Edward Glasscock, Ph.D.

Edward Glasscock, Ph.D.
Assistant Professor
Ph.D., 2005, University of California, Berkeley
Department of Cellular Biology and Anatomy
1501 Kings Highway
LSU Health Sciences Center
Shreveport, LA 71130
Phone: 318.675.8886
E-mail: aglas1@lsuhsc.edu

Major Research Interests: Dr. Glasscock’s research focuses on the molecular mechanisms that contribute to neurocardiacdysfunction in mouse models of epilepsy and sudden unexplained death in epilepsy (SUDEP). His lab seeks to answer the question of how ion channelopathies causing seizures can give rise to faulty brain-heart interactions leading to SUDEP, the most common cause of mortality in epilepsy.

Ongoing cardiovascular-related projects:

  1. Title:  Complex genetic interactions in mouse model of sudden death in epilepsy (SUDEP)
    Brief description: This project analyzes the ability of Scn2a-null allele heterozygosity to act as a protective modifier of sudden death, epilepsy, and cardiac dysfunction in Kv1.1 knockout mice.
    Names of collaborators / collaborating institutions: Leon Iasemidis (LaTech)
    Funding source: none
  2. Title:  Role of Kv1.1 channels in arrhythmia susceptibility
    Brief description: This project is analyzing the expression and function of Kv1.1 channels in relation to atrial fibrillation and inducible arrhythmias.
    Names of collaborators / collaborating institutions: Xander Wehrens (Baylor College of Medicine); Dobromir Dobrev (Univ. of Essen, Germany)
    Funding source: NIH/NHLBI
  3. Title:  Therapeutic efficacy of KCNQ channel opener drugs in the prevention of sudden death in epilepsy
    Brief description: This project is analyzing the utility of retigabine, a KCNQ potassium channel activator, as therapy to prevent sudden death, epilepsy, and cardiac dysfunction in Kv1.1 knockout mice.
    Names of collaborators / collaborating institutions: none.
    Funding source: none.

Planned cardiovascular-related projects:

  1. Examining the respiratory profile of seizures in Kv1.1 knockout mice and determining whether cardiac dysfunction is linked to respiratory dysfunction in this mouse model.
  2. Using Kv1.1 floxed mice to determine the tissue-specific origin of cardiac dysfunction due to Kv1.1 deficiency.

Methods and Available Resources:

  1. In vivo video simultaneous electroencephalography (EEG), electrocardiography (ECG), and plethysmography in awake freely moving mice. EEG and ECG could also be performed on rats theoretically.
  2. Brain slice immunohistochemistry.
  3. Cardiac myocyte patch clamp electrophysiology (coming soon)
  4. Brain slice extracellular electrophysiology (coming soon)

Publications: http://www.ncbi.nlm.nih.gov/pubmed/?term=Glasscock+E%5BAuthor%5D