神经科学
谷氨酸的
加巴能
突触可塑性
神经传递
变质塑性
兴奋性突触后电位
长时程增强
抑制性突触后电位
癫痫
海马体
突触疲劳
海马结构
稳态可塑性
神经可塑性
突触后电位
生物
谷氨酸受体
受体
生物化学
作者
Christian Bonansco,Marco Fuenzalida
摘要
Synaptic plasticity is the capacity generated by experience to modify the neural function and, thereby, adapt our behaviour. Long-term plasticity of glutamatergic and GABAergic transmission occurs in a concerted manner, finely adjusting the excitatory-inhibitory (E/I) balance. Imbalances of E/I function are related to several neurological diseases including epilepsy. Several evidences have demonstrated that astrocytes are able to control the synaptic plasticity, with astrocytes being active partners in synaptic physiology and E/I balance. Here, we revise molecular evidences showing the epileptic stage as an abnormal form of long-term brain plasticity and propose the possible participation of astrocytes to the abnormal increase of glutamatergic and decrease of GABAergic neurotransmission in epileptic networks.
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