5-HT_2受体-磷脂酶C的激活易化大鼠基底外侧杏仁核突触可塑性的研究

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。

Study of 5-HT2 receptor-phospholipase C system facilitating synaptic plasticity in the rat basolateral amygdala

To explore the modulation of synaptic plasticity by 5-HT2 receptor agonist 1-(2,5)-dimethoxy-4-iodophen-2-aminopropane (DOI) in the amygdala, field excitatory post-synaptic potentials (field potentials, fEPSPs) in the basolateral amygdala (BLA) were recorded in rat slice preparation. Single theta burst stimulation (TBS) was applied to induce synaptic plasticity in BLA. The effect of DOI on TBS-induced synaptic plasticity was observed and its mechanism was studied by using 5-HT2 receptor antagonists and phospholipase C (PLC) inhibitors. The results showed that single TBS only induced short-term potentiation lasting 10 min in BLA. Bath application of 100 μmol/L DOI for 20 min had no observable effect on the basal synaptic responses. However, TBS-induced synaptic potentiations were significantly facilitated and remained at potentiated levels for more than 30 min in all the slices treated with DOI. The potentiated slopes of field potentials remained at 162.5%±9.7% (n=9, P<0.01) of the baseline values 30 min after the onset of theta-burst stimulation. The facilitating effect of DOI on TBS-induced synaptic plasticity was blocked by the 5-HT2A/2C receptor antagonist ketanserin and PLC inhibitor U73122. These results indicate that 5-HT2A/2C receptor stimulation enhances synaptic function in BLA via a PLC-mediated mechanism.