William A. Pulsinelli, M.D., Ph.D.

William A. Pulsinelli, M.D., Ph.D.

Semmes-Murphey Professor

Department of Neurology
Department of Anatomy and Neurobiology

Center for Neurobiology of Brain Disease

The University of Tennessee Health Science Center
855 Monroe Avenue, Room 415
Memphis, TN 38163
Phone: (901) 448-6199
Fax: (901) 448-7440
Email: William A. Pulsinelli


  • M.D. Institution: University of Utah Medical College
  • Ph.D. Institution: University of Utah, Department of Biochemistry


Neurology - William A. Pulsinelli

Research Interests

My laboratory is engaged in human and animal research to define how disturbances of brain blood flow and chemistry cause cerebral dysfunction and damage to brain cells. Our long-range goal is to identify the molecular mechanisms responsible for ischemic injury to brain and for the phenomenon of "selective vulnerability;" i.e., the unique sensitivity of specific brain neurons to a lack of oxygen. Our research takes a multifaceted approach to solving the questions of selective vulnerability and ischemic brain injury. Current research focuses on the hypothesis that an imbalance between excitatory and inhibitory neurotransmitters, which occurs in the aftermath of cerebral ischemia, leads to uncontrolled neuronal excitation and the death of neurons. We are characterizing changes in neurotransmitter chemistry with particular emphasis placed on the excitatory amino acid neurotransmitters glutamate, aspartate, and their postsynaptic receptors. As a corollary to this hypothesis, we are measuring changes in potentially toxic ion shifts in brain during ischemia which include alterations of both hydrogen and calcium ions. Currently available techniques used in the laboratory include radioisotope techniques for the measurements of regional cerebral blood flow, metabolism, neurotransmitter chemistry, and calcium movement within the brain.

Representative Publications

  • Takeda Y, Zhao L, Jacewicz M, Pulsinelli WA, Nowak TS Jr. Metabolic and perfusion responses to recurrent peri-infarct depolarization during focal ischemia in the Spontaneously Hypertensive Rat: dominant contribution of sporadic CBF decrements to infarct expansion. J Cereb Blood Flow Metab. 2011 Sep;31(9):1863-73. doi: 10.1038/jcbfm.2011.62. Epub 2011 Apr 27. PubMed PMID: 21522165; PubMed Central PMCID: PMC3185883.
  • Kurasako T, Zhao L, Pulsinelli WA, Nowak TS Jr. Transient cooling during early reperfusion attenuates delayed edema and infarct progression in the Spontaneously Hypertensive Rat. Distribution and time course of regional brain temperature change in a model of postischemic hypothermic protection. J Cereb Blood Flow Metab. 2007 Dec;27(12):1919-30. Epub 2007 Apr 11. PubMed PMID: 17429346.
  • Kamiya T, Jacewicz M, Nowak TS Jr, Pulsinelli WA. Cerebral blood flow thresholds for mRNA synthesis after focal ischemia and the effect of MK-801. Stroke. 2005 Nov;36(11):2463-7. Epub 2005 Oct 13. PubMed PMID: 16224091.
  • Halaby IA, Takeda Y, Yufu K, Nowak TS Jr, Pulsinelli WA. Depolarization thresholds for hippocampal damage, ischemic preconditioning, and changes in gene expression after global ischemia in the rat. Neurosci Lett. 2004 Nov 30;372(1-2):12-6. PubMed PMID: 15531079.
  • Ren Y, Hashimoto M, Pulsinelli WA, Nowak TS Jr. Hypothermic protection in rat focal ischemia models: strain differences and relevance to "reperfusion injury". J Cereb Blood Flow Metab. 2004 Jan;24(1):42-53. PubMed PMID: 14688615.
  • Meade CA, Figueredo-Cardenas G, Fusco F, Nowak TS Jr, Pulsinelli WA, Reiner A. Transient global ischemia in rats yields striatal projection neuron and interneuron loss resembling that in Huntington's disease. Exp Neurol. 2000 Dec;166(2):307-23. PubMed PMID: 11085896.

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