Philip Schwartzkroin, Ph.D.

 Philip  Schwartzkroin, Ph.D.


  • Professor
  • Center for Neuroscience


Research Summary

Our research is focused on cellular mechanisms that control/modulate the level of excitability in the brain. We have been interested in issues of neuronal plasticity, particularly those processes that underlie the generation of pathological activities such as epileptic seizures. Toward these ends, we have focused on cellular and circuit properties of the hippocampus, a region implicated in both normal "higher brain functions" (e.g., learning and memory), and neuropathologies associated with epilepsy, stroke, Alzheimer's disease and other neurological disorders. The emphasis of our research is on elucidating the basic cellular mechanisms of the epilepsies, the effects of seizures (particularly in the immature brain), and the development of treatments that prevent (or cure) the epileptic state. Currently, our research focuses on three major themes:

1) How do developmental brain abnormalities lead to seizures and epilepsy? Using animal models of cortical dysplasia, we apply 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 animals models in which genes have been modified or deleted, we study seizure propensity and seek the underlying bases for that sensitivity. In a new study, we will try to replace missing genes (via viral vectors) to see if we can modify seizure activity in a genetically-epileptic mouse. We also pursue an interest in how those seizure-sensitive genes might interact with environmental insult (e.g., head trauma) to induce an epileptogenic process.

3) How do seizures affect neuronal viability, discharge patterns, and connectivity? What are the pathways by which cells die (or recover) during seizures? And do survivng neurons have normal electrical properties and synaptic interactions? These studies involve the elucidation of intracellular pathways that lead to cell death, and the characterization of neurons that remain after an excitotoxic challenge.

Select Publications

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

Tschuluun N, Wenzel HJ, Katleba K, Schwartzkroin PA (2005) 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.

Patel LS, Wenzel HJ, Schwartzkroin PA (2004) Physiological and morphological characterizationof dentate granule cells in the p35 knockout mouse hippocampus: evidence for an epileptic circuit. J.Neurosci., 24:9005-9014.

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

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

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

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

Bough KJ, Schwartzkroin PA, Rho, JM (2003) Calorie restriction and ketogenic diet minish neuronal excitability in rat dentate gyrus in vivo. Epilepsia, 44:752-760.

Wenzel,H.J., Robbins, C.A., Tsai,L.-H. and Schwartzkroin,P.A. (2001) Abnormal morphological and functional organization of the hippocampus in a p35 mutant model of cortical dysplasia assocaited with spontaneous seizures. J.Neurosci., 21:983-998.


Department of Neurological Surgery

Center for Neuroscience