David Akers Hosford
Adjunct Associate Professor in the Department of Neurology

Dr. David A. Hosford is P.I. in an Epilepsy Research Lab at
Duke University and Durham V.A. Medical Centers. The focus of Dr.
Hosford's lab is to identify the cellular and molecular mechanisms
that cause absence seizures in genetic models. The goal of these
studies is to provide a scientific framework that will lead to the
development of new antiabsence therapies for patients with absence

Dr. Hosford's lab uses a variety of molecular biologic,
genetic, biochemical, and electrophysiologic techniques to study
spontaneous absence seizures in a genetic model, the lethargic
(lh/lh) mouse. These mice express frequent (2-4/min) seizures that
demonstrate behavioral, electrographic, and pharmacologic features
typical of those in human absence seizures. The lab has
determined: i) that GABAB receptors are required for the expression
of these seizures; ii) that GABAB receptors are increased in number
in neocortex and discrete thalamic neuronal populations; iii) that
the functions of presynaptic and not postsynaptic GABAB receptors
in these populations are altered. The lab has also found that: i)
GABAA receptors regulate absence seizures in these mice; ii) GABAA
receptor isoforms are differentially expressed in critical thalamic
neuronal populations. Current studies are investigating the roles
of GABAB and GABAA receptors in these neuronal populations.
Other studies are investiating the roles of proteins encoded by absence genes in these animal models.

Dr. Hosford's expertise in GABAergic mechanisms underlying
absence seizures has been recognized by his service as a reviewer
on NIH grant review committees, and by his service as a reviewer
for V.A. Merit Review grants and for 6 peer-reviewed scientific
publications. He has been invited to speak at 4 international
scientific symposia dealing with absence seizures, and was recently
honored by an invitation to speak on absence seizures at the 15th
Annual Merritt-Putnam Symposium.

Key Words: absence seizures, lethargic mouse, GABAB receptors, GABAA receptors, thalamocortical neurons, nucleus reticularis thalami, absence genes

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