Rats are stressed by foot-shock or restraint that increases their tail flick latencies. This study looks at the time it takes for analgesia to take place with an exposure to another stressor, which would be the cold-water swim. The rats will be tested by putting them in a cold-water swim for about three and a half minutes, the water is about 35 degrees. After the cold-water swim, they had tail-pinch and flinch actions for about an hour. The tail-flick radiant heat for the rat and it lasted for over two hours, also increasing to help radiate heat and go back to homeostasis. The results show that the rat reacts to three different pain reflex perceptions; electric shock, heat and pressure, all can be changed by bringing in another stressor.
Evidence from recent studies show that there is a part of the brain system that functions to inhibit sensitivity to painful modalities. It is likely to be a neural pain relief system that has evolved. Painful stimuli can cause a reaction to protect or defend self, due to different environmental stimuli or threatening stimuli. In an emergency situation, when the sympathetic nervous system is activated, there are changes in heart rate, pupils are dilated, and muscle blood flow is increased displaying the ‘fight or flight’ reaction. The emergency response also shows to produce less pain and sensitivity in physically troublesome events. The original observation that rats increased their tail-flick tendencies after an exposure to severe stressors has started further research pn the analgesic mechanisms that underlie those stressors and extend the type of stressful stimuli that increase analgesia.
Method:
Forty-eight male rats were tested for flinch-jump thresholds. Electric shocks were given through
the floor by a current shock generator. With more intense shocks, the intensity made the rats increase the withdraw of their paws from the grid. The original jump threshold was the lowest of the intensities and each experiment began with a foot shock with an intensity of .1. The shocks were increased every 20 seconds by .05. After three days when the animals were stable, they were exposed to a cold-water bath and forced to swim for three and a half minutes. Following the cold-water bath, the rats were exposed to the flinch, initial jump, and jump thresholds were determined at one of four post swim intervals.
The tail-flick withdraw was tested on six male rats. A radiant heat source was mounted about a centimeter above the tail of a restrained rat, and the thermal stimulus was applied to the dorsum of the tail. The intensity of the thermal stimulus increased the production of the tail-flick. Experiments were fifteen minutes before the swim and immediately prior.
Tail pinch thresholds were with seven male rats. Increasing pressure by a motor driven analgesic meter was applied to the rail until a withdraw response from the forelimb or hind-limb. The results were scheduled before and after the cold-water bath.
Results:
Both jump thresholds were elevated at thirty minutes following the cold-water swim but then returned back to normal after 2 hours. With warm water control swim, did not produce any changes in either jump thresholds. Both jump thresholds in the cold-water stressed rats were higher than the warm water rats. Flinch-threshold rats were higher in cold-water stressed rats but not at other intervals, and there was no change across intervals. As the time between the swim and foot shock increased, the flinch differences in the cold water decreased, and the warm water increased. Tail-flick reactions to heat showed important increases for two hours after the cold-water swim. For the tail-pinch thresholds, the cold water stressed rats elevated tail pinch thresholds, and warm water rats were unaltered.
Discussion:
Measured by three different tests, analgesia was produced by the force of swim in cold water, but not by warm water. In the flinch-jump test the jump thresholds had an analgesic time of sixty minutes following the cold-water, while the tail-flick had a longer time. The time of the analgesia made by the cold-water swim is similar to the time course of avoidance learning deficits. It is compared to a “learned helplessness”. The animal has learned the negative response to the unavoidable shocks. There is a connection with the avoidance learning deficits to a deficiency in motor activation caused by norepinephrine decrease during exposure to the stressor. The study shows that stressed-induced analgesia is measured by increases in thresholds and may also contribute to avoidance of learning deficits.