Jaideep Kapur

Education

  • Residency, Medical College of Virginia, Virginia Commonwealth University
  • Internship, Eastern Virginia School of Medicine
  • PhD, University of Virginia
  • MB,BS, University of Delhi
  • Fellowship, University of Michigan

Primary Appointment

  • Professor, Neurology

Contact

Research Interest(s)

Pathophysiology of Status Epilepticus and Epilepsy; Plasticity of GABAergic Synaptic Transmission

Research Description

γ-Aminobutyric acid (GABA) mediates inhibitory neurotransmission in the brain and controls the excitability of neurons.  GABA mediates fast inhibitory neurotransmission by activating GABAA receptors, which are targets of numerous drugs such as sedatives, anesthetics, anticonvulsants and alcohol.  Alterations of GABAA receptor mediated inhibition are believed to play in important role in the pathogenesis of diseases such as epilepsy.  The laboratory is interested in understanding function and plasticity of inhibitory neurotransmission in the central nervous system.  We are particularly interested in alterations in GABA-mediated inhibition that occur in animal models of epilepsy.  Techniques used in the laboratory include EEG, patch clamp electrophysiology, immunohistochemistry, immunocytochemistry, and cellular imaging in collaboration with the Keck imaging center.  Studies are carried out on whole animals, brain slices, and neuronal cultures.  Recent studies have focused on trafficking of GABAA receptor during seizures and characterization of a novel form of inhibition, called tonic inhibition that is mediated by extrasynaptic GABAA receptors. 
Translational studies focus on novel treatment strategies for prolonged seizures (status epilepticus), which can be life threatening.  These studies also characterize alterations in excitatory neurotransmission during status epilepticus.

Selected Publications

  • Swanwick C, Murthy N, Mtchedlishvili Z, Sieghart W, Kapur J. Development of gamma-aminobutyric acidergic synapses in cultured hippocampal neurons. The Journal of comparative neurology. 2006;495(5): 497-510. PMID: 16498682 | PMCID: PMC2742963
  • Trotter S, Kapur J, Anzivino M, Lee K. GABAergic synaptic inhibition is reduced before seizure onset in a genetic model of cortical malformation. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2006;26(42): 10756-67. PMID: 17050714
  • Sun C, Mtchedlishvili Z, Bertram E, Erisir A, Kapur J. Selective loss of dentate hilar interneurons contributes to reduced synaptic inhibition of granule cells in an electrical stimulation-based animal model of temporal lobe epilepsy. The Journal of comparative neurology. 2006;500(5): 876-93. PMID: 17177260 | PMCID: PMC2844442
  • Rajasekaran K, Kapur J, Bertram E. Alterations in GABA(A) receptor mediated inhibition in adjacent dorsal midline thalamic nuclei in a rat model of chronic limbic epilepsy. Journal of neurophysiology. 2007;98(5): 2501-8. PMID: 17855591
  • Sun C, Mtchedlishvili Z, Erisir A, Kapur J. Diminished neurosteroid sensitivity of synaptic inhibition and altered location of the alpha4 subunit of GABA(A) receptors in an animal model of epilepsy. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2007;27(46): 12641-50. PMID: 18003843 | PMCID: PMC2878477
  • Martin B, Kapur J. A combination of ketamine and diazepam synergistically controls refractory status epilepticus induced by cholinergic stimulation. Epilepsia. 2007;49(2): 248-55. PMID: 17941842 | PMCID: PMC2844443
  • Goodkin H, Joshi S, Mtchedlishvili Z, Brar J, Kapur J. Subunit-specific trafficking of GABA(A) receptors during status epilepticus. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2008;28(10): 2527-38. PMID: 18322097 | PMCID: PMC2880323