IFNγ increases M2 muscarinic receptor expression in cultured sympathetic neurons

Ana Cristina G Grodzki, Atefeh Ghogha, Linley Mangini, Allison Fryer, Pamela J. Lein

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

M2 muscarinic receptors are expressed on both parasympathetic and sympathetic nerve endings where they function as autoinhibitory receptors to limit release of acetylcholine and norepinephrine, respectively. M2 muscarinic receptor expression on parasympathetic nerves is decreased by viral infection and by gamma-interferon (IFNγ) and increased by dexamethasone; and these effects are of clinical relevance in the etiology and treatment of asthma. Whether IFNÄ and dexamethasone similarly modulate M2 receptor expression on sympathetic nerves is not known. To address this question, we examined the effects of IFNγ and dexamethasone on M2 receptor expression at the mRNA and protein level in primary cultures of sympathetic neurons dissociated from the rat superior cervical ganglia (SCG). Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) indicated that neither IFNγ nor dexamethasone altered M2 receptor transcript levels. However, western blot analyses demonstrated that IFNγ, but not dexamethasone, increases M2 receptor protein expression in sympathetic neurons. Increased expression did not significantly alter subcellular localization of M2 receptors in sympathetic neurons as determined using immunocytochemistry. These findings indicate that M2 receptors are differentially regulated in different types of autonomic neurons, and they suggest a novel mechanism by which IFNγ may contribute to airway hyperreactivity in viral-induced asthma.

Original languageEnglish (US)
Pages (from-to)23-29
Number of pages7
JournalCurrent Neurobiology
Volume2
Issue number1
StatePublished - 2011

Fingerprint

Muscarinic M2 Receptors
Interferons
Dexamethasone
Neurons
Asthma
Superior Cervical Ganglion
Nerve Endings
Virus Diseases
Reverse Transcriptase Polymerase Chain Reaction
Acetylcholine
Interferon-gamma
Norepinephrine
Proteins
Western Blotting
Immunohistochemistry
Messenger RNA

Keywords

  • Dexamethasone
  • Ifnγ
  • M2 muscarinic receptor
  • Sympathetic nerves

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Grodzki, A. C. G., Ghogha, A., Mangini, L., Fryer, A., & Lein, P. J. (2011). IFNγ increases M2 muscarinic receptor expression in cultured sympathetic neurons. Current Neurobiology, 2(1), 23-29.

IFNγ increases M2 muscarinic receptor expression in cultured sympathetic neurons. / Grodzki, Ana Cristina G; Ghogha, Atefeh; Mangini, Linley; Fryer, Allison; Lein, Pamela J.

In: Current Neurobiology, Vol. 2, No. 1, 2011, p. 23-29.

Research output: Contribution to journalArticle

Grodzki, ACG, Ghogha, A, Mangini, L, Fryer, A & Lein, PJ 2011, 'IFNγ increases M2 muscarinic receptor expression in cultured sympathetic neurons', Current Neurobiology, vol. 2, no. 1, pp. 23-29.
Grodzki, Ana Cristina G ; Ghogha, Atefeh ; Mangini, Linley ; Fryer, Allison ; Lein, Pamela J. / IFNγ increases M2 muscarinic receptor expression in cultured sympathetic neurons. In: Current Neurobiology. 2011 ; Vol. 2, No. 1. pp. 23-29.
@article{fae5f69162b54761a730517afe3452d6,
title = "IFNγ increases M2 muscarinic receptor expression in cultured sympathetic neurons",
abstract = "M2 muscarinic receptors are expressed on both parasympathetic and sympathetic nerve endings where they function as autoinhibitory receptors to limit release of acetylcholine and norepinephrine, respectively. M2 muscarinic receptor expression on parasympathetic nerves is decreased by viral infection and by gamma-interferon (IFNγ) and increased by dexamethasone; and these effects are of clinical relevance in the etiology and treatment of asthma. Whether IFN{\"A} and dexamethasone similarly modulate M2 receptor expression on sympathetic nerves is not known. To address this question, we examined the effects of IFNγ and dexamethasone on M2 receptor expression at the mRNA and protein level in primary cultures of sympathetic neurons dissociated from the rat superior cervical ganglia (SCG). Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) indicated that neither IFNγ nor dexamethasone altered M2 receptor transcript levels. However, western blot analyses demonstrated that IFNγ, but not dexamethasone, increases M2 receptor protein expression in sympathetic neurons. Increased expression did not significantly alter subcellular localization of M2 receptors in sympathetic neurons as determined using immunocytochemistry. These findings indicate that M2 receptors are differentially regulated in different types of autonomic neurons, and they suggest a novel mechanism by which IFNγ may contribute to airway hyperreactivity in viral-induced asthma.",
keywords = "Dexamethasone, Ifnγ, M2 muscarinic receptor, Sympathetic nerves",
author = "Grodzki, {Ana Cristina G} and Atefeh Ghogha and Linley Mangini and Allison Fryer and Lein, {Pamela J.}",
year = "2011",
language = "English (US)",
volume = "2",
pages = "23--29",
journal = "Current Neurobiology",
issn = "0975-9042",
publisher = "Scientific Publishers of India",
number = "1",

