Archived AES Symposia 2004
Astrocytes and Epileptogenesis
Program Length: 1 hrs 54 min
The role of astrocytes in the development of seizures and epilepsy remains elusive. This symposium explores recent advances in understanding astrocytic contributions to normal brain development and epileptogenesis. The radial glial cell is a subtype of astrocyte now recognized as the neural stem cell that gives rise to most, if not all, cerebral neurons. The stem cell function of radial glia and their potential involvement in seizure-induced neurogenesis will be described. Astrocytes are also pivotal in the generation of hyperexcitability and seizures in many localization-related epilepsies. Astrocyte dysfunction is specifically implicated in epilepsy pathogenesis in mesial temporal sclerosis, cortical dysplasia, tuberous sclerosis and cerebral gliomas. Potential mechanisms underlying altered astrocytic function, including dysregulated glutamate handling and potassium buffering, will be described for each of these disorders. An improved understanding of astrocyte biology and the involvement of glial cells in epileptogenesis offers the potential for developing novel pharmacological strategies to treat epilepsy.
At the conclusion of this activity, participants should be able to:
- Describe the role of radial glia in brain development
- Understand how astrocyte function changes in human and experimental temporal lobe epilepsy
- Discuss how altered glutamate handling may contribute to seizures caused by brain tumors
- Describe epileptogenic mechanisms of astrocyte dysfunction in cortical dysplasia and tuberous sclerosis complex.
Practitioners who treat persons with epilepsy, and researchers interested in epilepsy.
Chair: Jack M. Parent, M.D.
- Functional and Molecular Changes in Astrocytes of Human Epileptogenic Hippocampus: Relevance to Seizure Generation
Christian Steinhäuser, Ph.D.
- Glutamate Release from Astrocyte-Derived Tumors and Its Contributions to Peritumoral Seizures
Harald Sontheimer, Ph.D.
- Astrocytes and Epileptogenesis in Tuberous Sclerosis Complex
Peter B. Crino, M.D., Ph.D.
Dr. Crino has indicated that he has no relationships to disclose.
Dr. Goetz has indicated that she has no relationships to disclose.
Dr. Sontheimer has indicated that he receives grants/research support from Goldhirsh Foundation and is a consultant for NIH.
Dr. Steinhäuser has indicated that he has no relationships to disclose.