Differing mechanisms for proactive effects of intermittent and single shock on gastric ulceration.

Rats exposed to either 80 5-s shocks on a VT 60-s or to a single 400-s shock plus 80-min rest in the shock apparatus show dramatically increased degree of ulceration induced 72 h later by exposure to 75-min restraint-in-water stress (at 19 degrees C). However, the proactive effect of the 80 shocks on later gastric ulceration was blocked by SC injection of 7 mg/kg naltrexone 20 min prior to the shock session; naltrexone treatment prior to the single shock session had no ameliorating effect. A second experiment confirmed opioid involvement in the proactive augmentation of vulnerability by showing that when a 20 mg/kg injection of morphine replaced the shocks, rats showed a comparable increase in vulnerability. A third experiment replicated the basic findings from the first experiments that 80 intermittent shocks increase vulnerability to the ulcerogenicity of restraint-in-water and that this effect can be mimicked by replacing the shock stress with a 20 mg/kg injection of morphine; however, other groups showed that injection of 40 mg/kg produced a similar effect whereas 10 mg/kg was ineffective as a mimic. This suggests that there are at least two types of proactive effects from shock experiences that can increase later vulnerability to shock-induced gastric ulceration; one is opioid mediated and the other is not. This finding parallels reports made about mediation of prior shock-induced hypoalgesias and expands the spectrum to psychosomatic phenomenon.