While cortical and limbic regions are known to be highly susceptible to seizures, converging evidence suggests that subcortical structures critically regulate when and how seizures start and propagate. We are determining how seizures hijack subcortical neuromodulatory networks, and whether those networks can in turn be harnessed to regulate ictogenesis.
Neuromodulatory neurons, clustered in small nuclei deep within the brain (hypothalamus, brainstem), send widespread ascending projections throughout the central nervous system to modulate brain networks on a global scale. These neuronal populations and their projections have been studied extensively in the context of sleep and arousal; we are building upon that work to examine their roles in the context of epilepsy.
- Are neuromodulatory neurons inhibited during seizures?
- Does direct activation of arousal networks inhibit or curtail seizures?
- How does chronic epilepsy alter the properties of neuromodulatory neurons and of their projections?