To save 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 saving content to .
To save 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 saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved 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.
Disinhibition of REM sleep is a characteristic finding in patients with major depression. REM disinhibition includes shortened REM latency, prolonged first REM periods, and increased REM density (measure of the frequency of rapid eye movements). REM latency, but not REM density, is influenced by age. REM-sleep changes appear to be closely related to the development and the course of depression. A relationship between REM-sleep changes before treatment and treatment outcome is suggested by several studies. REM density is elevated in healthy subjects who have a high genetic load for affective disorders. Most antidepressants suppress REM sleep in patients, normal controls, and laboratory animals. REM-sleep suppression appears to be a distinct hint for the antidepressive properties of a substance, whereas it is not absolutely required. REM-sleep variables during treatment with antidepressants appear to predict the course of the illness. The noradrenergic locus coeruleus and the serotonergic dorsal raphe nuclei, the cholinergic nuclei, and the nucleus of the solitary tract (NTS) are involved in sleep and mood regulation. Hyperaldosteronism has been demonstrated in major depression. Subchronic aldosterone administration can induce anxiety-like behavior. Because of the unusual presence within the brain of both mineralocorticoid receptors and 11-β hydroxysteroid dehydrogenase (11-β HSD), the NTS can act as the gate of the influence of peripheral aldosterone into the brain. Importantly, aldosterone secretion is closely related to the REM/non-REM cycle and is sensitive to sleep manipulations. Hypersecretion of corticotropin-releasing hormone (CRH), the key hormone of the hypothalamo–pituitary–adrenocortical system appears to participate in the pathophysiology of REM-sleep disinhibition. This is supported by increased time spent in REM sleep in mice overexpressing corticotropin-releasing hormone (CRH) in the brain. Furthermore CRH-receptor-type 1 antagonism seems to induce normalization of the REM-sleep changes related to the depression.