Sun M K, Nelson T J, Alkon D L
Laboratory of Adaptive Systems, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):12300-5. doi: 10.1073/pnas.210396697.
The role of the ryanodine receptor (RyR) in modifiability of synapses made by the basket interneurons onto the hippocampal CA1 pyramidal cells was examined in rats. Associating single-cell RyR activation with postsynaptic depolarization increased intracellular free Ca(2+) concentrations and reversed the basket interneuron-CA1 inhibitory postsynaptic potential into an excitatory postsynaptic potential. This synaptic transformation was accompanied by a shift of the reversal potential from that of chloride toward that of bicarbonate. This inhibitory postsynaptic potential-excitatory postsynaptic potential transformation was prevented by blocking RyR or carbonic anhydrase. Associated postsynaptic depolarization and RyR activation, therefore, changes GABAergic synapses from excitation filters to amplifier and, thereby, shapes information flow through the hippocampal network.
在大鼠中研究了兰尼碱受体（RyR）在篮状中间神经元与海马CA1锥体细胞形成的突触可塑性中的作用。将单细胞RyR激活与突触后去极化相关联，可增加细胞内游离Ca(2+)浓度，并将篮状中间神经元 - CA1抑制性突触后电位转变为兴奋性突触后电位。这种突触转变伴随着反转电位从氯离子的反转电位向碳酸氢根的反转电位的转变。通过阻断RyR或碳酸酐酶可防止这种抑制性突触后电位 - 兴奋性突触后电位的转变。因此，相关的突触后去极化和RyR激活将GABA能突触从兴奋过滤器转变为放大器，从而塑造了通过海马网络的信息流。
