Research Overview

In our first line of research, we seek to understand the cellular and molecular mechanisms underlying brain injury in order to provide a rational basis for preventing and treating important neurological disorders and diseases. We are investigating how expression and function of the brain's major glutamate transporter, GLT1, is regulated at normal synapses and how GLT1 function is compromised in acute and chronic neurodegenerative diseases. In addition, we are working to characterize pathways of programmed cell death in neurons and oligodendrocytes. In our second line of research, we are investigating the biochemical and molecular basis of behavioral state regulation, with a particular focus on the role of nitric oxide and adenosine in regulating behavioral states (sleeping and waking).

About Paul Rosenberg

Paul Rosenberg received his MD and PhD degrees from Albert Einstein College of Medicine. He completed an internship at University Hospital, Boston, a neurology residency through the Harvard-Longwood Neurological Training Program and a fellowship in cellular neurobiology at Boston Children's Hospital.

Researcher Services

Researcher Areas

  • Physiology and Pathology of Glutamate Transporters in the Central Nervous System
  • Molecular Mechanisms of Brain Injury
  • Mechanisms of Homeostatic Sleep Regulation

Research Departments

Researcher Programs

Researcher Centers


  • Rimmele TS, Rosenberg PA (2016) GLT-1: The elusive presynaptic glutamate transporter. Neurochem Int 98:19-28.
  • Petr GT, Sun Y, Frederick NM, Zhou Y, Dhamne SC, Hameed MQ, Miranda C, Bedoya EA, Fischer KD, Armsen W, Wang J, Danbolt NC, Rotenberg A, Aoki CJ, Rosenberg PA (2015) Conditional deletion of the glutamate transporter GLT-1 reveals that astrocytic GLT-1 protects against fatal epilepsy while neuronal GLT-1 contributes significantly to glutamate uptake into synaptosomes. J Neurosci 35:5187-5201.
  • Kabakov AY, Rosenberg PA (2015) GLT-1 transport stoichiometry Is constant at low and high glutamate concentrations when chloride Is substituted by gluconate. PLoS One10:e0136111.
  • Frederick NM, Bertho J, Patel KK, Petr GT, Bakradze E, Smith SB, Rosenberg PA (2014) Dysregulation of system xc(-) expression induced by mutant huntingtin in a striatal neuronal cell line and in R6/2 mice. Neurochem Int 76:59-69.
  • Elitt CM, Rosenberg PA (2014) The challenge of understanding cerebral white matter injury in the premature infant. Neuroscience 276:216-238.
  • Back SA, Rosenberg PA (2014) Pathophysiology of glia in perinatal white matter injury. Glia 62:1790-1815.
  • Petr GT, Schultheis LA, Hussey KC, Sun Y, Dubinsky JM, Aoki C, Rosenberg PA (2013) Decreased expression of GLT-1 in the R6/2 model of Huntington's disease does not worsen disease progression. Eur J Neurosci 38:2477-2490.
  • Petr GT, Bakradze E, Frederick NM, Wang J, Armsen W, Aizenman E, Rosenberg PA (2013) Glutamate transporter expression and function in a striatal neuronal model of Huntington's disease. Neurochem Int 62:973-981.
  • DeSilva TM, Borenstein NS, Volpe JJ, Kinney HC, Rosenberg PA (2012) Expression of EAAT2 in neurons and protoplasmic astrocytes during human cortical development. J Comp Neurol 520:3912-3932.
  • Volpe JJ, Kinney HC, Jensen FE, Rosenberg PA (2011) The developing oligodendrocyte: key cellular target in brain injury in the premature infant. Int J Dev Neurosci 29:423-440.