Brain-derived neurotrophic factor (BDNF) reverses the effects of rapid eye movement sleep deprivation (REMSD) on developmentally regulated, long-term potentiation (LTP) in visual cortex slices.
Brain-derived neurotrophic factor (BDNF) reverses the effects of rapid eye movement sleep deprivation (REMSD) on developmentally regulated, long-term potentiation (LTP) in visual cortex slices.
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DOI：
10.1016/j.neulet.2012.02.012
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发表时间：
2012-03-28
影响因子：
2.5
通讯作者：
Roffwarg HP
中科院分区：
文献类型：
--
作者：
Shaffery JP;Lopez J;Roffwarg HP
本实验室的工作证实了关键期（CP）、出生后17-30天（P）的快速眼动睡眠（REMS）在视皮层突触可塑性中的作用。对青春期大鼠的研究表明，REMS剥夺（REMSD）重新启动了一种发育调节形式的突触可塑性，否则只在CP动物中观察到。随后的工作表明，REMSD影响被认为参与终止CP的抑制机制。神经营养因子参与突触可塑性，这是视皮层中CP成熟和CP最终闭合的基础。脑源性神经营养因子（BDNF）的表达依赖于神经元的活动，REMSD可以阻断BDNF的表达。我们认为，REMS有助于通过调节BDNF的表达和随之而来的，下游增加皮质抑制音的视皮层的成熟。在这项研究中，渗透微型泵将脑源性神经营养因子输送到大脑一侧的视觉皮质。对侧半球未植入，用作内部对照。我们检验了BDNF被青春期晚期大鼠的REMSD阻断的假设，并研究了替代BDNF是否能阻止θ爆发刺激（TBS）诱导LTPWM-III。我们还评估了类似的REMSD和BDNF注入动物的视觉皮层与配对脉冲刺激（PPS）的相对抑制音。在REMSD后，平行制备两个半球用于体外突触可塑性研究（LTPWM-III或PPS）。在接受BDNF输注一侧的REMSD大鼠（8只动物中的8只）的视觉皮层中，TBS始终未能诱导LTPWM-III。相比之下，在匹配的非输注半球中获得LTPWM-III（5/5只动物），与该年龄大鼠中的预期一致。单侧输注生理盐水的REMSD动物在两个半球产生LTPWM-III。在另一组单侧BDNF输注的REMSD动物中进行的PPS研究显示，BDNF输注侧（5/5）的第二反应受到年龄相关的抑制，而在非输注侧观察到易化（3/3）。皮质内注入BDNF在REMSD青少年大鼠似乎恢复必要的终止CP发育调节突触可塑性在视觉皮层的神经化学过程。结果表明，REMSD阻断BDNF的表达和成熟的抑制过程在青少年的视觉皮层。这些数据支持REMS在大脑发育中的功能。
Work in this laboratory demonstrated a role for rapid eye movement sleep (REMS) in critical period (CP), postnatal days (P)17-30, synaptic plasticity in visual cortex. Studies in adolescent rats showed that REMS deprivation (REMSD) reinitiates a developmentally regulated form of synaptic plasticity that otherwise is observed only in CP animals. Subsequent work showed that REMSD affects inhibitory mechanisms that are thought to be involved in terminating the CP. Neurotrophins are implicated in the synaptic plasticity that underlies CP maturation and also final closure of the CP in visual cortex. Expression of brain-derived neurotrophic factor (BDNF) is dependent upon neuronal activity, and REMSD may block BDNF expression. We propose that REMS contributes to the maturation of visual cortex through regulation of BDNF expression and consequent, downstream increase in cortical inhibitory tone. In this study, osmotic minipumps delivered BDNF into visual cortex on one side of brain. The opposite hemisphere was not implanted and served as an internal control. We tested the hypothesis that BDNF is blocked by REMSD in late-adolescent rats and investigated whether replacing BDNF prevents induction of LTPWM-III by theta burst stimulation (TBS). We also assessed relative inhibitory tone in visual cortex with paired-pulse stimulation (PPS) in animals that were similarly REMSD- and BDNF-infused. After REMSD, both hemispheres were prepared in parallel for in vitro synaptic plasticity studies (LTPWM-III or PPS). In visual cortex of REMSD rats on the side receiving BDNF infusions (8 of 8 animals), TBS consistently failed to induce LTPWM-III. In contrast, LTPWM-III was obtained (5 of 5 animals) in the matched non-infused hemisphere, as expected in rats of this age. REMSD animals that were unilaterally infused with saline produced LTPWM-III in both hemispheres. PPS studies in another group of REMSD animals that were unilaterally BDNF-infused displayed age-appropriate inhibition of the second response on the BDNF-infused side (5/5), whereas on the non-infused side facilitation was observed (3/3). Intracortical infusion of BDNF in REMSD adolescent rats appears to restore neurochemical processes necessary for termination of the CP for developmentally regulated synaptic plasticity in visual cortex. The results suggest that REMSD blocks BDNF expression and also maturation of inhibitory processes in adolescent visual cortex. These data support REMS’ function in brain development.
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