Mechanisms of hypercapnia-induced arousal from sleep

Carbon dioxide potently induces arousal form sleep. Serotonin (5-HT) neurons comprise part of the ascending arousal system (AAS) and as such are involved in sleep wake regulation. 5-HT neurons, including those that may contribute to the AAS, are chemosensitive, increasing their firing rate in response to acidosis. With his mentor, George Richerson, Dr. Buchanan has shown that 5-HT neurons are important for CO2-induced arousal from sleep. Work in our lab continues to probe mechanisms of CO2-induced arousal from sleep. 

Ongoing studies are aimed at determining which serotonergic neuron populations are responsible for CO2-induced arousal, identifying downstream effecter sites after stimulation of 5-HT neurons with CO2, and understanding larger network mechanisms underlying CO2 induced arousal.

Mechanisms of seizure-related death with relevance to sudden unexpected death in epilepsy (SUDEP):

SUDEP is the leading cause of death in patients with epilepsy. Respiratory, cardiac, autonomic and primary electrocerebral etiologies have been proposed for SUDEP. A second on-going line of research in the lab is geared toward understanding how a seizure can result in death. 

We have first been attempting to establish models of increased seizure susceptibility and mortality. We are beginning to employ these models to understand serotonergic mechanisms in cardio-respiratory control during and after a seizure, post-ictal arousal mechanisms, and seizure-related death.