Abstract

Previous studies have reported that a novel environment renders animals hypoalgesic and this novelty-induced hypoalgesia(NIHA) is not reversed by naloxone-pretreatment; in fact, the NIHA seems to be mediated through the monoaminergic system such as serotoninergic- and noradrenergic substrate, according to the studies on the effects of i.p. injection of those receptor ligands on the NIHA. The present study is conducted to investigate not only whether the central amygdaloid nucleus(ACe), which is known as mediating anti-nociceptive response as well as emotional/cognitive ones including fear/anxiety response, is responsible for the NE-mediated NIHA, but also whether the opiate system modulates this kind of NE mediation. In the present experiment, all rats were first given bilateral cannulae-implantations into the ACe. 7 days later, after these rats were randomly assigned into two groups named 'exposure group(EXP)' and 'non-exposure group(NON)', only the EXP started to be exposed to the non-functional floor of the Hot-Plate Apparatus (at the temperature of 23℃) 5 minutes every day for 7 consecutive days. On the 8th day, after being divided into two subgroups such as yohimbine group and saline group and being supplied with bilaterally-microinjected yohimbine or saline equivalent to its condition into the ACe, each group received a hot-plate(49℃) test. The latency to lick a hind-paw was manually recorded. As soon as picked out of the Apparatus all the rats were re-provided with naloxone, one of opiate receptor antagonists, and were re-tested under the same conditions mentioned. The result is that the novelty rats produced more hypoalgesia than the adapted rats in the hindpaw-licking latency, and that the bilateral micro-injection of yohimbine, an a₂-NE receptor antagonist increaing NE release in the brain-neuron synaptic cleft by blocking the presynaptic autoreceptors, potentiated the hypoalgesia, only in the novelty rats; which indicates that the novelty-induced hypoalgesia appears to be carried through the NE substrate and that the ACe is the chief forebrain site conducting the NE-potentiated novety-induced hypoalgesia. As far as the effect of naloxone injection under the influence of the preinjected yohimbine and saline is concerned, the hypoalgesia was reduced only under the condition of novelty yohimbine, neither under that of novelty saline nor under that of non-novelty yohimbine and saline; which implicates the opiate substrast may participate in the hypoalgesia necessarily as the NE-substrate-dependant pattern rather than by itself. Thus, the NE system may play more important role than opiate system in mediating the novelty-induced hypoalgesia.