Functional evidence for different roles of GABA(A) and GABA(B) receptors in modulating mouse gastric tone.

Rosa Maria Serio, Flavia Mule', Alessandra Rotondo

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Abstract

The aims of the present study were to investigate, using mouse whole stomach in vitro, the effects ofg-aminobutyric acid (GABA) and GABA receptor agonists on the spontaneous gastric tone, to examine thesubtypes of GABA receptors involved in the responses and to determine the possible site(s) of action.GABA induced gastric relaxation, which was antagonized by the GABAA-receptor antagonist, bicuculline,potentiated by phaclofen, GABAB-receptor antagonist, but not affected by 1,2,5,6-Tetrahydropyridin-4-yl methylphosphinic acid hydrate (TPMPA), GABAC-receptor antagonist. Muscimol,GABAA-receptor agonist, mimicked GABA effects inducing relaxation, which was significantly reduced bybicuculline, Nu-nitro-L-arginine methyl ester (L-NAME), inhibitor of NO synthase or apamin, inhibitor ofsmall conductance Ca2þ-dependent Kþ channels, which blocks the purinergic transmission in thispreparation. It was abolished by tetrodotoxin (TTX) or L-NAME plus apamin. Baclofen, a specific GABABreceptoragonist, induced an increase in the gastric tone, which was antagonized by phaclofenand abolished by TTX or atropine. Bicuculline, but not phaclofen or TPMPA, per se induced an increase ingastric tone, which was prevented by L-NAME. In conclusion, our results suggest that GABA is involvedin the regulation of mouse gastric tone, through modulation of intrinsic neurons. Activation of GABAAreceptorsmediates relaxation through neural release of NO and neurotransmitters, activating Ca2þ-dependent Kþ channels, likely purines, while activation of GABAB-receptors leads to contraction throughacetylcholine release.
Lingua originaleEnglish
pagine (da-a)1033-1037
Numero di pagine5
RivistaNeuropharmacology
Volume58
Stato di pubblicazionePublished - 2010

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GABA-B Receptors
gamma-Aminobutyric Acid
Stomach
NG-Nitroarginine Methyl Ester
Apamin
Bicuculline
Tetrodotoxin
GABA Agents
GABA-A Receptor Agonists
GABA Agonists
Aminobutyrates
GABA-A Receptor Antagonists
Purines
Baclofen
GABA Receptors
GABA-A Receptors
Atropine
Nitric Oxide Synthase
Neurotransmitter Agents
Neurons

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Cellular and Molecular Neuroscience

Cita questo

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title = "Functional evidence for different roles of GABA(A) and GABA(B) receptors in modulating mouse gastric tone.",
abstract = "The aims of the present study were to investigate, using mouse whole stomach in vitro, the effects ofg-aminobutyric acid (GABA) and GABA receptor agonists on the spontaneous gastric tone, to examine thesubtypes of GABA receptors involved in the responses and to determine the possible site(s) of action.GABA induced gastric relaxation, which was antagonized by the GABAA-receptor antagonist, bicuculline,potentiated by phaclofen, GABAB-receptor antagonist, but not affected by 1,2,5,6-Tetrahydropyridin-4-yl methylphosphinic acid hydrate (TPMPA), GABAC-receptor antagonist. Muscimol,GABAA-receptor agonist, mimicked GABA effects inducing relaxation, which was significantly reduced bybicuculline, Nu-nitro-L-arginine methyl ester (L-NAME), inhibitor of NO synthase or apamin, inhibitor ofsmall conductance Ca2{\th}-dependent K{\th} channels, which blocks the purinergic transmission in thispreparation. It was abolished by tetrodotoxin (TTX) or L-NAME plus apamin. Baclofen, a specific GABABreceptoragonist, induced an increase in the gastric tone, which was antagonized by phaclofenand abolished by TTX or atropine. Bicuculline, but not phaclofen or TPMPA, per se induced an increase ingastric tone, which was prevented by L-NAME. In conclusion, our results suggest that GABA is involvedin the regulation of mouse gastric tone, through modulation of intrinsic neurons. Activation of GABAAreceptorsmediates relaxation through neural release of NO and neurotransmitters, activating Ca2{\th}-dependent K{\th} channels, likely purines, while activation of GABAB-receptors leads to contraction throughacetylcholine release.",
keywords = "GABA, GABA receptors, NANC inhibitory nerves., cholinergic excitatory nerves, stomach",
author = "Serio, {Rosa Maria} and Flavia Mule' and Alessandra Rotondo",
year = "2010",
language = "English",
volume = "58",
pages = "1033--1037",
journal = "Neuropharmacology",
issn = "0028-3908",
publisher = "Elsevier Limited",

}

TY - JOUR

T1 - Functional evidence for different roles of GABA(A) and GABA(B) receptors in modulating mouse gastric tone.

