56 rats were divided into 4 groups: (a) controls

(b) elerctoacupu- ncture-(EAP-) treated

(c) morphine-treated and (d) morphine plus EAP treated. Besides using the PAP technique of Sternberger for immunocyto- chemical demonstration of SP and ENK and the KarnovskyRoots' method for the histochemical visualization of ACHE

additional sections stained for SP and AChE were prepared for electron microscopic (EM) observati- ons. A semi-quantitative analysis of tissue sections was also accomplished. After EAP the elevation of pain threshold was correlated with the enhanced staining of SP-LI in Rexed's lamina Ⅱ (P<0.001 as compared with the control group). However

ENK-LI in the same regions appeared decreased (P<0.001) . After morphine

SP-LI in lamina Ⅱ became increased (P<0.001) rese- mbling that after EAP. However

when the morphine-treated animals were also subjected to EAP

SP-LI became diminished instead (P<0.001

compared with the morphine group) . As for the histochemical changes of AChE in dorsal horn

the levels of enzymic activity of animals in various groups were different

e.g. 3.855 ±0.550 (in control group)

4.225±0.477 (EAP)

3.252±0.405 (morphine) and 3.775±0.401 (morphine plus EAP group). Indeed Rexed's lamina Ⅱ is rich in both SP-LI and AChE. EM obser- vations showed that SP-LI material appears in and around clear synaptic vesicles in the axonal ending of "thin" diameter

whereas AChE activity distributes mostly within axon of "coarse" caliber. The foregoing results indicate that the effects of EAP and morphine analgesia are similar with regard to the change of SP-LI

but opposite with respect to the change of AChE activity. It is suggested that the separate effect of EAP and morphine on SP-LI and ENK-LI can be expla- ined by Jessell-Iversen model of spinal processing. And a possible func- tional relationship between SP and acetylcholine can not be excluded. The AChE-marked neurons may influence SP release.