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REGULATION OF SYNAPTIC RESPONSES TO HIGH-FREQUENCY STIMULATION AND LTP BY NEUROTROPHINS IN THE HIPPOCAMPUS

机译:神经营养素对海马神经突触对高频刺激和LTP的调节

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摘要

NEUROTROPHINS promote neuronal survival and differentiation, but the fact that their expression is modified by neuronal activity, suggests a role in regulating synapse development and plasticity(1-3). In developing hippocampus, the expression of brain-derived neurotrophic factor (BDNF) and its receptor TrkB(4-7) increases in parallel with the ability to undergo long-term potentiation (LTP)(8-10). Here me report a mechanism by which BDNF modulates hippocampal LTP. Exogenous BDNF promoted the induction of LTP by tetanic stimulation in young (postnatal day 12-13) hippocampal slices, which in the absence of BDNF show only short-term potentiation (STP), This effect was due to an enhanced ability of hippocampal synapses to respond to tetanic stimulation, rather than to a direct modulation of the LTP-triggering mechanism. A TrkB-IgG fusion protein, which scavenges endogenous BDNF11, reduced the synaptic responses to tetanus as well as the magnitude of LTP in adult hippocampus. [References: 30]
机译:神经营养素可以促进神经元的存活和分化,但神经元的活性会修饰神经元的表达,这表明神经元在调节突触的发育和可塑性中发挥作用(1-3)。在发育中的海马中,脑源性神经营养因子(BDNF)及其受体TrkB(4-7)的表达与经历长期增强(LTP)的能力平行增加(8-10)。在这里,我报告了BDNF调节海马LTP的机制。外源性BDNF通过强直刺激在年轻(出生后第12-13天)海马切片中促进LTP的诱导,在缺乏BDNF的情况下,海马切片仅表现出短期增强作用(STP),此作用是由于海马突触的能力增强对破伤风刺激做出反应,而不是对LTP触发机制的直接调节。清除内源性BDNF11的TrkB-IgG融合蛋白可减少对破伤风的突触反应以及成年海马的LTP强度。 [参考:30]

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