RESUMEN
Recurrent seizures lead to abnormal expression of synaptic proteins,reorganization of synapse and formation of abnormal neuron network.Recently,it is identified that the synaptic proteins are involved in epileptogenesis.The abnormal expression of several synaptic regulatory proteins and postsynaptic membrane receptor proteins may result in epilepsy.The ion channels usually are the action target of most antiepileptic drugs.However,carbamazepine and zonisamide may interact with syntaxin and/or soluble N-ethylmaleimide-sensitive factor attachment protein receptor complex to exert its function of anti-epilepsy.The synaptic vesicle protein 2A is the action target for new anti-epileptic drugs,including levetiracetam,brivaracetam and seletracetam.
RESUMEN
Alcoholic dementia is increasingly becoming both a severe medical issue and a social problem;the unknown overall mecha-nism is the bottleneck for effective intervention and treatment of alcoholic brain injury. As the primary structure for the release, transmission of neurotransmitter and information integration between neurons, synapse plays a significant role in performing the advanced function of brain, such as learning and memory. Based on the neurobiological principles of synaptic structure and function, the changes in process and efficiency of synaptic transmission and information integration stressed by alcoholic molecular were reviewed in comparison with the nor-mal process. The molecular mechanisms for alcoholic brain damage in learning and memory abilities were systematically discussed from the levels of synaptic morphology, material components, and signal transduction, respectively, and the repairing strategies for the damaged syn-aptic structure were proposed accordingly. Hopefully, this review could provide a deep insight into understanding the molecular mechanism of alcoholic brain damage, and draw ideas for the memory-enhancing peptides development.
RESUMEN
@#Alcoholic dementia is increasingly becoming both a severe medical issue and a social problem; the unknown overall mechanism is the bottleneck for effective intervention and treatment of alcoholic brain injury. As the primary structure for the release, transmission of neurotransmitter and information integration between neurons, synapse plays a significant role in performing the advanced function of brain, such as learning and memory. Based on the neurobiological principles of synaptic structure and function, the changes in process and efficiency of synaptic transmission and information integration stressed by alcoholic molecular were reviewed in comparison with the normal process. The molecular mechanisms for alcoholic brain damage in learning and memory abilities were systematically discussed from the levels of synaptic morphology, material components, and signal transduction, respectively, and the repairing strategies for the damaged synaptic structure were proposed accordingly. Hopefully, this review could provide a deep insight into understanding the molecular mechanism of alcoholic brain damage, and draw ideas for the memory-enhancing peptides development.