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Richard W. Keller, Jr. , Ph.D.
Professor and Associate Dean for Graduate Studies


1978 - Ph.D. from University of Kansas
1972 - University of Delaware
1988 - University of Pittsburgh - Research Assistant Professor

Current Research

Dr. Keller is currently serving as the Associate Dean for Graduate Studies. 

While he is conducting research in collaboration with Dr. Mongin,

he is not currently accepting students into his lab.


With enhanced use of imaging techniques, it has become apparent over the last several years that there is a much higher rate of neonatal stroke than was originally appreciated. The rate for neonatal stroke is now recognized to be in the range of 1 in 4000 term births. As in adult stroke, neonatal stroke is most commonly ischemic (blockade of blood flow) and most frequently occurs in the region of the brain which receives its oxygen and nutrients via the middle cerebral artery; however, the neurological impairments are dramatically reduced in the neonate. While half the cases of neonatal stroke involve some degree of neurological or cognitive impairment, the degree of impairment seen in the infant is significantly less than the impairment observed in adults. This reduction in the behavioral signs of stroke has lead to an underestimation and underdiagnosis of neonatal stroke. Adult rat models of stroke focusing on temporary disruption of blood flow in the middle cerebral artery have existed for years and are relatively well characterized. To date most ischemia studies in rat pups have focused on disruptions of blood flow associated with the birthing process and have utilized the hypoxic-ischemic model which not as regionally focused as the adult stroke models. Our lab is using a more recently developed ischemia model in infant rats which, like the adult rat stroke models, is focused on disruption of blood flow in the middle cerebral artery. We are doing this in hopes of making direct comparisons with work done in adult rats as we look for differences in mechanisms of damage between adult and infant. The model we are using is called a "transient unilateral focal ischemia" and is performed in 7-day-old rat pups as described by Renolleau, et al., Stroke 29 1454-1461 (1998). At a neurochemical level, the initial stages of stroke damage appear to be associated with the release of significant quantities of the excitatory neurotransmitter, glutamate, leading to excitotoxicity. This excitotoxicity is associated with an influx of calcium into the cell and generation of the rather damaging free radicals that can, in significant quantities, result in cell death. Our studies indicate that glutamate is released with a different time profile and possibly by a different mechanism in the rat pup. Similarly, there are differences in the generation and release of the free radicals. There are also differences in the excitability of these cells as demonstrated by examining the activation of immediate early genes. More recently we have begun to examine the effects of this ischemia on more long term changes related to inflammation. At a behavioral level we find that these pups, even with very large brain lesions, display very little in the way of neurological impairments - consistent with the reduced deficits seen in human infants after a stroke. Exposed to an entire battery of behavioral measures we have found no significant behavioral deficits up to six weeks of age. Since infant stroke is more prevalent and more damaging in cases where the infant is exposed to infection, we are also beginning studies in this area of research. We have preliminary evidence that in utero exposure to infection can result in enhanced stroke damage when the stroke is administered 7 days after birth. We hope that our findings will lead to a better understanding of how infants are relatively protected from the effects of stroke and, furthermore, how this information might be translated into therapies for both infant and adult stroke victims.


Below are some sample publications.

For a list of all my publications click here:

PubMed Publications

  1. Dohare, P., Hyzinski-García, M.C., Vipani, A., Bowens, N.H., Nalwalk, J.W., Feustel, P.J., Keller, R.W. Jr., Jourd'heuil, D. and Mongin, A.A., The neuroprotective properties of the superoxide dismutase mimetic tempol correlate with its ability to reduce pathological glutamate release in an animal model of stroke. Free Radical Biology & Medicine 77, 168-182 (2014).

  2. Mongin, A.A., Hyzinski-García, M.C., Vincent, M.Y., and Keller, R.W., Jr., A simple method for measuring intracellular glutamine synthetase and glutaminase activities in glial cells. Am. J. Physiol. Cell Physiol. 301, C814-C822. (2011).

  3. Hyzinski-García, M.C., Vincent, M.Y., Haskew-Layton, R.E., Dohare, P., Keller, R.W. Jr., Mongin, A.A., Hypoosmotic swelling modifies glutamate-glutamine cycle in the rat brain in vivo and in cultured astrocytes. J. Neurochem., 118, 140-152 (2011).

  4. Pabello,N.G., Tracy,S.J., Snyder-Keller,A., and Keller,R.W. Jr., Regional expression of constitutive and inducible transcription factors following transient focal ischemia in the neonatal rat: Influence of hypothermia., Brain Res., 1038: 11-21 (2005).

  5. Pabello,N.G., Tracy,S.J., and Keller,R.W.Jr., Protective effects of brief intra- and delayed postischemic hypothermia in a transient focal ischemia model in the neonatal rat., Brain Res.,995: 29-38 (2004).

  6. Seki, U., Feustel, P.J., Kimelberg, H.K., Keller, R.W.,Jr., Charniga, C., Chandra, A. & Tranmer, B.I., Mechanisms of ischemia-induced glutamate release in rat striatum: An in vivo brain microdialysis study. Stroke 30, 433-440 (1999).