Possible Modulation of Dopamine (D2) Signalling in Alcohol Induced Neuropathic Pain in Rats

The present study has been designed to investigate the possible modulation of Dopamine (D2) signalling in alcohol induced Neuropathic Pain in rats. Wistar albino rats of either sex (180-220g) (n=6) were employed in present study. Rats were pair fed with isocaloric liquid diets containing 30% (2.5ml each) of ethanol for 4 weeks. Chronic alcohol administration was reported to induce increased pain perception. Two weeks prior to initiating the experiment, rats were adapted to the liquid diet by incrementing the ethanol content 0% to 11.8%, 23.6% and then 37% of caloric content model followed by daily drug treatment of Metoclopramide (1.25-2.5mg/kg, i. p. /day) which is d2 receptor antagonist and Bromocriptine (2.5mg/kg, i. p. /day) which is d2 receptor agonist. The periodic checkup of neuropathic pain was carried out by using hot plate, hot immersion and cold allodynia test. Serum biochemical lipid peroxidation, NO and GSH level was assessed on 28th day. Chronic ethanol exposure induced Neuropathy showed elevated hyperalgesia, allodynia response, serum biochemical lipid peroxidation and NO, decreases GSH level. Treatment with bromocriptine results in increased sensation of pain, metoclopramide antagonize D2 receptor results in lowering of neuropathic pain perception, serum biochemical lipid peroxidation and NO measurement, finds increase in GSH level. The finding from the present study may conclude that the down regulation of Dopamine D2 cascade in amelioration of nervous sensitization on chronic intake of alcohol in rats and thereby reducing pain perception in the condition of alcoholic Neuropathy.