AU - Serio, Rosa Maria

AU - Mule', Flavia

AU - Rotondo, Alessandra

PY - 2010

Y1 - 2010

N2 - The aims of the present study were to investigate, using mouse whole stomach in vitro, the effects ofg-aminobutyric acid (GABA) and GABA receptor agonists on the spontaneous gastric tone, to examine thesubtypes of GABA receptors involved in the responses and to determine the possible site(s) of action.GABA induced gastric relaxation, which was antagonized by the GABAA-receptor antagonist, bicuculline,potentiated by phaclofen, GABAB-receptor antagonist, but not affected by 1,2,5,6-Tetrahydropyridin-4-yl methylphosphinic acid hydrate (TPMPA), GABAC-receptor antagonist. Muscimol,GABAA-receptor agonist, mimicked GABA effects inducing relaxation, which was significantly reduced bybicuculline, Nu-nitro-L-arginine methyl ester (L-NAME), inhibitor of NO synthase or apamin, inhibitor ofsmall conductance Ca2þ-dependent Kþ channels, which blocks the purinergic transmission in thispreparation. It was abolished by tetrodotoxin (TTX) or L-NAME plus apamin. Baclofen, a specific GABABreceptoragonist, induced an increase in the gastric tone, which was antagonized by phaclofenand abolished by TTX or atropine. Bicuculline, but not phaclofen or TPMPA, per se induced an increase ingastric tone, which was prevented by L-NAME. In conclusion, our results suggest that GABA is involvedin the regulation of mouse gastric tone, through modulation of intrinsic neurons. Activation of GABAAreceptorsmediates relaxation through neural release of NO and neurotransmitters, activating Ca2þ-dependent Kþ channels, likely purines, while activation of GABAB-receptors leads to contraction throughacetylcholine release.

AB - The aims of the present study were to investigate, using mouse whole stomach in vitro, the effects ofg-aminobutyric acid (GABA) and GABA receptor agonists on the spontaneous gastric tone, to examine thesubtypes of GABA receptors involved in the responses and to determine the possible site(s) of action.GABA induced gastric relaxation, which was antagonized by the GABAA-receptor antagonist, bicuculline,potentiated by phaclofen, GABAB-receptor antagonist, but not affected by 1,2,5,6-Tetrahydropyridin-4-yl methylphosphinic acid hydrate (TPMPA), GABAC-receptor antagonist. Muscimol,GABAA-receptor agonist, mimicked GABA effects inducing relaxation, which was significantly reduced bybicuculline, Nu-nitro-L-arginine methyl ester (L-NAME), inhibitor of NO synthase or apamin, inhibitor ofsmall conductance Ca2þ-dependent Kþ channels, which blocks the purinergic transmission in thispreparation. It was abolished by tetrodotoxin (TTX) or L-NAME plus apamin. Baclofen, a specific GABABreceptoragonist, induced an increase in the gastric tone, which was antagonized by phaclofenand abolished by TTX or atropine. Bicuculline, but not phaclofen or TPMPA, per se induced an increase ingastric tone, which was prevented by L-NAME. In conclusion, our results suggest that GABA is involvedin the regulation of mouse gastric tone, through modulation of intrinsic neurons. Activation of GABAAreceptorsmediates relaxation through neural release of NO and neurotransmitters, activating Ca2þ-dependent Kþ channels, likely purines, while activation of GABAB-receptors leads to contraction throughacetylcholine release.

KW - GABA

KW - GABA receptors

KW - NANC inhibitory nerves.

KW - cholinergic excitatory nerves

KW - stomach

UR - http://hdl.handle.net/10447/51816

M3 - Article

VL - 58

SP - 1033

EP - 1037

JO - Neuropharmacology

JF - Neuropharmacology

SN - 0028-3908

ER -