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The Journal of Neuroscience, March 24, 2004, 24(12):2866-2876; doi:10.1523/JNEUROSCI.5051-03.2004

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Neurobiology of Disease
Neuron-Specific mRNA Complexity Responses during Hippocampal Apoptosis after Traumatic Brain Injury

Paolo G. Marciano,¹ Julia Brettschneider,⁶ Elisabetta Manduchi,⁴ Jason E. Davis,³ Scott Eastman,⁷ Ramesh Raghupathi,³ Kathryn E. Saatman,³ Terence P. Speed,⁶ Christian J. Stoeckert, Jr,⁴ James H. Eberwine,^2 * and Tracy K. McIntosh^3,5 *

Departments of ¹Neuroscience, ²Pharmacology, and ³Neurosurgery and ⁴Center for Bioinformatics, University of Pennsylvania, Philadelphia, Pennsylvania 19104, ⁵Veterans Administration Medical Center, Philadelphia, Pennsylvania 19104, ⁶Department of Statistics, University of California, Berkeley, California 94720, and ⁷Incyte Genomics, Fremont, California 94304

In an effort to understand the complexity of genomic responses within selectively vulnerable regions after experimental brain injury, we examined whether single apoptotic neurons from both the CA3 and dentate differed from those in an uninjured brain. The mRNA from individual active caspase 3(+)/terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling [TUNEL(–)] and active caspase 3(+)/TUNEL(+) pyramidal and granule neurons in brain-injured mice were amplified and compared with those from nonlabeled neurons in uninjured brains. Gene analysis revealed that overall expression of mRNAs increased with activation of caspase 3 and decreased to below uninjured levels with TUNEL reactivity. Cell type specificity of the apoptotic response was observed with both regionally distinct expression of mRNAs and differences in those mRNAs that were maximally regulated. Immunohistochemical analysis for two of the most highly differentially expressed genes (prion and Sos2) demonstrated a correlation between the observed differential gene expression after traumatic brain injury and corresponding protein translation.

Key words: apoptosis; traumatic brain injury; hippocampus; CA3; dentate; single-cell amplification; microarray; cell death; differential expression; real-time quantitative PCR

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Received Nov 13, 2003; revised January 27, 2004; accepted January 29, 2004.

This article has been cited by other articles:

				H. Tsuchiya, T. Oka, K. Nakamura, A. Ichikawa, C. B. Saper, and Y. Sugimoto Prostaglandin E2 Attenuates Preoptic Expression of GABAA Receptors via EP3 Receptors J. Biol. Chem., April 18, 2008; 283(16): 11064 - 11071. [Abstract] [Full Text] [PDF]

				R. Linden, V. R. Martins, M. A. M. Prado, M. Cammarota, I. Izquierdo, and R. R. Brentani Physiology of the Prion Protein Physiol Rev, April 1, 2008; 88(2): 673 - 728. [Abstract] [Full Text] [PDF]

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