Heinemann U, Hamon B, Konnerth A
Neurosci Lett. 1984 Jun 29;47(3):295-300. doi: 10.1016/0304-3940(84)90529-9.
Reductions in extracellular free Ca2+-concentration [( Ca2+]o) result from neuronal activation and can be induced by repetitive electrical stimulation or by application of excitatory amino acids. They reflect Ca2+-movements along its electrochemical gradient into pre- and postsynaptic elements. Amino acid-induced reductions in [Ca2+]o are predominantly caused by postsynaptic Ca2+ entry. Under conditions of blocked chemical synaptic transmission, a presynaptic component of extracellular Ca2+ loss becomes apparent during stimulation of the Schaffer collateral/commissural fibers system in stratum radiatum/moleculare. GABA, both iontophoretically and bath applied, always reduces pre- and postsynaptic components of [Ca2+]o changes. Baclofen regularly affects postsynaptic Ca2+ entry and has frequently also a suppressant action on presynaptic Ca2+ entry in area CA1.
细胞外游离钙离子浓度([Ca2+]o)的降低是由神经元激活引起的,可通过重复性电刺激或应用兴奋性氨基酸诱导产生。它们反映了钙离子沿其电化学梯度向突触前和突触后成分的移动。氨基酸诱导的[Ca2+]o降低主要是由突触后钙离子内流引起的。在化学性突触传递受阻的情况下,在刺激辐射层/分子层的Schaffer侧支/联合纤维系统时,细胞外钙离子丢失的突触前成分变得明显。离子导入和浴用的GABA总是会降低[Ca2+]o变化的突触前和突触后成分。巴氯芬经常影响突触后钙离子内流,并且在CA1区对突触前钙离子内流也经常具有抑制作用。