidate the role of SP in modulating hypoxic chemotransmission, we have used quantitative in situ hybridization histochemistry, to determine the effect of hypoxia on SP gene induction, and the localization of neurokinin 1 (NK-1) receptor mRNA in the carotid body and petrosal ganglia complex in rats at 21 days post-natal age. For comparison, we also determined: (1) the effect of hypoxia on tyrosine hydroxylase (TH) gene induction and (2) the localization of the mRNA encoding the D2-dopamine receptor. SP mRNA was not detected in the rat carotid body during normoxia and its expression was not induced after a 1 h of exposure to hypoxia (10% O2/90% N2), a stimulus that was sufficient to cause a significant increase (P2-dopamine receptor mRNA was abundantly expressed in the rat carotid body, we found no evidence of NK-1 receptor mRNA in the carotid body. In contrast, both NK-1 receptor mRNA and D2-dopamine receptor mRNA were present in petrosal ganglion cells. In the rat, SP does not appear to modulate hypoxic chemotransmission by being made in and released from type 1 cells in the carotid body, and neither does SP modulate the activity of type 1 cells by binding to NK-1 receptors on these cells. Copyright (C) 1998 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)100-108
Number of pages9
JournalJournal of the Autonomic Nervous System
Volume74
Issue number2-3
DOIs
StatePublished - Dec 11 1998

Fingerprint

Neurokinin-1 Receptors
Carotid Body
Substance P
Gene Expression
Messenger RNA
Neurotransmitter Agents
Dopamine D2 Receptors
Ganglia
Tachykinins
Carotid Sinus
Neurotransmitter Receptor
Dopamine Receptors
Tyrosine 3-Monooxygenase
Hypoxia
Genes
In Situ Hybridization

Keywords

  • Arterial chemoreceptors
  • In situ hybridization
  • Neurokinin 1 receptor mRNA
  • Petrosal ganglion
  • Preprotachykinin mRNA

ASJC Scopus subject areas

  • Physiology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

@article{96ca9cb8896449cd8f5c6190c44a8e1e,
title = "Lack of induction of substance P gene expression by hypoxia and absence of neurokinin 1-receptor mRNAs in the rat carotid body",
abstract = "Peripheral chemoreceptors are commonly thought to respond to hypoxia by releasing neurotransmitters from the type 1 cells of the carotid body; these molecules then bind to post-synaptic receptors on the carotid sinus nerve. The tachykinin substance P (SP) may act as an important neurotransmitter/neuromodulator in hypoxic chemotransmission in peripheral arterial chemoreceptors. In order to elucidate the role of SP in modulating hypoxic chemotransmission, we have used quantitative in situ hybridization histochemistry, to determine the effect of hypoxia on SP gene induction, and the localization of neurokinin 1 (NK-1) receptor mRNA in the carotid body and petrosal ganglia complex in rats at 21 days post-natal age. For comparison, we also determined: (1) the effect of hypoxia on tyrosine hydroxylase (TH) gene induction and (2) the localization of the mRNA encoding the D2-dopamine receptor. SP mRNA was not detected in the rat carotid body during normoxia and its expression was not induced after a 1 h of exposure to hypoxia (10{\%} O2/90{\%} N2), a stimulus that was sufficient to cause a significant increase (P2-dopamine receptor mRNA was abundantly expressed in the rat carotid body, we found no evidence of NK-1 receptor mRNA in the carotid body. In contrast, both NK-1 receptor mRNA and D2-dopamine receptor mRNA were present in petrosal ganglion cells. In the rat, SP does not appear to modulate hypoxic chemotransmission by being made in and released from type 1 cells in the carotid body, and neither does SP modulate the activity of type 1 cells by binding to NK-1 receptors on these cells. Copyright (C) 1998 Elsevier Science B.V.",
keywords = "Arterial chemoreceptors, In situ hybridization, Neurokinin 1 receptor mRNA, Petrosal ganglion, Preprotachykinin mRNA",
author = "Gauda, {Estelle B} and Bamford, {O. S.} and Frances Northington",
year = "1998",
month = "12",
day = "11",
doi = "10.1016/S0165-1838(98)00141-6",
language = "English (US)",
volume = "74",
pages = "100--108",
journal = "Autonomic Neuroscience: Basic and Clinical",
issn = "1566-0702",
publisher = "Elsevier",
number = "2-3",

}

TY - JOUR

T1 - Lack of induction of substance P gene expression by hypoxia and absence of neurokinin 1-receptor mRNAs in the rat carotid body

AU - Gauda, Estelle B

AU - Bamford, O. S.

