Røed A
Eur J Pharmacol. 1982 Sep 10;83(1-2):83-90. doi: 10.1016/0014-2999(82)90288-6.
Caffeine, 10(2) M, blocked the indirectly stimulated rat phrenic nerve-diaphragm preparation at 37 degrees C. Dantrolene, above 2.25 x 10(-7) M, reversed the blockade. Microelectrode recordings showed a gradual reduction of the end plate potential (EPP) amplitude following a period of facilitation. An increased frequency of miniature (EPPs was still recorded after complete EPP blockade. A presynaptic blockade of stimulus-secretion coupling caused by an effect upon Ca2+ balance is suggested. Caffeine may release and deplete Ca2+ from the smooth endoplasmic reticulum (SER) in the nerve terminals. This Ca2+ may be sequestered by the mitochondria. The blockade suggests that the SER may also supply Ca2+ to another intraterminal release site which is necessary for stimulus-secretion coupling. This site is unaffected by caffeine and dantrolene. The dantrolene reversal may result from inhibition of the caffeine-induced release from the same Ca2+ pool. The facilitatory effects of caffeine were not antagonized by dantrolene and may result from Ca2+ release from another pool.
10（2）M的咖啡因在37摄氏度时阻断间接刺激的大鼠膈神经-膈肌标本。高于2.25×10（-7）M的丹曲林可逆转这种阻断作用。微电极记录显示，在一段易化期后终板电位（EPP）幅度逐渐降低。在EPP完全阻断后仍记录到微小终板电位（MEPP）频率增加。提示是对Ca2+平衡的影响导致突触前刺激-分泌偶联的阻断。咖啡因可能从神经末梢的滑面内质网（SER）释放并耗尽Ca2+。这种Ca2+可能被线粒体螯合。这种阻断表明SER也可能向另一个终末内释放位点供应Ca2+，这是刺激-分泌偶联所必需的。该位点不受咖啡因和丹曲林的影响。丹曲林的逆转作用可能是由于抑制了咖啡因诱导的从同一Ca2+池的释放。咖啡因的易化作用未被丹曲林拮抗，可能是由于从另一个池释放Ca2+所致。
