Blockade of GABA, type A, receptors in the rat pontine reticular formation induces rapid eye movement sleep that is dependent upon the cholinergic system

G. A. Marks, O. W. Sachs, C. G. Birabil

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

The brainstem reticular formation is an area important to the control of rapid eye movement (REM) sleep. The antagonist of GABA-type A (GABAA) receptors, bicuculline methiodide (BMI), injected into the rat nucleus pontis oralis (PnO) of the reticular formation resulted in a long-lasting increase in REM sleep. Thus, one factor controlling REM sleep appears to be the number of functional GABAA receptors in the PnO. The long-lasting effect produced by BMI may result from secondary influences on other neurotransmitter systems known to have long-lasting effects. To study this question, rats were surgically prepared for chronic sleep recording and additionally implanted with guide cannulas aimed at sites in the PnO. Multiple, 60 nl, unilateral injections were made either singly or in combination. GABAA receptor antagonists, BMI and gabazine (GBZ), produced dose-dependent increases in REM sleep with GBZ being approximately 35 times more potent than BMI. GBZ and the cholinergic agonist, carbachol, produced very similar results, both increasing REM sleep for about 8 h, mainly through increased period frequency, with little reduction in REM latency. Pre-injection of the muscarinic antagonist, atropine, completely blocked the REM sleep-increase by GBZ. GABAergic control of REM sleep in the PnO requires the cholinergic system and may be acting through presynaptic modulation of acetylcholine release.

Original languageEnglish (US)
Pages (from-to)1-10
Number of pages10
JournalNeuroscience
Volume156
Issue number1
DOIs
StatePublished - Sep 22 2008

Fingerprint

REM Sleep
GABA-A Receptors
Cholinergic Agents
Sleep
GABA-A Receptor Antagonists
Reticular Formation
Cholinergic Agonists
Injections
Muscarinic Antagonists
Pontine Tegmentum
Carbachol
Atropine
Brain Stem
Acetylcholine
Neurotransmitter Agents
bicuculline methiodide
gabazine

Keywords

  • bicuculline
  • gabazine
  • intracerebral injection
  • muscarinic
  • nucleus pontis oralis
  • sublaterodorsal nucleus

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Blockade of GABA, type A, receptors in the rat pontine reticular formation induces rapid eye movement sleep that is dependent upon the cholinergic system. / Marks, G. A.; Sachs, O. W.; Birabil, C. G.

In: Neuroscience, Vol. 156, No. 1, 22.09.2008, p. 1-10.

Research output: Contribution to journalArticle

@article{10346e4d676641679e2cfee920d642db,
title = "Blockade of GABA, type A, receptors in the rat pontine reticular formation induces rapid eye movement sleep that is dependent upon the cholinergic system",
abstract = "The brainstem reticular formation is an area important to the control of rapid eye movement (REM) sleep. The antagonist of GABA-type A (GABAA) receptors, bicuculline methiodide (BMI), injected into the rat nucleus pontis oralis (PnO) of the reticular formation resulted in a long-lasting increase in REM sleep. Thus, one factor controlling REM sleep appears to be the number of functional GABAA receptors in the PnO. The long-lasting effect produced by BMI may result from secondary influences on other neurotransmitter systems known to have long-lasting effects. To study this question, rats were surgically prepared for chronic sleep recording and additionally implanted with guide cannulas aimed at sites in the PnO. Multiple, 60 nl, unilateral injections were made either singly or in combination. GABAA receptor antagonists, BMI and gabazine (GBZ), produced dose-dependent increases in REM sleep with GBZ being approximately 35 times more potent than BMI. GBZ and the cholinergic agonist, carbachol, produced very similar results, both increasing REM sleep for about 8 h, mainly through increased period frequency, with little reduction in REM latency. Pre-injection of the muscarinic antagonist, atropine, completely blocked the REM sleep-increase by GBZ. GABAergic control of REM sleep in the PnO requires the cholinergic system and may be acting through presynaptic modulation of acetylcholine release.",
keywords = "bicuculline, gabazine, intracerebral injection, muscarinic, nucleus pontis oralis, sublaterodorsal nucleus",
author = "Marks, {G. A.} and Sachs, {O. W.} and Birabil, {C. G.}",
year = "2008",
month = "9",
day = "22",
doi = "10.1016/j.neuroscience.2008.06.067",
language = "English (US)",
volume = "156",
pages = "1--10",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "1",

