Regulation of cortical activity and arousal by the matrix cells of the ventromedial thalamic nucleus.
Regulation of cortical activity and arousal by the matrix cells of the ventromedial thalamic nucleus.
复制标题
DOI：
10.1038/s41467-018-04497-x
复制
发表时间：
2018-05-29
影响因子：
16.6
通讯作者：
Cirelli C
中科院分区：
文献类型：
--
作者：
Honjoh S;Sasai S;Schiereck SS;Nagai H;Tononi G;Cirelli C
丘脑腹内侧核(Vm)由于其弥漫的、浅表的投射，长期以来一直被认为是调节皮质觉醒的候选区域，但缺乏直接的证据。在这里，我们在小鼠身上显示，在觉醒和REM睡眠中，VM calbindin1阳性基质细胞的活性高，在NREM睡眠中低，在睡眠到觉醒转换时，在皮质活动之前增加。对Vm细胞的光遗传刺激迅速将所有小鼠从NREM睡眠中唤醒，并在慢波麻醉下持续引起脑电激活，而在REM睡眠中没有唤醒。相反，抑制Vm的化学发生可缩短觉醒时间。“特定的”腹后内侧核(VPM)的光遗传激活不会引起NREM或REM睡眠的唤醒。因此，在NREM睡眠和慢波麻醉期间，VM中的基质细胞产生唤醒和广泛的皮质激活，这种方式解释了经典上归因于“非特异性”丘脑核团的影响。丘脑腹内侧核(Vm)被认为通过其向皮质的弥漫性投射来控制皮质的觉醒。在这里，作者记录和操纵了VM中calbindin1阳性基质细胞的活动，并表明它们双向调节睡眠-觉醒转换。
The “non-specific” ventromedial thalamic nucleus (VM) has long been considered a candidate for mediating cortical arousal due to its diffuse, superficial projections, but direct evidence was lacking. Here, we show in mice that the activity of VM calbindin1-positive matrix cells is high in wake and REM sleep and low in NREM sleep, and increases before cortical activity at the sleep-to-wake transition. Optogenetic stimulation of VM cells rapidly awoke all mice from NREM sleep and consistently caused EEG activation during slow wave anesthesia, while arousal did not occur from REM sleep. Conversely, chemogenetic inhibition of VM decreased wake duration. Optogenetic activation of the “specific” ventral posteromedial nucleus (VPM) did not cause arousal from either NREM or REM sleep. Thus, matrix cells in VM produce arousal and broad cortical activation during NREM sleep and slow wave anesthesia in a way that accounts for the effects classically attributed to “non-specific” thalamic nuclei. The ventromedial thalamus (VM) is thought to control cortical arousal through its diffuse projections to cortex. Here the authors record and manipulate the activity of calbindin1-positive matrix cells in VM and show that they bidirectionally regulate the sleep-wake transition.
登录
查看更多内容
影响因子：
3.5
作者：
Chen Z;Wimmer RD;Wilson MA;Halassa MM
通讯作者：
Halassa MM
影响因子：
16.6
作者：
Anaclet C;Pedersen NP;Ferrari LL;Venner A;Bass CE;Arrigoni E;Fuller PM
通讯作者：
Fuller PM
影响因子：
--
作者：
Dempsey, EW;Morison, RS
通讯作者：
Morison, RS
影响因子：
25
作者：
Eban-Rothschild A;Rothschild G;Giardino WJ;Jones JR;de Lecea L
通讯作者：
de Lecea L
影响因子：
3.3
作者：
ARBUTHNOTT, GW;MACLEOD, NK;WRIGHT, AK
通讯作者：
WRIGHT, AK