To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Sleep has been generally divided into rapid eye movement (REM) sleep and non-REM (NREM) sleep in higher order mammals, including humans. Several theories have proposed various functions of different stages of sleep. We hypothesized that REM sleep maintains brain excitability. In this chapter, we discuss the significance of REM sleep in the maintenance of neuronal electrochemical homeostasis, which governs brain excitability. Selective REM-sleep loss increases the activity of Na-K ATPase, a membrane-bound enzyme that maintains neuronal Na+ and K+ homeostasis and, thus, the neuronal resting membrane potential. Further, the REM sleep deprivation-induced increase in Na-K ATPase activity has been attributed to an increased level of norepinephrine in the brain.
Aserinsky & Kleitman (1953) identified within sleep a physiological state that expresses several signs apparently similar to those that occur during wakefulness. This state was termed rapid eye movement (REM) sleep. REM sleep may play a significant role in maintaining normal physiological functions, as its loss has serious detrimental psychopathological effects. The mechanism of REM sleep regulation is still unknown. The pontine cholinergic and noradrenergic transmissions in the brain undergo reciprocal variations in activity associated with the transformation from non-REM sleep to a REM sleep state and vice versa. The cessation of noradrenergic neuronal firing in the locus coeruleus (LC) plays a crucial role in the regulation of REM sleep. Disinhibition of the LC neurons may result in increased levels of noradrenaline (NA) in the brain, and this increased brain NA is likely to be responsible for the pathophysiological effects associated with REM sleep deprivation. Based on recent findings, we discuss the modulation as well as the role of LC neurons and NA in the modulation of REM sleep and the pathophysiological conditions associated with its deprivation. We propose that LC NA neurons are negative executive neurons for the regulation of REM sleep.
One of the important characteristics of living beings is to alternate between active and rest phases, but the underlying mechanism/s and functions are not yet known.
Email your librarian or administrator to recommend adding this to your organisation's collection.