Neurobiology of Arousal and Sleep: Updates and Insights Into Neurological Disorders

Miranda M. Lim, Ronald Szymusiak

Research output: Contribution to journalReview articlepeer-review

12 Scopus citations


Brain activation during wakefulness is sustained by multiple arousal systems. Dysfunction of one or more arousal systems is a feature of neurological disorders associated with hypersomnolence and/or sleep-wake cycle disturbance. Narcolepsy, Alzheimer’s disease (AD), Parkinson’s disease (PD), and traumatic brain injury appear to involve hypocretin (HCT) and possibly histamine insufficiency as a mechanism related to excessive daytime sleepiness. Loss of cholinergic neurons in AD and of dopamine neurons in PD contributes to sleep-wake disturbance. GABAergic neurons in the preoptic hypothalamus and rostral medulla promote sleep through inhibition of arousal systems. Pathology of preoptic sleep regulatory circuits is correlated with sleep disturbance in AD. An unidentified endogenous somnogen that potentiates the actions of gamma-aminobutyric acid (GABA) is present in the cerebrospinal fluid (CSF) of patients with primary hypersomnia. Descending pathways from the dorsal lateral pons to the ventral medulla and spinal cord are responsible for the inhibition of spinal motoneurons during rapid eye movement (REM) sleep and are implicated in human REM sleep behavior disorder.

Original languageEnglish (US)
Pages (from-to)91-100
Number of pages10
JournalCurrent Sleep Medicine Reports
Issue number2
StatePublished - Jun 1 2015


  • Acetylcholine
  • Alzheimer’s disease
  • Basal forebrain
  • Dopamine
  • Galanin
  • Glutamate
  • Hypocretin
  • Laterodorsal tegmentum
  • Locus coeruleus
  • Monoamines
  • Orexin
  • Parkinson’s disease
  • Preoptic hypothalamus
  • Traumatic brain injury
  • Tuberomammillary nucleus

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Neurology
  • Clinical Neurology


Dive into the research topics of 'Neurobiology of Arousal and Sleep: Updates and Insights Into Neurological Disorders'. Together they form a unique fingerprint.

Cite this