Introduction to Neural Plasticity Mechanism  被引量:1

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作  者:Bogdan Feliks Kania Danuta Wronska Dorota Zieba 

机构地区:[1]Veterinary Institute,University Center for Veterinary Medicine Jagiellonian University&Agriculture University,Hugon Kollataj Agricultural University in Cracow,Cracow,Poland [2]Department of Physiology and Endocrinology of Animals,Faculty of Animal Sciences,Hugon Kollataj Agricultural University in Cracow,Cracow,Poland [3]Department of Animal Biotechnology,Faculty of Animal Sciences,Hugon Kollataj Agricultural University in Cracow,ul.Redzina1B,Cracow,Poland

出  处:《Journal of Behavioral and Brain Science》2017年第2期41-49,共9页行为与脑科学期刊(英文)

摘  要:In researches that examine neuroplasticity, many studies that are performed directly on isolated neurons in the pyramidal cells of CA1 area (CA1) and slices of the hippocampus indicate that changes occur at the molecular and cellular levels during long-term synaptic potentiation (LTP), and these changes are dependent on N-methyl-D-aspartate (NMDA) acid receptors and/or purinergic receptors. Electrophysiological studies and the chemical induction of LTP of synaptic neurotransmissions provide key evidence that LTP is dependent on the volume of Ca2+ influx through postsynaptic NMDA receptors, in addition to the subsequent activation and autophosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and the increase in the density of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors on postsynaptic neuronal membranes. The primary peculiarity of LTP in the central nervous system (CNS) excitatory synapses is the synthesis of additional AMPA receptors in the postsynaptic elements. Furthermore, the proteolysis of the extracellular matrix (ECM) has an important role in the synaptic neuroplasticity of the CNS. Proteases from the serine family and metalloproteinases of the extracellular matrix are localized within the synapses and are released into the extracellular space in proportion to the degree of neuronal excitation. These enzymes cause changes in the morphology, shape and size, as well as the overall number of synapses and synthesize new synaptic connections. The proteinases also change the function of receptors, and consequently, the secretions of neurotransmitters from the presynaptic elements are strengthened or weakened.In researches that examine neuroplasticity, many studies that are performed directly on isolated neurons in the pyramidal cells of CA1 area (CA1) and slices of the hippocampus indicate that changes occur at the molecular and cellular levels during long-term synaptic potentiation (LTP), and these changes are dependent on N-methyl-D-aspartate (NMDA) acid receptors and/or purinergic receptors. Electrophysiological studies and the chemical induction of LTP of synaptic neurotransmissions provide key evidence that LTP is dependent on the volume of Ca2+ influx through postsynaptic NMDA receptors, in addition to the subsequent activation and autophosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and the increase in the density of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors on postsynaptic neuronal membranes. The primary peculiarity of LTP in the central nervous system (CNS) excitatory synapses is the synthesis of additional AMPA receptors in the postsynaptic elements. Furthermore, the proteolysis of the extracellular matrix (ECM) has an important role in the synaptic neuroplasticity of the CNS. Proteases from the serine family and metalloproteinases of the extracellular matrix are localized within the synapses and are released into the extracellular space in proportion to the degree of neuronal excitation. These enzymes cause changes in the morphology, shape and size, as well as the overall number of synapses and synthesize new synaptic connections. The proteinases also change the function of receptors, and consequently, the secretions of neurotransmitters from the presynaptic elements are strengthened or weakened.

关 键 词:NEUROPLASTICITY Heterosynaptic Metaplasticity SUBJECTS 

分 类 号:R73[医药卫生—肿瘤]

 

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