Rapid eye movement sleep deprivation in post-critical period, adolescent rats alters the balance between inhibitory and excitatory mechanisms in visual cortex.
Rapid eye movement sleep deprivation in post-critical period, adolescent rats alters the balance between inhibitory and excitatory mechanisms in visual cortex.
复制标题
快速眼动睡眠剥夺在关键期后，青春期大鼠改变了视觉皮层抑制和兴奋机制之间的平衡。
DOI：
10.1016/j.neulet.2005.09.051
复制
发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Roffwarg,HowardP
中科院分区：
文献类型：
--
作者：
Shaffery,JamesP;Lopez,Jorge;Bissette,Garth;Roffwarg,HowardP
在发育中的动物中抑制快速眼动睡眠（REMS）具有解剖学和生理学后果。我们最近已经表明，在年轻大鼠的关键期结束之前启动REMS剥夺（REMSD）延迟了视觉皮层中关键期（CP）的终止，因此，支持发育调节形式的长时程增强（LTP）的突触可塑性机制维持在不成熟状态[J. P. Shaffery，C.M.辛顿，G. Bisset，H.P. Roffwarg，G.A. Marks，Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats，Neuroscience，110（2002）431-443]。在CP动物中，针对视皮层下方的白色物质（WM）的高频θ爆发刺激（TBS）在II/III层（LTPWM-III）中的突触后细胞中产生LTP。然而，LTPWM-III可以在取自REMS剥夺动物的皮质组织中诱导，持续时间超过CP的通常结束时间长达一周[J. P. Shaffery，C.M.辛顿，G. Bisset，H.P. Roffwarg，G.A. Marks，Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats，Neuroscience，110（2002）431-443]。此外，在CP后的青春期动物中（迟至出生后第60天），REMSD似乎揭示了允许产生发育调节的LTPWM-III的突触可塑性机制[J. P. Shaffery，J.洛佩斯，G. Bissette，H. P. Roffwarg，快速眼动睡眠剥夺恢复了后临界期大鼠视觉皮层中发育调节的突触可塑性的一种形式，神经科学快报，（2005），出版中]。已经提出，REMSD对LTPWM-III产生的影响是由抑制机制效率的降低引起的，该抑制机制被认为促使脑发育的CP终止[J. P. Shaffery，J.洛佩斯，G. Bissette，H. P. Roffwarg，快速眼动睡眠剥夺恢复了后临界期大鼠视觉皮层中发育调节的突触可塑性的一种形式，神经科学快报，（2005），出版中]。在这项研究中，我们测试的假设，低频刺激（LFS）的纤维的WM，这通常会产生相关形式的突触可塑性，长期抑郁症（LTD），也将反映减少抑制音。我们在这里报告说，LFS协议，在正常睡眠，青春期大鼠通常产生LTD或没有变化的反应幅度，在REMS剥夺，青春期大鼠更有可能产生LTP。
Suppression of rapid eye movement sleep (REMS) in developing animals has both anatomical and physiological consequences. We have recently shown that initiating REMS deprivation (REMSD) prior to the end of the critical period in young rats delays termination of the critical period (CP) in visual cortex, and, consequently, the synaptic plasticity mechanisms that support a developmentally regulated form of long-term potentiation (LTP) are maintained in an immature state [J.P. Shaffery, C.M. Sinton, G. Bisset, H.P. Roffwarg, G.A. Marks, Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats, Neuroscience, 110 (2002) 431–443]. In CP animals, high-frequency, theta burst stimulation (TBS) directed at the white matter (WM) below visual cortex produces LTP in the post-synaptic cells in layer II/III (LTPWM-III). However, LTPWM-III can be induced in cortical tissue taken from REMS-deprived animals for up to a week beyond the usual end of the CP [J.P. Shaffery, C.M. Sinton, G. Bisset, H.P. Roffwarg, G.A. Marks, Rapid eye movement sleep deprivation modifies expression of long-term potentiation in visual cortex of immature rats, Neuroscience, 110 (2002) 431–443]. Further, in post-CP, adolescent animals (as late as postnatal day 60), REMSD appears to unmask synaptic plasticity mechanisms that allow for production of developmentally regulated LTPWM-III [J.P. Shaffery, J. Lopez, G. Bissette, H.P. Roffwarg, Rapid eye movement sleep deprivation revives a form of developmentally regulated synaptic plasticity in the visual cortex of post-critical period rats, Neurosci Lett., (2005), in press]. It has been proposed that REMSD's effects on production of LTPWM-III result from a reduction in efficiency of the inhibitory mechanisms thought to precipitate termination of the CP of brain development [J.P. Shaffery, J. Lopez, G. Bissette, H.P. Roffwarg, Rapid eye movement sleep deprivation revives a form of developmentally regulated synaptic plasticity in the visual cortex of post-critical period rats, Neurosci Lett., (2005), in press]. In this study we tested the hypothesis that low-frequency stimulation (LFS) of the fibers of the WM, which usually produces the related form of synaptic plasticity, long-term depression (LTD), will also reflect the reduction in inhibitory tone. We report here that LFS protocols, which in normally sleeping, adolescent rats usually produce either LTD or no change in response magnitude, in REMS-deprived, adolescent rats are more likely to produce LTP.