大鼠杏仁核5—HT3受体参与免疫调制

实验通过大鼠侧脑室和杏仁核给予5－HT3受体激动剂1－phenylbiguanide(PBG),用3H－TdR掺入法测定脾细胞丝裂原（concanavalin A,Con A和lipopolysaccharide,LPS)刺激增殖效应,用活化脾细胞增殖法测定IL－2生成,MTT法测定自然杀伤（natural killer,NK)细胞活性和用放射免疫测定血浆皮质酮水平,以探讨大鼠杏仁核5－HT3受体在免疫调控中的作用。结果表明：5－HT3受体拮抗剂granisetron(GNT,0.1-0.4mg/kg ip)剂量依赖地增强Con A和LPS刺激的脾细胞增殖,作用在连续给药5d最明显,双侧脑室给予PBG（5ug/side)可增强ConA和LPS刺激的脾细胞增殖效应,作用在连续给药3d最明显,双侧和单侧中共杏仁核给予PBG0．5ug均增强ConA刺激的脾细胞增殖和IL－2生成,底内侧杏仁核给予同剂量PBG仅增强LPS刺激的脾细胞增殖效应,不影响ConA刺激的脾细胞增殖和IL－2生成,中央杏仁核给予PBG升高血浆皮质酮的作用较底侧杏仁核给予等量PBG引起的升高血浆皮质酮作用明显（P＜0．01）,侧脑室,中央杏仁核和底内杏仁核给予PBG对丝裂原刺激的脾细胞增殖效应影响不同,但均被同时同部位给予GNT所拮抗,提示杏仁核中央核和底内侧核的5－HT3受体可能以不同方式参与ConA或LPS刺激的脾细胞增殖效应的调制。

5-HT3 receptors in amygdala mediate neuroimmunomodulation in rats

The present study was to explore the possible immunomodulatory role of 5-HT3 receptors in the amygdala in rats. Concanovalin A (Con A)- and lipopolysaccharide (LPS)-stimulated splenocyte proliferation response (SPR), production of IL-2, activity of natural killer (NK) cells and serum cortisol were measured by 3H-TdR incorporating method, MTT method and RIA, respectively. The Con A- and LPS-stimulated SPR was enhanced in a dose-dependent manner by 5-HT3 receptor antagonist granisetron (GNT) (0.1-0.4 mg/kg, i.p.). SPR was also enhanced by intracerebroventricular (icv) administration of 1-phenylbiguanide (PBG, 10 micrograms/d). Con A-stimulated SPR and production of IL-2 were increased either by bilateral or by unilateral central amygdala (CeA) microinfusion of PBG (0.5 microgram/side), but LPS-induced SPR and NK cell activity were not affected. On the contrary, the LPS-induced SPR was increased by either bilateral or unilateral basomedial amygdala (BmA) microinfusion of PBG (0.5 microgram/side). The plasma cortisol level was significantly raised by CeA or BmA PBG microinfusion, but the effect induced by PBG intra-CeA was greater than that induced by PBG intra-BmA (P < 0.01). The effects of icv PBG and intra-amygdala infusion were antagonized by granisetron. Asymmetrical modulation of immune reactivity by 5-HT3 receptors in CeA or BmA was not observed in these experiments. It is suggested that 5-HT3 receptors within the amygdala may modulate rat mitogen-stimulated SPR in different manners.