中国药理学与毒理学杂志
中國藥理學與毒理學雜誌
중국약이학여독이학잡지
CHINESE JOURNAL OF PHARMACOLOGY AND TOXICOLOGY
2002年
6期
432-437
,共6页
钟桂生%阮迪云%葛少宇%汪铭%陈聚涛
鐘桂生%阮迪雲%葛少宇%汪銘%陳聚濤
종계생%원적운%갈소우%왕명%진취도
锂%海马%电位测定法,长时程增强%双脉冲易化
鋰%海馬%電位測定法,長時程增彊%雙脈遲易化
리%해마%전위측정법,장시정증강%쌍맥충역화
lithium%hippocampus%potentiometry,long-term potentiation%paired-pulse facilitation
目的从齿状回长时程增强效应(LTP)方面研究锂的治疗作用机理.方法细胞外记录离体海马脑片神经元兴奋性突触后电位(EPSP).结果锂可逆地增强EPSP的幅度.高频刺激 (100 Hz, 1 s)对照组大鼠海马穿通纤维,在海马齿状回(DG)区记录的EPSP幅度会持续增高,可以诱导出明显的突触后LTP.若用10 mmol*L-1锂处理大鼠海马脑片,则诱导的LTP幅度明显降低,但低浓度锂(2, 6 mmol*L-1)不影响LTP的幅度;10 mmol*L-1锂明显抑制海马脑片DG区的脉冲间隔(IPI)为50 ms的双脉冲易化效应(PPF),而低浓度锂(2, 6 mmol*L-1)处理则不影响PPF(IPI, 50 ms);在不同的细胞外钙浓度下,用10 mmol*L-1锂处理过的海马脑片PPF受到的抑制程度不同.结论锂可能通过突触前的机理来抑制海马DG区LTP的幅度,这种抑制效应与锂的临床治疗狂躁症及其副作用之间的关系尚需进一步的研究.
目的從齒狀迴長時程增彊效應(LTP)方麵研究鋰的治療作用機理.方法細胞外記錄離體海馬腦片神經元興奮性突觸後電位(EPSP).結果鋰可逆地增彊EPSP的幅度.高頻刺激 (100 Hz, 1 s)對照組大鼠海馬穿通纖維,在海馬齒狀迴(DG)區記錄的EPSP幅度會持續增高,可以誘導齣明顯的突觸後LTP.若用10 mmol*L-1鋰處理大鼠海馬腦片,則誘導的LTP幅度明顯降低,但低濃度鋰(2, 6 mmol*L-1)不影響LTP的幅度;10 mmol*L-1鋰明顯抑製海馬腦片DG區的脈遲間隔(IPI)為50 ms的雙脈遲易化效應(PPF),而低濃度鋰(2, 6 mmol*L-1)處理則不影響PPF(IPI, 50 ms);在不同的細胞外鈣濃度下,用10 mmol*L-1鋰處理過的海馬腦片PPF受到的抑製程度不同.結論鋰可能通過突觸前的機理來抑製海馬DG區LTP的幅度,這種抑製效應與鋰的臨床治療狂躁癥及其副作用之間的關繫尚需進一步的研究.
목적종치상회장시정증강효응(LTP)방면연구리적치료작용궤리.방법세포외기록리체해마뇌편신경원흥강성돌촉후전위(EPSP).결과리가역지증강EPSP적폭도.고빈자격 (100 Hz, 1 s)대조조대서해마천통섬유,재해마치상회(DG)구기록적EPSP폭도회지속증고,가이유도출명현적돌촉후LTP.약용10 mmol*L-1리처리대서해마뇌편,칙유도적LTP폭도명현강저,단저농도리(2, 6 mmol*L-1)불영향LTP적폭도;10 mmol*L-1리명현억제해마뇌편DG구적맥충간격(IPI)위50 ms적쌍맥충역화효응(PPF),이저농도리(2, 6 mmol*L-1)처리칙불영향PPF(IPI, 50 ms);재불동적세포외개농도하,용10 mmol*L-1리처리과적해마뇌편PPF수도적억제정도불동.결론리가능통과돌촉전적궤리래억제해마DG구LTP적폭도,저충억제효응여리적림상치료광조증급기부작용지간적관계상수진일보적연구.
AIM To investigate the mechanism of the-rapeutic action of lithium with respect to long-term potentiation(LTP) elicited in dentate gyrus(DG) region of rat hippocampus. METHODS To use conventional extracellular recording technique in hippocampal slices in vitro. RESULTS Lithium was found to reversibly increase excitatory postsynaptic potentials in the DG region of rat hippocampus. Under control conditions, titanic stimulation (100 Hz, 1 s) of medial perforans pathway induced LTP. Acute treatment of low concentration lithium (2, 6 mmol*L-1) did not affect the LTP induced by titanic stimulation, while its higher concentration (10 mmol*L-1) inhibited the amplitude of LTP in the DG region of rat hippocampus. Furthermore, lithium treatment (10 mmol*L-1) decreased paired-pulse facilitation (PPF) measured at 50 ms inter-pulse interval while, at lower concentrations, lithium treatments (2, 6 mmol*L-1) did not affect PPF significantly. We also found that the effects of lithium (10 mmol*L-1) on PPF were different at different [Ca2+]o. CONCLUSIONLithium can inhibit the LTP magnitude in rat hippocampus probably through presynaptic mechanisms. These alterations of neurophysiological responses may be related to the therapeutic action of lithium salts in mania and depression as well as producing side effects of lithium chemotherapy.