Clinical/Research Interests

Dr. Schwartzkroin studies cellular mechanisms that control/modulate excitability in the brain, particularly those involved in epilepsy and seizures, as well as the neurobiology of pediatric epilepsies, particularly those associated with abnormal brain development and cortical dysplasia. Dr. Schwartzkroin's laboratory is interested in issues of neuronal plasticity, ranging from those processes that underlie normal learning to those involved in the generation of pathological activities such as epileptic seizures. They have focused on cellular and circuit properties of the hippocampus, a region implicated in both higher brain functions (such as learning and memory), as well as in neuropathologies associated with epilepsy, traumatic brain injury, autism and other neurological disorders. The laboratory employs a variety of experimental techniques, including: electrophysiology of individual neurons in in vitro preparations; stimulation and recording in intact animal seizure models; morphological and immunocytochemical (light and electron microscopic) assessment of brain tissue; and behavioral/electrophysiological/morphological characterization of genetically manipulated animals (rats/mice). Currently, Dr. Schwartzkroin's laboratory focuses on three major sets of research questions: (1) How do developmental brain abnormalities lead to seizures and epilepsy? Using animal models of cortical dysplasia, the laboratory uses cellular electrophysiological analyses to determine changes in cellular or circuit properties that might underlie seizure/epilepsy development. Single-cell recording and histochemical staining procedures are used to establish structure-function relationships. (2) What genes contribute to seizure susceptibility and/or to the development of an epileptic state? Using animal models in which genes have been modified or deleted, the laboratory studies seizure propensity and seeks the underlying bases for that sensitivity. In a new pilot study, Dr. Schwartzkroin and colleagues have begun to replace missing genes (via viral vectors) to see if they can modify seizure activity in a genetically epileptic mouse. They also are developing an animal model in which to study how seizure-sensitivity genes might interact with environmental insult (traumatic brain injury) to induce an epileptogenic process. (3) How are seizures related to traumatic brain injury? These studies focus on the possibility of preventing post-traumatic epilepsy by treting animals (e.g., with the ketogenic diet) to reduce neuronal cell injury/loss associated with the insult.

In addition to his epilepsy-related research, Dr. Schwartzkroin has been active in a number of major editing projects: Co-Editor-in-Chief of the journal Epilepsia, and Editor-in-Chief of The Encyclopedia of Basic Epilepsy Research.

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Select Recent Publications:

Wenzel HJ, Vacher H, Clark E, Trimmer JS, Lee AL, Sapolsky RM, Tempel BL, Schwartzkroin PA (2007) Structural consequences of Kcna1 gene deletion and transfer in the mouse hippocampus. Epilepsia 48:2023-2046 (doi: 10.1111/j.1528-1167. 2007. 01189.x)

Tschuluun N, Wenzel HJ, Schwartzkroin PA. Irradiation exacerbates cortical cytopathology in the Eker rat model of Tuberous Sclerosis Complex, but does not induce hyperexcitability. Epilepsy Res, (doi: 10.1016/j.eplepsyres. 2006. 08.003) 73:53-64.

Wenzel HJ, Tamse CT, Schwartzkroin PA. Dentate development in organotypic hippocampal slice cultures from p35 knock-out mice. Developmental Neurosci, 2006. 29:99-112.

Keogh BP, Cordes D, Stanberry L, Figler BD, Robbins CA, Tempel BL, Green CG, Emmi A, Maravilla KM, Schwartzkroin PA. BOLD-fMRI of PTZ-induced seizures in rats. Epilepsy Res, 66:75-90, 2005.

Tschuluun N, Wenzel HJ, Katleba K, Schwartzkroin PA. Initiation and spread of epileptiform discharges in the methylazoxymethanol acetate rat model of cortical dysplasia: Functional and structural connectivity between CA1 heterotopia and hippocampus/neocortex. Neuroscience, 133:327-342, 2005.

Patel LS, Wenzel HJ, Schwartzkroin PA. Physiological and morphological characterization of dentate granule cells in the p35 knock-out mouse hippocampus: Evidence for an epileptic circuit. J Neurosci, 24:9005-9014, 2004.

Wenzel HJ, Patel LS, Robbins CA, Emmi A, Yeung RS, Schwartzkroin PA. Morphology of cerebral lesions in the Eker rat model of tuberous sclerosis. Act Neuropath, 108:97-108, 2004.

Galvan CD, Wenzel HJ, Dineley KT, Lam TT, Schwartzkroin PA, Sweatt JD, Swann JW. Postsynaptic contributions to hippocampal network hyperexcitability induced by chronic activity blockade in vivo. Eur J Neurosci, 18:1861-1872, 2003.

McKhann GM, Wenzel HJ, Robbins CA, Sosunov AA, Schwartzkroin PA. Mouse strain differences in kainic acid sensitivity, seizure behavior, mortality and hippocampal pathology. Neuroscience, 122:551-561, 2003.

Lopantsev V, Tempel BL, Schwartzkroin PA. Hyperexcitability of CA3 pyramidal cells in mice lacking the Kv1.1 potassium channel. Epilepsia, 44:1506-1512, 2003.