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为了探讨5-HT2受体激动剂盐酸2,5-二甲氧基-4-碘苯基丙烷(DOI)对杏仁核突触可塑性的调节作用,本研究在杏仁核脑片上记录基底外侧杏仁核(BLA)场电位,应用单串的θ频率波刺激(TBS)诱导突触可塑性,观察DOI对TBS诱导的突触可塑性的影响,及5-HT2受体拮抗剂、磷脂酶C抑制剂能否抑制DOI的作用。结果显示:单串的TBS刺激外囊,在BLA仅诱导约为10min的短时程增强。灌流液中加入100μmol/L DOI 20min,对基础的场电位没有作用。但在DOI存在的情况下,单串的TBS即可诱导长时程增强,强直刺激30min后,增强的场电位斜率仍维持在基础值的(162.5±9.7)%(n=9,P<0.01)。DOI对TBS诱导的突触可塑性的易化作用可被5-HT2A/2C受体拮抗剂ketanserin和PLC抑制剂U73122所抑制。以上结果提示5-HT2A/2C受体的激活可通过磷脂酶C通路易化杏仁核的突触可塑性。
In order to investigate the regulatory effect of 5-HT2 receptor agonist 2,5-dimethoxy-4-iodophenyl propane (DOI) on the synaptic plasticity of amygdala, this study recorded basolateral amygdala in amygdala (BLA) field potentials, synaptic plasticity was induced by single-strand β-frequency wave stimulation (TBS), and the effect of DOI on TBS-induced synaptic plasticity was observed, and whether 5-HT2 receptor antagonist and phospholipase C inhibitor Inhibit the role of DOI. The results showed that: a single string of TBS stimulated the outer capsule, BLA induced only about 10min short-term enhancement. The perfusate added 100μmol / L DOI 20min, no effect on the basic field potential. However, in the presence of DOI, long-term potentiation was induced by single-strand TBS, and the slope of field potentials was maintained at 162.5 ± 9.7% (n = 9, P <0.01) ). The facilitatory effect of DOI on TBS-induced synaptic plasticity can be inhibited by 5-HT2A / 2C receptor antagonist ketanserin and PLC inhibitor U73122. The above results suggest that activation of the 5-HT2A / 2C receptor facilitates the synaptic plasticity of the amygdala via the phospholipase C pathway.