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Calcium channel  untuk tidur nyenyak  telah  diidentifikasi

Date:

June 27, 2015

Source:

Marine Biological Laboratory

Summary:

Para ilmuwan telah menemukan, Sebuah saluran kalsium tertentu memainkan peran penting di dalam, tidur gelombang lambat . Ini adalah langkah kunci menuju pemahaman kedua fungsi otak bangun normal dan abnormal .

............... Untuk mengatasi pertanyaan luas tentang tidur, Llinás dan rekan-rekannya terfokus pada satu bagian penting dari teka-teki pada tikus. Saluran kalsium, gerbang selektif dalam dinding neuron, yang integral dalam neuron firing , memastikan bahwa semua bagian dari otak terus berbicara dengan yang lain. Tapi selama tidur, aktivitas saluran kalsium meningkat, menjaga irama lambat yang berbeda dari pola yang ditemukan selama terjaga. Berdasarkan petunjuk ini, para ilmuwan menghapus satu jenis saluran kalsium, Cav3.1, dan melihat bagaimana tidak adanya kegiatan saluran yang  menmpengaruhi  fungsi otak tikus.

Calcium channel ini ternyata menjadi pemain kunci dalam tidur normal. Tikus tanpa bekerjanya  saluran kalsium Cav3.1  membutuhkan waktu lebih lama untuk tertidur daripada tikus normal, dan tertidur untuk waktu yang lebih pendek. "Mereka pada dasarnya mengambil tidur siangnya  kucing," kata Llinás. Aktivitas otak mereka juga normal, lebih seperti terjaga normal daripada tidur. Yang paling penting, tikus-tikus ini tidak pernah mencapai hingga mendalam, tidur gelombang lambat. "Ini berarti bahwa kita telah menemukan bahwa Cav3.1 adalah saluran yang pada akhirnya mendukung tidur nyenyak," kata Llinás.....more

Calcium channel essential for deep sleep identified

Date:

June 27, 2015

Source:

Marine Biological Laboratory

Summary:

A specific calcium channel plays a crucial role in deep, slow-wave sleep, scientists have discovered. This is a key step toward understanding both normal and abnormal waking brain functions.

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Sleep seems simple enough, a state of rest and restoration that almost every vertebrate creature must enter regularly in order to survive. But the brain responds differently to stimuli when asleep than when awake, and it is not clear what brain changes happen during sleep. "It is the same brain, same neurons and similar requirements for oxygen and so on, so what is the difference between these two states?" asks Rodolfo Llinás, a professor of neuroscience at New York University School of Medicine and a Whitman Center Investigator at the Marine Biological Laboratory (MBL) in Woods Hole. In a recent paper, Choi, Yu, Lee, and Llinás announced that a specific calcium channel plays a crucial role in healthy sleep, a key step toward understanding both normal and abnormal waking brain functions.

To tackle the broad question of sleep, Llinás and his colleagues focused on one crucial part of the puzzle in mice. Calcium channels, selective gates in neuron walls, are integral in neuron firing, ensuring that all parts of the brain keep talking to one other. But during sleep, calcium channel activity is increased, keeping a slow rhythm that is different from patterns found during wakefulness. Based on this clue, the scientists removed one type of calcium channel, Cav3.1, and looked at how the absence of that channel's activity affected mouse brain function.

This calcium channel turns out to be a key player in normal sleep. The mice without working Cav3.1 calcium channels took longer to fall asleep than normal mice, and stayed asleep for much shorter periods. "They basically took cat naps," says Llinás. Their brain activity was also abnormal, more like normal wakefulness than sleep. Most importantly, these mice never reached deep, slow-wave sleep. "This means that we have discovered that Cav3.1 is the channel that ultimately supports deep sleep," Llinás says.

Because these mice completely lack the ability to sleep deeply, they eventually express a syndrome similar to psychiatric disorders in humans. Llinás believes that studying how the brain functions during unconsciousness is key to understanding normal consciousness, as well as abnormal brain activity. This paper begins to uncover one of the key mechanisms of normal sleep, as well as the role for one important calcium channel in overall brain function.

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Story Source:

The above post is reprinted from materials provided by Marine Biological Laboratory. The original item was written by Kelsey Calhoun. Note: Materials may be edited for content and length.

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Journal Reference:

1.    Choi, S, Yu E, Lee S, Llinás RR. Altered thalamocortical rhythmicity and connectivity in mice lacking CaV3.1 T-type Ca2 channels in unconsciousness. Proc, Natl. Acad. Sci., June 2015 DOI: 10.1073/1420983112

http://www.sciencedaily.com/releases/2015/06/150627081214.htm

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