DEFECTIVE HABITUATION TO NOCICEPTIVE STIMULATION IN ALCOHOL-AVOIDING ANA RATS

Brain opioidergic mechanisms participate in the regulation of motivational and ingestive behaviours. Since alcohol is believed to activate endogenous opiold systems and to produce opioid-mediated antinociception, the present experiments were performed to find out if alcohol-induced antinociception differs between the alcohol-preferring AA and alcohol-avoiding ANA rat lines. Alcohol doses relevant to the voluntary alcohol intake by the AA rats (0.5-1.0 g/kg, intraperitoneally) failed to alter tail-flick (TF) latency in a 55 degrees C water bath by either rat line. However, repeated measurement of TF latency, even without any alcohol treatment, prolonged tail-flick latencies in AA but not in ANA rats. Prolongation of TF latency was also seen in non-selected Wistar rats, indicating that the ANA rats respond abnormally in this test. The antinociceptive effects of swimming-induced stress (3 min at 15 degrees C) and those of cumulative morphine administration (0.5-16.0 mg/kg, subcutaneously) were similar in both rat lines. Using higher, motor-impairing alcohol doses with repeated baseline TF determinations, it was observed that a dose of 1.5 g/kg induced slight antinociception only in the AA rats, while 2.0 g/kg produced similar effects in both rat lines. It is thus concluded that the alcohol-preferring AA rats do not show any enhanced alcohol-induced antinociception at relevant alcohol doses. However, the alcohol-avoiding ANA rats appear to have a defective ability to habituate to repeated sensory stimuli, which could contribute to their alcohol avoidance by preventing the development of tolerance to aversive effects of alcohol.