Modulation of gamma-aminobutyric acid on painful sense in central nervous system of morphine-dependent rats.
- Author:
Yan XU
1
;
Man-Ying XU
;
Xia LI
Author Information
- Publication Type:Journal Article
- MeSH: Action Potentials; drug effects; physiology; Animals; Bicuculline; pharmacology; Disease Models, Animal; Drug Administration Schedule; Electric Stimulation; adverse effects; Female; GABA Antagonists; pharmacology; Injections, Intraventricular; methods; Male; Morphine; administration & dosage; Morphine Dependence; etiology; pathology; physiopathology; Narcotics; administration & dosage; Nucleus Accumbens; metabolism; physiopathology; Pain; etiology; physiopathology; Pain Threshold; drug effects; physiology; Rats; Rats, Wistar; Reaction Time; drug effects; physiology; Time Factors; gamma-Aminobutyric Acid; metabolism; pharmacology
- From: Neuroscience Bulletin 2008;24(5):278-282
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo observe the effects of gamma-aminobutyric acid (GABA) on the electric activities of pain-excited neurons (PEN) in nucleus accumbens (NAc) in central nervous system (CNS) of morphine-dependent rats.
METHODSAfter GABA or the GABA(A)-receptor antagonist, bicuculline (Bic), was injected into cerebral ventricles or NAc, right sciatic nerve was stimulated by electrical pulses, which was considered as traumatic pain stimulation. Extracellular recordings methods were used to record the electric activities of PEN in NAc.
RESULTSWhen GABA was injected into intracerebroventricle (ICV) as well as NAc, it could decrease the pain-evoked discharge frequency and prolong the latency of PEN. Bic could interdict the above effects of GABA on the electric activities of PEN.
CONCLUSIONExogenous GABA might have an inhibitory effect on the central pain adjustment. Furthermore, GABA and GABA(A) receptor participate and mediate the traumatic information transmission process in CNS.
