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Eur Neuropsychopharmacol ; 13(4): 281-8, 2003 Aug.
Article in English | MEDLINE | ID: mdl-12888188

ABSTRACT

The effects of intracerebroventricular (i.c.v.) and intrathecal (i.t.) 3-isobutyl-1-methylxanthine (IBMX), cholera toxin (CTX) and pertussis toxin (PTX) administration on immobilization-induced antinociception were studied in ICR mice. Antinociception was assessed by the tail-flick assay. Immobilization of the mouse increased inhibition of the tail-flick response for at least 1 h. The pretreatment with i.t. IBMX (0.01-1 ng), but not i.c.v. IBMX, significantly attenuated immobilization-induced inhibition of the tail-flick response. The pretreatments with i.c.v. PTX (0.05-0.5 microg) as well as i.t. CTX, but neither i.c.v. CTX (0.05-0.5 microg) nor i.t. PTX, potentiated the inhibition of the tail-flick response induced by immobilization stress. Our results suggest that spinally located phosphodiesterase appears to be involved in the production of immobilization stress-induced antinociception. In addition, inactivation of supraspinally located PTX-sensitive G-proteins and spinally located CTX-sensitive G-proteins may modulate immobilization stress-induced antinociception.


Subject(s)
1-Methyl-3-isobutylxanthine/pharmacology , Cholera Toxin/pharmacology , Pain Threshold/drug effects , Pertussis Toxin/pharmacology , Phosphodiesterase Inhibitors/pharmacology , Stress, Physiological/physiopathology , Analysis of Variance , Animals , Dose-Response Relationship, Drug , Immobilization , Injections, Intraventricular/methods , Injections, Spinal/methods , Male , Mice , Mice, Inbred ICR , Motor Activity , Pain Measurement/drug effects , Pain Threshold/physiology , Reaction Time , Time Factors
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