[Effects of strong and weak electroacupuncture on endotoxin-induced changes of electrical activities of heat-sensitive neurons in preoptic area and anterior hypothalamus in rabbits].

OBJECTIVE

To observe the effects of weak and strong electroacupuncture (EA) on endotoxin (ET) thermolysis-induced changes of discharges of neurons in the preoptic region and anterior hypothalamus (PO-AH) so as to explore its underlying mechanism in antipyretic and thermolytic actions and its relation to the receptive system of acupoints.

METHODS

Eighteen New Zealand rabbits were randomly divided into ET group, ET + weak-EA group and ET + strong-EA group. Extracellular discharges of the PO-AH neurons were recorded by using tungsten microelectrodes. A "U"-shape stainless steel tube was implanted in the region (P0.4-A4.4, L0.5-1.7) crossing the hypothalamus for changing local temperature by perfusion of cool (25 degrees C) or warm (41 degrees C) solution in order to distinguish the heat sensitive neurons (HSN), cold sensitive neurons (CSN) and insensitve neurons to temperature changes. Intravenous injection of endotoxin (25 EU/rabbit) was given to rabbits to induce increase of tempe rature. EA (8 Hz, wave width 0.1 ms, weak stimulation: 4.5 V, strong stimulation: 25 V) was applied to bilateral "Yongquan" (KI 1) for observing changes of firing rates of HSN in PO-AH.

RESULTS

Compared with the basal values of firing rates of PO-AH neurons in each group, the average changing ratios of both ET and ET + weak-EA groups decreased significantly from 55-60 min on in ET group and from 40-45 min on in ET + weak-EA group after intravenous injection of ET (P<0.05), suggesting no marked effect of weak EA for preventing discharges of PO-AH neurons from decrease. While in ET + strong-EA group, the firing rates of HSN of PO-AH kept stable after injection of ET during EA and after cease of EA (P>0.05 vs basal value), suggesting that strong EA could antagonize ET thermolysis-induced decrease of firing rates of PO-AH neurons.

CONCLUSION

Stronger EA stimulation of KI1 can antagonize ET thermolysis-induced effect on electrical activities of PO-AH HSN, which may be initiated by the activation of the high-threshold thin nerve fibers in the acupoint region.