Dorsal Raphe Serotonin Neurons Mediate CO-Induced Arousal from Sleep.

Arousal from sleep in response to CO is a critical protective phenomenon. Dysregulation of CO-induced arousal contributes to morbidity and mortality from prevalent diseases, such as obstructive sleep apnea and sudden infant death syndrome. Despite the critical nature of this protective reflex, the precise mechanism for CO-induced arousal is unknown.

5-HT2A receptor activation is necessary for CO2-induced arousal.

Hypercapnia-induced arousal from sleep is an important protective mechanism pertinent to a number of diseases. Most notably among these are the sudden infant death syndrome, obstructive sleep apnea and sudden unexpected death in epilepsy. Serotonin (5-HT) plays a significant role in hypercapnia-induced arousal.

Corticostriatal interactions in the generation of tic-like behaviors after local striatal disinhibition.

The pathophysiology of the tics that define Gilles de la Tourette syndrome (TS) is not well understood. Local disinhibition within the striatum has been hypothesized to play a pathogenic role. In support of this, experimental disinhibition by local antagonism of GABA-A receptors within the striatum produces tic-like phenomenology in monkey and rat.