CAJ | 학술논문

目的评价海马神经元N受体α4β2亚型在异氟醚抑制大鼠海马突触长时程增强(LTP)中的作用.方法健康成年雄性SD大鼠,取海马组织,制备海马脑片.取70张脑片,随机分为10组(n=7):各组用正常人工脑脊液(aCSF)灌流海马脑片,记录稳定正常的细胞外群峰电位(PS)30 min,LTP组继续给予正常的aCSF灌流,其余各组分别用含异氟醚0.125 mmol/L(I1组)、0.25 mmol/L(I2组)、0.5 mmol/L(I3组)、地棘蛙素0.1 mmol/L(E1组)、1.0 μmol/L(E2组)、地棘蛙素0.1 μmol/L+异氟醚0.25 mmol/L(E1+I2组)、地棘蛙素1.0 μmol/L+异氟醚0.25 mmol/L(E2+I2组)、双氢β-刺酮碱(DHβE)0.1μmol/L(D组)、DHβE0.1μmol/L+异氟醚0.125 mmol/L(D+I1组)的aCSF灌流.采用细胞外微电极记录技术,记录海马脑片CA1区细胞外PS 30 min后,施以高频强直刺激(HFS)15 min,诱发LTP,记录各组HFS结束后5、10、15、20、25、30、40、50、60 min时的PS幅值.结果与LTP组比较,I1.2.3组、D组、D+I1组、E1+I2组HFS后PS幅值降低,E1.2组HFS后PS幅值升高(P＜0.05),E2+I2组HFS后PS幅值差异无统计学意义(P＞0.05).与I1组比较,D+I1组HFS后PS幅值降低(P＜0.05).与I2组比较,E1+I2组、E2+I2组HFS后PS幅值升高(P＜0.01).结论异氟醚通过拮抗海马神经元N受体α4β2亚型从而抑制了突触LTP的形成.
목적 평개해마신경원N수체α4β2아형재이불미억제대서해마돌촉장시정증강(LTP)중적작용.방법 건강성년웅성SD대서,취해마조직,제비해마뇌편.취70장뇌편,수궤분위10조(n=7):각조용정상인공뇌척액(aCSF)관류해마뇌편,기록은정정상적세포외군봉전위(PS)30 min,LTP조계속급여정상적aCSF관류,기여각조분별용함이불미0.125 mmol/L(I1조)、0.25 mmol/L(I2조)、0.5 mmol/L(I3조)、지극와소0.1 mmol/L(E1조)、1.0 μmol/L(E2조)、지극와소0.1 μmol/L+이불미0.25 mmol/L(E1+I2조)、지극와소1.0 μmol/L+이불미0.25 mmol/L(E2+I2조)、쌍경β-자동감(DHβE)0.1μmol/L(D조)、DHβE0.1μmol/L+이불미0.125 mmol/L(D+I1조)적aCSF관류.채용세포외미전겁기록기술,기록해마뇌편CA1구세포외PS 30 min후,시이고빈강직자격(HFS)15 min,유발LTP,기록각조HFS결속후5、10、15、20、25、30、40、50、60 min시적PS폭치.결과 여LTP조비교,I1.2.3조、D조、D+I1조、E1+I2조HFS후PS폭치강저,E1.2조HFS후PS폭치승고(P＜0.05),E2+I2조HFS후PS폭치차이무통계학의의(P＞0.05).여I1조비교,D+I1조HFS후PS폭치강저(P＜0.05).여I2조비교,E1+I2조、E2+I2조HFS후PS폭치승고(P＜0.01).결론 이불미통과길항해마신경원N수체α4β2아형종이억제료돌촉LTP적형성.
Objective To evaluate the role of alpha4 beta2 neuronal nicotinic acetylcholine receptor in the inhibition of synaptic long-term potentiation (LTP) by isoflurane in the CA1 area of rat hippocampal slices.Methods Hippocampal slices (400 μm thick) were prepared from the brains of adult male SD rats, 2 months old, weighing 200-250 g, anesthetized with ether and decapitated. The slices were incubated in artificial cerebrospinal fluid (aCSF) at room temperature for at least 2 h before use. Seventy slices were randomly divided into 10 groups ( n = 7 each): Ⅰ LTP group in which the slices were perfused with aCSF; Ⅱ , Ⅲ and Ⅳ group in which the slices were perfused with aCSF containing isoflurane 0.125, 0.25 and 0.5 mmol/L respectively (group Ⅰ1-3 );Ⅴ and Ⅵ group in which the slices were perfused with aCSF containing epibatidine 0.1 and 1.0 μmol/L respectively (group E1.2 ); Ⅶ group epibatidine 0.1 μmol/L + isoflurane 0.25 mmol/L (group E1 + I2 ); Ⅷgroup epibatidine 1.0 μmol/L + isoflurane 0.25 mmol/L (group E2 + I2); Ⅸ group DHβE 0.1 μmol/L (group D); Ⅹ group DHβE 0.1 μmol/L + isoflurane 0.125 mmol/L (group D + I1 ). Population spikes (PS) were recorded for at least 30 min before LTP in each group. For LTP induction, high-frequency stimulation (HFS) was applied to the Schaffer collateral-commissural pathway of hippocampus and maintained for 15 min using a stimulating electrode.The changes in PS amplitude were analyzed at 5, 10, 15, 20, 25, 30, 40, 50 and 60 min after HFS in each group. Results Compared with group LTP, the PS amplitude was significantly decreased after HFS in group I1 ,I2, I3 , D, D + I1 and E1 + I2 ( P ＜ 0.05), while increased after HFS in group E1 .2 ( P ＜ 0.05 ), but no significant change was found after HFS in group E2 + I2 ( P ＞ 0.05). The PS amplitude was significantly decreased after HFS in group D + I1 compared with group I1 (P ＜ 0.05). The PS amplitude was significantly increased after HFS in group E1 + I2 and F2 + I2 compared with group I2 ( P ＜ 0.01 ). Conclusion Isoflurane inhibits LTP induction via inhibiting the activation of alpha4 beta2 nicotinic acetylcholine receptor in rat hippocampus.