}

TY - JOUR

T1 - IFNγ increases M2 muscarinic receptor expression in cultured sympathetic neurons

AU - Grodzki, Ana Cristina G

AU - Ghogha, Atefeh

AU - Mangini, Linley

AU - Fryer, Allison

AU - Lein, Pamela J.

PY - 2011

Y1 - 2011

N2 - M2 muscarinic receptors are expressed on both parasympathetic and sympathetic nerve endings where they function as autoinhibitory receptors to limit release of acetylcholine and norepinephrine, respectively. M2 muscarinic receptor expression on parasympathetic nerves is decreased by viral infection and by gamma-interferon (IFNγ) and increased by dexamethasone; and these effects are of clinical relevance in the etiology and treatment of asthma. Whether IFNÄ and dexamethasone similarly modulate M2 receptor expression on sympathetic nerves is not known. To address this question, we examined the effects of IFNγ and dexamethasone on M2 receptor expression at the mRNA and protein level in primary cultures of sympathetic neurons dissociated from the rat superior cervical ganglia (SCG). Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) indicated that neither IFNγ nor dexamethasone altered M2 receptor transcript levels. However, western blot analyses demonstrated that IFNγ, but not dexamethasone, increases M2 receptor protein expression in sympathetic neurons. Increased expression did not significantly alter subcellular localization of M2 receptors in sympathetic neurons as determined using immunocytochemistry. These findings indicate that M2 receptors are differentially regulated in different types of autonomic neurons, and they suggest a novel mechanism by which IFNγ may contribute to airway hyperreactivity in viral-induced asthma.

AB - M2 muscarinic receptors are expressed on both parasympathetic and sympathetic nerve endings where they function as autoinhibitory receptors to limit release of acetylcholine and norepinephrine, respectively. M2 muscarinic receptor expression on parasympathetic nerves is decreased by viral infection and by gamma-interferon (IFNγ) and increased by dexamethasone; and these effects are of clinical relevance in the etiology and treatment of asthma. Whether IFNÄ and dexamethasone similarly modulate M2 receptor expression on sympathetic nerves is not known. To address this question, we examined the effects of IFNγ and dexamethasone on M2 receptor expression at the mRNA and protein level in primary cultures of sympathetic neurons dissociated from the rat superior cervical ganglia (SCG). Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) indicated that neither IFNγ nor dexamethasone altered M2 receptor transcript levels. However, western blot analyses demonstrated that IFNγ, but not dexamethasone, increases M2 receptor protein expression in sympathetic neurons. Increased expression did not significantly alter subcellular localization of M2 receptors in sympathetic neurons as determined using immunocytochemistry. These findings indicate that M2 receptors are differentially regulated in different types of autonomic neurons, and they suggest a novel mechanism by which IFNγ may contribute to airway hyperreactivity in viral-induced asthma.

KW - Dexamethasone

KW - Ifnγ

KW - M2 muscarinic receptor

KW - Sympathetic nerves

UR - http://www.scopus.com/inward/record.url?scp=82655175461&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=82655175461&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:82655175461

VL - 2

SP - 23

EP - 29

JO - Current Neurobiology

JF - Current Neurobiology

SN - 0975-9042

IS - 1

ER -