One goal of our research is to translate basic science into new potential therapeutic targets for the treatment of neurological disorders.  In the brain, synapses are the principal means of communication between nerve cells. Most disorders of the nervous system result from the breakdown or the alteration of this synaptic information transfer. We want to gain insight into the causes of specific neurological disorders by studying the physiology/pharmacology of healthy and diseased synaptic transmission.  We employ electrophysiological techniques, such as whole-cell patch clamp recording, excised patch recording, or in vivo electroencephalogram (EEG) recording as well as molecular and biochemical techniques, such as Western blotting, quantitative real-time PCR, and immunohistochemistry to examine alterations in synaptic transmission between healthy and diseased states. 

We aim to investigate if there are specific alterations in synaptic transmission and/or network activity associated with specific disease states.  To study the pathogenesis of neurological disease, we employ both pharmacological models of diseases, such as the pilocarpine or kainate models of epilepsy, and transgenic mouse models, such as a mouse model of Huntington’s disease and a mouse model of Autosomal Dominant Noctornal Frontal Lobe Epilepsy (ADNFLE).

Current projects involve studying the molecular events responsible for the pathological changes in synaptic transmission that take place during different types of epilepsy, alcoholism, premenstrual dysphoric disorder (PMDD), postpartum depression, or Huntington’s Disease.  Our studies are beginning to unravel how disruption in the regulation of synaptic transmission can lead to an altered state of neuronal excitability thus causing specific neurological disorders.