}

TY - JOUR

T1 - Blockade of GABA, type A, receptors in the rat pontine reticular formation induces rapid eye movement sleep that is dependent upon the cholinergic system

AU - Marks, G. A.

AU - Sachs, O. W.

AU - Birabil, C. G.

PY - 2008/9/22

Y1 - 2008/9/22

N2 - The brainstem reticular formation is an area important to the control of rapid eye movement (REM) sleep. The antagonist of GABA-type A (GABAA) receptors, bicuculline methiodide (BMI), injected into the rat nucleus pontis oralis (PnO) of the reticular formation resulted in a long-lasting increase in REM sleep. Thus, one factor controlling REM sleep appears to be the number of functional GABAA receptors in the PnO. The long-lasting effect produced by BMI may result from secondary influences on other neurotransmitter systems known to have long-lasting effects. To study this question, rats were surgically prepared for chronic sleep recording and additionally implanted with guide cannulas aimed at sites in the PnO. Multiple, 60 nl, unilateral injections were made either singly or in combination. GABAA receptor antagonists, BMI and gabazine (GBZ), produced dose-dependent increases in REM sleep with GBZ being approximately 35 times more potent than BMI. GBZ and the cholinergic agonist, carbachol, produced very similar results, both increasing REM sleep for about 8 h, mainly through increased period frequency, with little reduction in REM latency. Pre-injection of the muscarinic antagonist, atropine, completely blocked the REM sleep-increase by GBZ. GABAergic control of REM sleep in the PnO requires the cholinergic system and may be acting through presynaptic modulation of acetylcholine release.

AB - The brainstem reticular formation is an area important to the control of rapid eye movement (REM) sleep. The antagonist of GABA-type A (GABAA) receptors, bicuculline methiodide (BMI), injected into the rat nucleus pontis oralis (PnO) of the reticular formation resulted in a long-lasting increase in REM sleep. Thus, one factor controlling REM sleep appears to be the number of functional GABAA receptors in the PnO. The long-lasting effect produced by BMI may result from secondary influences on other neurotransmitter systems known to have long-lasting effects. To study this question, rats were surgically prepared for chronic sleep recording and additionally implanted with guide cannulas aimed at sites in the PnO. Multiple, 60 nl, unilateral injections were made either singly or in combination. GABAA receptor antagonists, BMI and gabazine (GBZ), produced dose-dependent increases in REM sleep with GBZ being approximately 35 times more potent than BMI. GBZ and the cholinergic agonist, carbachol, produced very similar results, both increasing REM sleep for about 8 h, mainly through increased period frequency, with little reduction in REM latency. Pre-injection of the muscarinic antagonist, atropine, completely blocked the REM sleep-increase by GBZ. GABAergic control of REM sleep in the PnO requires the cholinergic system and may be acting through presynaptic modulation of acetylcholine release.

KW - bicuculline

KW - gabazine

KW - intracerebral injection

KW - muscarinic

KW - nucleus pontis oralis

KW - sublaterodorsal nucleus

UR - http://www.scopus.com/inward/record.url?scp=51449091381&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=51449091381&partnerID=8YFLogxK

U2 - 10.1016/j.neuroscience.2008.06.067

DO - 10.1016/j.neuroscience.2008.06.067

M3 - Article

C2 - 18706488

AN - SCOPUS:51449091381

VL - 156

SP - 1

EP - 10

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 1

ER -