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GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior.

GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior. Research Abstract Details 

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  • GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior. Abstract Text:

    stacey c lagraizeStacey C LaGraize,perry n fuchsPerry N Fuchs,

    The rostral anterior cingulate cortex (rACC) is involved in supraspinal nociceptive processing. ACC lesions relieve persistent pain, but do not affect the patient's ability to localize a noxious stimulus. Since the rACC has a high density of GABA receptors, it is possible that pain processing is influenced by these receptors in the rACC. The present experiments examined the involvement of rat rACC GABA(A) and GABA(B) receptors in regard to sensitivity to mechanical stimulation and escape/avoidance behavior in response to a noxious stimulus following L5 spinal nerve ligation. Rats were or were not afflicted with a neuropathic pain condition by an L5 spinal nerve ligation. rACC microinjection of 10 microg/microl GABA, a GABA(A) agonist (0.001 microg/microl, 0.1 microg/microl, or 0.5 microg/microl muscimol), a GABA(B) agonist (0.1 microg/microl, 1 microg/microl, or 5 microg/microl baclofen), or saline, did not alter mechanical withdrawal thresholds. Importantly, following 10 microg/microl GABA, 0.1 microg/microl, or 0.5 microg/microl muscimol microinjected into the rACC, place escape/avoidance behavior to a noxious mechanical stimulus was attenuated in injured animals. The attenuation was specific to the rACC and was blocked by a preadministered microinjection of the appropriate antagonist(s) into the rACC. In conclusion, microinjection of GABA and higher doses of muscimol did not decrease mechanical hyperalgesia but did attenuate place escape/avoidance behavior that is associated with mechanical stimulation of the ligated paw. These results provide additional support for the role of the rACC in higher order supraspinal processing of noxious events and suggest that rACC GABA(A) receptors significantly contribute to this processing.

    GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior. Publishing Authors By Initials

    sc lagraizeSC LaGraize,pn fuchsPN Fuchs,

    For similar organic chemicals: carboxylic acids: acids, acyclic: butyric acids: aminobutyric acids: gamma-aminobutyric acid research abstracts see: organic chemicals: carboxylic acids: acids, acyclic: butyric acids: aminobutyric acids: gamma-aminobutyric acid research

    PUBMED ID PMID:

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    GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Experimental neurology

    VOLUME: 204

    Page Numbers: 182-94

    Journal Abbreviation: Exp. Neurol.

    ISSN: 0014-4886

    DAY: 4

    MONTH: 12

    YEAR: 2006

    GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 370712

    GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior. Keywords Mesh Terms:

    KEYWORDS: gamma-Aminobutyric Acid

    MESH TERMS: pharmacology

    Chemical & Substance for Abstract: GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior. Information

    Substance Name: gamma-Aminobutyric Acid

    Registry Number: 56-12-2

    Grant and Affiliation Information for GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior.

    AFFILIATION: Department of Psychology, University of Texas at Arlington, Arlington, TX 76019, USA. SLagraize@umaryland.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDA

    GRANT: R15 DA015350-01A1

    ACRONYM: DA

    MEDLINETA: Exp Neurol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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