Teyler T J, Cavus I, Coussens C
Neurobiology Department, NE Ohio College of Medicine, Rootstown 44272, USA.
J Neurosci Methods. 1995 Jun;59(1):11-7. doi: 10.1016/0165-0270(94)00188-m.
There are 3 known forms of synaptic plasticity at CNS synapses: long-term potentiation (LTP) mediated by NMDA receptor activation, LTP mediated by voltage-dependent calcium channel (VDCC) activation, and long-term depression (LTD) mediated by the NMDA receptor. All 3 forms of synaptic plasticity can be observed in hippocampal CAl cells, all are induced by afferent activation, all involve Ca2+ influx, and all activate Ca(2+)-dependent mechanisms. We consider the functional consequences of the presence of 3, sometime opposing, forms of synaptic plasticity at the same synapse. We suggest that the 2 forms of LTP have different consequences for the synapse. We postulate that the co-existence of potentiating and depressing capabilities influences the network processing capabilities of neural networks.
中枢神经系统（CNS）突触存在三种已知的突触可塑性形式：由N-甲基-D-天冬氨酸（NMDA）受体激活介导的长时程增强（LTP）、由电压依赖性钙通道（VDCC）激活介导的LTP以及由NMDA受体介导的长时程抑制（LTD）。这三种突触可塑性形式均可在海马CA1细胞中观察到，均由传入激活诱导产生，均涉及Ca2+内流，且均激活Ca(2+)依赖性机制。我们探讨了同一突触处存在三种有时相互对立的突触可塑性形式所产生的功能后果。我们认为两种LTP形式对突触具有不同的影响。我们推测增强和抑制能力并存会影响神经网络的网络处理能力。
