The role of tail skin temperature in the facilitation of the tail-flick reflex after spinal transection or interference with descending serotonergic neurotransmission

Abstract

We examined in mice whether tail skin temperatures and tail-flick reflexes were changed after spinal transection or intrathecal (i.th.) injection of the serotonin (5-HT) neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) or the 5-HT receptor antagonist metergoline. Transection of the spinal cord reduced tail-flick latency (the time needed to evoke the tail-flick reflex by radiant heat) and increased tail skin temperature 15-21 days after surgery. Analysis of covariance showed that the effect of tail skin temperature on tail-flick latency was far more pronounced than the effect of spinal transection. Intrathecal injection of 5,6-DHT (5 or 10 micrograms mouse-1), which extensively reduced the spinal levels of 5-HT, reduced tail-flick latency and increased tail skin temperature 1-5 days after treatment. Similarly, tail-flick latency was shortened and tail skin temperature elevated 15 min after i.th. injection of metergoline (0.5 micrograms mouse-1). Analysis of covariance showed no significant effect of i.th. 5,6-DHT or i.th. metergoline on tail-flick latency. Tail skin temperature, on the other hand, had a highly significant effect on tail-flick latency. The results show that the facilitation of the tail-flick reflex in spinally transected mice and mice injected i.th. with 5,6-DHT or metergoline is mainly caused by increased tail skin temperature. The data do not indicate that descending 5-HT pathways tonically inhibit the tail-flick reflex.