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老年记忆缺陷大鼠海马中突触增强过程受损。

Impaired synaptic potentiation processes in the hippocampus of aged, memory-deficient rats.

作者信息

Landfield P W, McGaugh J L, Lynch G

出版信息

Brain Res. 1978 Jul 7;150(1):85-101. doi: 10.1016/0006-8993(78)90655-8.

Abstract

A series of neurophysiological experiments was performed on the Schaffercommissural system of the hippocampus of aged and young anesthetized Fischer rats. The aged Fisher rats were previously found to exhibit retention performance deficits. No obvious differences were found between aged and young animals in amplitude, latency, stimulation threshold, or wave forms of typical synaptic responses when these were elicited by control (0.3 Hz) stimulation pulses. Further, the temporal curves of facilitation during a paired-pulse series were not different in aged and young animals. However, aged and young synapses showed consistently different responses during repetitive stimulation. Synapses of aged animals were deficient in frequency potentiation processes during 12 Hz stimulation; and the aged animals exhibited a delayed rise of post-tetanic synaptic potentiation following a 5 sec, 100 Hz stimulation train. Moreover, aged synapses 'exhausted' more rapidly during continuous 4 Hz stimulation. Throughout these studies a biphasic pattern of potentiation was observed during repetitive stimulation (brief potentiation, depression, renewed potentiation). Aged animals were deficient primarily in development of the second phase of potentiation. This pattern suggests an age-related impairment of some secondary process of potentiation, leading to an increased tendency to synaptic depression during and after stimulation. The possibility that the impaired hippocampal synaptic plasticity may be related to reported deficient behavioral plasticity in the aged animals is considered.

摘要

在老年和年轻的麻醉Fischer大鼠海马的Schaffer连合系统上进行了一系列神经生理学实验。先前发现老年Fisher大鼠表现出记忆保持能力缺陷。当通过对照(0.3Hz)刺激脉冲引发典型突触反应时,在老年和年轻动物之间未发现振幅、潜伏期、刺激阈值或波形有明显差异。此外,在配对脉冲系列期间促进作用的时间曲线在老年和年轻动物中并无不同。然而,在重复刺激期间,老年和年轻的突触表现出始终不同的反应。在12Hz刺激期间,老年动物的突触在频率增强过程中存在缺陷;并且在5秒100Hz刺激序列后,老年动物的强直后突触增强出现延迟上升。此外,在连续4Hz刺激期间,老年突触更快地“耗尽”。在这些研究中,在重复刺激期间观察到双相增强模式(短暂增强、抑制、再次增强)。老年动物主要在增强的第二阶段发育中存在缺陷。这种模式表明与年龄相关的某种增强的次级过程受损,导致在刺激期间和之后突触抑制的倾向增加。考虑了受损的海马突触可塑性可能与老年动物中报道的行为可塑性缺陷相关的可能性。

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