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 firstname.lastname@example.org
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.
This chapter examines possible neuronal networks and mechanisms responsible for the switch from waking to non-rapid eye movement (NREM) and REM sleep. The activated cortical state during waking is induced by the activity of multiple waking neurochemical systems. In contrast to the complex and extensive neurochemical network involved in waking, the neurons inducing slow-wave sleep (SWS) are localized in the lateral preoptic area and the adjacent basal forebrain. A cluster of these neurons is localized in a small nucleus called the ventrolateral preoptic nucleus (VLPO), which is situated above the optic chiasm. Neurons specifically active during paradoxical sleep (PS) were recorded in the posterior hypothalamus (PH) of cats or head-restrained rats. One-third of these GABAergic neurons were immunoreactive for the neuropeptide melanin concentrating hormone (MCH). PS onset would be due to the activation of glutamatergic PS-on neurons from the sublaterodorsal tegmental nucleus (SLD).