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.
This chapter presents results from studies showing strong evidence for pronounced heritability of waking and rapid eye movement (REM) and non-REM sleep electroencephalographic (EEG) activity. Genes regulate the expression and function of the neurobiological systems that modulate sleep and wakefulness. The most commonly employed method for identifying genes involved in some aspect of physiological or behavioral regulation is the candidate gene approach. In this approach, individuals with genetic polymorphisms thought to be involved in sleep-wake regulation or neurobehavioral vulnerability to sleep loss are subjected to sleep loss in the laboratory, and neurobehavioral measures are assessed throughout. The chapter determines whether functional polymorphisms of the catechol-O-methyltransferase (COMT) gene moderate responsivity to other psychostimulants that also act via dopaminergic signaling. Genetic variations also appear to control individual responsivity to stimulants. Evidence indicates that the COMT Val158Met polymorphism controls individual responsivity to the stimulant modafinil during sleep loss.
Histamine (HA) is a biogenic amine, providing a number of functional roles throughout the body. HA release triggers inflammatory responses as a protective reaction against foreign pathogens. Released from basophils and mast cells in the periphery, HA causes increased vascular permeability and dilation of blood vessels to allow increased fluid infiltration into tissues which in turn induces swelling. Research designed to test the role of HA in mediating central nervous system (CNS) activity demonstrated that HA immunoreactive brain neurons actively fire action potentials and release HA during the wake phase but are essentially silent during sleep, supporting the hypothesis that increased HA tone is related to levels of wakefulness. Results of experiments investigating the effects of HA in the CNS, either through direct injection of HA or through pharmacological inhibition of its synthesis, show that increases in HA are positively correlated with amounts of wakefulness.
Email your librarian or administrator to recommend adding this to your organisation's collection.