Rochelle D. Schwartz-Bloom
Professor in the Program in Education
Dr. Schwartz-Bloom is a co-principal investigator for the National Science Foundation Phase II Noyce Fellowship program.
The Schwartz-Bloom laboratory has completed 18 years of research investigating novel pharmacologic approaches to prevent neuronal death caused by cerebral ischemia associated with cardiac arrest and stroke. The group studied how GABA neurotransmission dysfunction contributes to the death of hippocampal neurons after ischemia in vivo or in vitro. Dr. Schwartz-Bloom’s research program continues now exclusively in science education, which she started in 1996. With funds provided by the Duke Provost in 2007, Dr. Schwartz-Bloom established Duke Center for Science Education, an umbrella for all Duke-related activities in science education. She coordinates Duke faculty and student interests in curriculum development, research, and outreach activities in science education for the K-16 grades. Dr. Schwartz-Bloom also directs RISE (Raising Interest in Science Education, http://sites.duke.edu/rise), an office within the Department of Pharmacology and Cancer Biology, where she develops and provides novel science education curricular materials in the area of pharmacology to the K-12 and college community. One of the major programs that she developed is the Pharmacology Education Partnership (http://sites.duke.edu/thepepproject), a series of pharmacology- and drug abuse-related science education modules for high school biology and chemistry students. Testing of over 15,000 high school students has revealed that student performance in biology and chemistry improves when they use the pharmacology curriculum developed by her team. Dr. Schwartz-Bloom provides several opportunities for Duke Pharmacology graduate students and post-doctoral fellows to obtain experience in teaching.
- Ph.D., Georgetown University 1983
Schwartz, R. D., et al. “Diazepam, given postischemia, protects selectively vulnerable neurons in the rat hippocampus and striatum.” Journal of Neuroscience, vol. 15, no. 1 II, Jan. 1995, pp. 529–39.
Schwartz, R. D., et al. “Postischemic diazepam is neuroprotective in the gerbil hippocampus..” Brain Research, vol. 647, no. 1, May 1994, pp. 153–60. Epmc, doi:10.1016/0006-8993(94)91411-7. Full Text
Schwartz, R. D., et al. “Bidirectional modulation of GABA-gated chloride channels by divalent cations: inhibition by Ca2+ and enhancement by Mg2+..” Journal of Neurochemistry, vol. 62, no. 3, Mar. 1994, pp. 916–22.
Schwartz, R. D., et al. “Erratum: Postischemic diazepam is neuroprotective in the gerbil hippocampus (Brain Research 647 (1994) (153-160)) (BRES 26140).” Brain Research, vol. 655, no. 1–2, Jan. 1994, pp. 279–80. Scopus, doi:10.1016/0006-8993(94)91629-2. Full Text
Li, H., et al. “Rapid decline of GABAA receptor subunit mRNA expression in hippocampus following transient cerebral ischemia in the gerbil..” Hippocampus, vol. 3, no. 4, Oct. 1993, pp. 527–37. Epmc, doi:10.1002/hipo.450030412. Full Text
Schwartz, R. D., and X. Yu. “Inhibition of GABA-gated chloride channel function by arachidonic acid..” Brain Research, vol. 585, no. 1–2, July 1992, pp. 405–10. Epmc, doi:10.1016/0006-8993(92)91246-b. Full Text
Edgar, P. P., and R. D. Schwartz. “Functionally relevant gamma-aminobutyric acidA receptors: equivalence between receptor affinity (Kd) and potency (EC50)?.” Molecular Pharmacology, vol. 41, no. 6, June 1992, pp. 1124–29.
Mileson, B. E., et al. “Alterations in the gamma-aminobutyric acid-gated chloride channel following transient forebrain ischemia in the gerbil..” Journal of Neurochemistry, vol. 58, no. 2, Feb. 1992, pp. 600–07. Epmc, doi:10.1111/j.1471-4159.1992.tb09761.x. Full Text
Schwartz, R. D., et al. “Cellular regulation of the benzodiazepine/GABA receptor: arachidonic acid, calcium, and cerebral ischemia..” Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, vol. 6, no. 2, Feb. 1992, pp. 119–25.
McCown, T. J., et al. “Unilateral kindling of the inferior collicular cortex does not transfer to the contralateral seizure sensitive site or alter [3H]flunitrazepam and [35S]TBPS binding..” Epilepsy Research, vol. 9, no. 2, July 1991, pp. 132–38. Epmc, doi:10.1016/0920-1211(91)90024-a. Full Text