AU - Northington, Frances

PY - 1998/12/11

Y1 - 1998/12/11

N2 - Peripheral chemoreceptors are commonly thought to respond to hypoxia by releasing neurotransmitters from the type 1 cells of the carotid body; these molecules then bind to post-synaptic receptors on the carotid sinus nerve. The tachykinin substance P (SP) may act as an important neurotransmitter/neuromodulator in hypoxic chemotransmission in peripheral arterial chemoreceptors. In order to elucidate the role of SP in modulating hypoxic chemotransmission, we have used quantitative in situ hybridization histochemistry, to determine the effect of hypoxia on SP gene induction, and the localization of neurokinin 1 (NK-1) receptor mRNA in the carotid body and petrosal ganglia complex in rats at 21 days post-natal age. For comparison, we also determined: (1) the effect of hypoxia on tyrosine hydroxylase (TH) gene induction and (2) the localization of the mRNA encoding the D2-dopamine receptor. SP mRNA was not detected in the rat carotid body during normoxia and its expression was not induced after a 1 h of exposure to hypoxia (10% O2/90% N2), a stimulus that was sufficient to cause a significant increase (P2-dopamine receptor mRNA was abundantly expressed in the rat carotid body, we found no evidence of NK-1 receptor mRNA in the carotid body. In contrast, both NK-1 receptor mRNA and D2-dopamine receptor mRNA were present in petrosal ganglion cells. In the rat, SP does not appear to modulate hypoxic chemotransmission by being made in and released from type 1 cells in the carotid body, and neither does SP modulate the activity of type 1 cells by binding to NK-1 receptors on these cells. Copyright (C) 1998 Elsevier Science B.V.

AB - Peripheral chemoreceptors are commonly thought to respond to hypoxia by releasing neurotransmitters from the type 1 cells of the carotid body; these molecules then bind to post-synaptic receptors on the carotid sinus nerve. The tachykinin substance P (SP) may act as an important neurotransmitter/neuromodulator in hypoxic chemotransmission in peripheral arterial chemoreceptors. In order to elucidate the role of SP in modulating hypoxic chemotransmission, we have used quantitative in situ hybridization histochemistry, to determine the effect of hypoxia on SP gene induction, and the localization of neurokinin 1 (NK-1) receptor mRNA in the carotid body and petrosal ganglia complex in rats at 21 days post-natal age. For comparison, we also determined: (1) the effect of hypoxia on tyrosine hydroxylase (TH) gene induction and (2) the localization of the mRNA encoding the D2-dopamine receptor. SP mRNA was not detected in the rat carotid body during normoxia and its expression was not induced after a 1 h of exposure to hypoxia (10% O2/90% N2), a stimulus that was sufficient to cause a significant increase (P2-dopamine receptor mRNA was abundantly expressed in the rat carotid body, we found no evidence of NK-1 receptor mRNA in the carotid body. In contrast, both NK-1 receptor mRNA and D2-dopamine receptor mRNA were present in petrosal ganglion cells. In the rat, SP does not appear to modulate hypoxic chemotransmission by being made in and released from type 1 cells in the carotid body, and neither does SP modulate the activity of type 1 cells by binding to NK-1 receptors on these cells. Copyright (C) 1998 Elsevier Science B.V.

KW - Arterial chemoreceptors

KW - In situ hybridization

KW - Neurokinin 1 receptor mRNA

KW - Petrosal ganglion

KW - Preprotachykinin mRNA

UR - http://www.scopus.com/inward/record.url?scp=0032435863&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032435863&partnerID=8YFLogxK

U2 - 10.1016/S0165-1838(98)00141-6

DO - 10.1016/S0165-1838(98)00141-6

M3 - Article

C2 - 9915624

AN - SCOPUS:0032435863

VL - 74

SP - 100

EP - 108

JO - Autonomic Neuroscience: Basic and Clinical

JF - Autonomic Neuroscience: Basic and Clinical

SN - 1566-0702

IS - 2-3

ER -