MODULATION OF ALCOHOL PREFERENCE BY NMDA ANTAGONISTS IN MALE RATS

Chronic alcoholization by alcohol inhalation was used to studythe properties of magnesium, a non-competitive NMDA receptorantagonist, and CGP 39551, a competitive NMDA receptor antagonist,on behavioural dependence as estimated by the free-choice paradigm[alcohol 10% (v/v) vs. water], on the hypermotility after alcoholwithdrawal, and finally on the cortical vascularization. Thefirst experimental group received the drugs per os during thewhole alcoholization period. Magnesium (20 mg/kg/day) decreasedthe alcohol dependence while CGP 39551 (5 and 10 mg/kg/day)increased, in a dose-dependent manner, the dependence to alcohol.A second group of animals received the same drugs at the samedosages, not simultaneously during chronic alcoholization, butimmediately after alcoholization in one shot i.p. injection.In this case, rats receiving 5 mg/kg CGP 39551 never showedany dependence towards alcohol, while 10 mg/kg CGP 39551 or20 mg/kg magnesium prolonged the number of days of alcohol dependence.These results thus indicate the close interaction between NMDAreceptor function and dependence for alcohol. Magnesium hadno effects on hypermotility, while CGP 39551-treated animalspresented a decrease in the hypermotility observed after alcoholwithdrawal. Neither drug affected the hypervasculanzation accompanyingthe chronic alcoholization.     

Interleukin-5 immunoreactivity and mRNA expression in gut mucosa from patients with food allergy

BACKGROUND: Mast cell activation has been assumed to play a role in dermal neurogenic inflammation: C fibre-derived neuropeptides activating mast cells and releasing histamine, which in turn would activate C fibres. OBJECTIVE: To test this hypothesis mast cell tryptase (MCT) was measured inside the axon reflex flare area. Axon reflexes were elicited by histamine or compound 48/80, a polyanionic mast cell-degranulating substance. The time course of plasma extravasation and release of histamine and MCT from dermal mast cells in neurogenic inflammation was measured in vivo by intradermal microdialysis in humans. METHODS: Single hollow plasmapheresis fibres (pore cutoff size: 3000 kDa) were inserted intracutaneously at the volar forearm and perfused with Ringer's solution (4 microL/min) with one microdialysis fibre located at the planned stimulation site and a second inside the axon reflex area. Neurogenic inflammation was induced by intraprobe delivery of either histamine or the mast cell-degranulating agent compound 48/80. Mediator release was measured at the stimulation sites and inside the arising axon reflex flare area. RESULTS: Mast cell degranulation induced marked plasma protein extravasation (PPE 0.25 +/- 0.04-1.31 +/- 0.6 mg/mL; pre- and post-stimulation, mean +/- sem, n = 7) and release of histamine (2.0 +/- 0.9-38.7 +/- 1.4 ng/mL) and MCT (9.84 +/- 2.4-92.2 +/- 21.6 ng/mL). Interestingly, in addition to increasing PPE (0.33 +/- 0. 11-1.85 +/- 0.9 mg/mL), histamine also induced a slight but significant increase in MCT (11.3 +/- 3.0-12.4 +/- 2.3 ng/mL). No evidence for mast cell activation was observed inside the axon reflex areas, where PPE (0.34 +/- 0.03-0.25 +/- 0.02 mg/mL), histamine (1.64 +/- 0.5-1.46 +/- 0.4 ng/mL) and MCT concentration (11.6 +/- 3.1-7.6 +/- 1.7 ng/mL) gradually decreased. CONCLUSION: It is concluded that dermal neurogenic inflammation does not degranulate mast cells.     

ADRENALECTOMY PROTECTS ETHANOL-WITHDRAWN RATS FROM HARMINE-INDUCED TREMOR

Abstract-A growing number of studies have implicated the hypothalamic-pituitary-adrenal(HPA) axis in acute and chronic alcoholization and in ethanolwithdrawal. In order to study the ethanol/HPA axis interactionduring alcohol withdrawal, we performed experiments using adrenalectomized(ADX) male rats alcoholized by a chronic pulmonary alcoholizationprocedure. Eight hours after the 3 weeks of the alcoholizationprocedure, the rats were evaluated for a tremor activity Inorder to reduce the great variability of the withdrawal tremors,we estimated the supersensitivity of the withdrawn rats to thetremorogenic compound harmine. We also studied the effect ofa hydrocortisone treatment given in the drinking bottle duringthe alcoholization procedure on the harmine-induccd tremorsof ADX and sham rats. Alcohol withdrawal resulted in increasedtremor response to 10 mg/kg harmine, and a protective effectof adrenalectomy on this effect was observed. Hydrocortisoneadministration to ADX or sham rats did not affect the tremorprofile of the alcohol withdrawn rats.