Paul A Rosenberg

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Mature myelin basic protein-expressing oligodendrocytes are insensitive to kainate toxicity
    Paul A Rosenberg
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci Res 71:237-45. 2003
  2. pmc Regulation of glutamate transport in developing rat oligodendrocytes
    Tara M Desilva
    Department of Neurology and F M Kirby Neurobiology Center, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 29:7898-908. 2009
  3. ncbi request reprint Glutamate receptor-mediated oligodendrocyte toxicity in periventricular leukomalacia: a protective role for topiramate
    Pamela L Follett
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 24:4412-20. 2004
  4. ncbi request reprint Oligodendrocyte excitotoxicity determined by local glutamate accumulation and mitochondrial function
    Wenbin Deng
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Neurochem 98:213-22. 2006
  5. ncbi request reprint Developmental lag in superoxide dismutases relative to other antioxidant enzymes in premyelinated human telencephalic white matter
    Rebecca D Folkerth
    From Departments of Pathology Neuropathology, Children s Hospital, Boston, USA
    J Neuropathol Exp Neurol 63:990-9. 2004
  6. ncbi request reprint Developmental up-regulation of MnSOD in rat oligodendrocytes confers protection against oxidative injury
    Olivier Baud
    Department of Neurology, Children s Hospital and Harvard Medical School, 300 Longwood Ave, Boston, MA 02115, USA
    Eur J Neurosci 20:29-40. 2004
  7. pmc 17beta-estradiol protects against hypoxic/ischemic white matter damage in the neonatal rat brain
    Bettina Gerstner
    Department of Neurology, Children s Hospital Boston, Boston, MA 02115, USA
    J Neurosci Res 87:2078-86. 2009
  8. pmc Peroxynitrite-induced neuronal apoptosis is mediated by intracellular zinc release and 12-lipoxygenase activation
    Yumin Zhang
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 24:10616-27. 2004
  9. ncbi request reprint Intracellular zinc release and ERK phosphorylation are required upstream of 12-lipoxygenase activation in peroxynitrite toxicity to mature rat oligodendrocytes
    Yumin Zhang
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Mass 02115, USA
    J Biol Chem 281:9460-70. 2006
  10. pmc Vitamin K prevents oxidative cell death by inhibiting activation of 12-lipoxygenase in developing oligodendrocytes
    Jianrong Li
    The F M Kirby Neurobiology Center, Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
    J Neurosci Res 87:1997-2005. 2009

Collaborators

Detail Information

Publications51

  1. ncbi request reprint Mature myelin basic protein-expressing oligodendrocytes are insensitive to kainate toxicity
    Paul A Rosenberg
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci Res 71:237-45. 2003
    ....
  2. pmc Regulation of glutamate transport in developing rat oligodendrocytes
    Tara M Desilva
    Department of Neurology and F M Kirby Neurobiology Center, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 29:7898-908. 2009
    ..The absence of GLT1 in mature OLs in the rat corpus callosum and its presence in mature rat cultured OLs may indicate that a signaling process in vivo is not activated in vitro...
  3. ncbi request reprint Glutamate receptor-mediated oligodendrocyte toxicity in periventricular leukomalacia: a protective role for topiramate
    Pamela L Follett
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 24:4412-20. 2004
    ....
  4. ncbi request reprint Oligodendrocyte excitotoxicity determined by local glutamate accumulation and mitochondrial function
    Wenbin Deng
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Neurochem 98:213-22. 2006
    ..Therapeutic strategies targeting local glutamate concentration and mitochondrial injury during hypoxia-ischemia may be relevant to human disorders associated with pre-OL excitotoxicity...
  5. ncbi request reprint Developmental lag in superoxide dismutases relative to other antioxidant enzymes in premyelinated human telencephalic white matter
    Rebecca D Folkerth
    From Departments of Pathology Neuropathology, Children s Hospital, Boston, USA
    J Neuropathol Exp Neurol 63:990-9. 2004
    ..The previously unrecognized dissociation between the expression of the SODs and that of catalase and GPx in the fetal period has potential implications for future antioxidant therapy in PVL...
  6. ncbi request reprint Developmental up-regulation of MnSOD in rat oligodendrocytes confers protection against oxidative injury
    Olivier Baud
    Department of Neurology, Children s Hospital and Harvard Medical School, 300 Longwood Ave, Boston, MA 02115, USA
    Eur J Neurosci 20:29-40. 2004
    ..These data suggest a primary involvement of superoxide in glutathione depletion toxicity in developing OLs, and suggest an important role for MnSOD in the resistance observed in mature OLs...
  7. pmc 17beta-estradiol protects against hypoxic/ischemic white matter damage in the neonatal rat brain
    Bettina Gerstner
    Department of Neurology, Children s Hospital Boston, Boston, MA 02115, USA
    J Neurosci Res 87:2078-86. 2009
    ..These results suggest a potential role for estrogens in attenuation of hypoxic-ischemic and oxidative injury to developing OLs and in the prevention of periventricular leukomalacia...
  8. pmc Peroxynitrite-induced neuronal apoptosis is mediated by intracellular zinc release and 12-lipoxygenase activation
    Yumin Zhang
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 24:10616-27. 2004
    ....
  9. ncbi request reprint Intracellular zinc release and ERK phosphorylation are required upstream of 12-lipoxygenase activation in peroxynitrite toxicity to mature rat oligodendrocytes
    Yumin Zhang
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Mass 02115, USA
    J Biol Chem 281:9460-70. 2006
    ....
  10. pmc Vitamin K prevents oxidative cell death by inhibiting activation of 12-lipoxygenase in developing oligodendrocytes
    Jianrong Li
    The F M Kirby Neurobiology Center, Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
    J Neurosci Res 87:1997-2005. 2009
    ..In summary, our data indicate that vitamin K prevents oxidative cell death by blocking activation of 12-LOX and ROS generation...
  11. pmc Tumor necrosis factor alpha mediates lipopolysaccharide-induced microglial toxicity to developing oligodendrocytes when astrocytes are present
    Jianrong Li
    Department of Neurology and the F M Kirby Neurobiology Center, Children s Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 28:5321-30. 2008
    ....
  12. ncbi request reprint Elevation of intracellular cAMP evokes activity-dependent release of adenosine in cultured rat forebrain neurons
    Yin Lu
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Eur J Neurosci 19:2669-81. 2004
    ..These data suggest the existence of a homeostatic negative feedback loop in which increases in neuronal activity are damped by release of adenosine following activation of glutamate receptors...
  13. pmc Glutamate transporter EAAT2 expression is up-regulated in reactive astrocytes in human periventricular leukomalacia
    Tara M Desilva
    Department of Neurology, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Comp Neurol 508:238-48. 2008
    ..The previously unrecognized up-regulation of EAAT2 in reactive astrocytes and its presence in macrophages in PVL reported here may reflect a response to either hypoxic-ischemic injury or inflammation...
  14. pmc Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway
    Seija Lehnardt
    Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 100:8514-9. 2003
    ..In contrast, animals bearing a loss-of-function mutation in the tlr4 gene are resistant to neuronal injury in the same model. The present study demonstrates a mechanistic link among innate immunity, TLRs, and neurodegeneration...
  15. pmc Decreased expression of GLT-1 in the R6/2 model of Huntington's disease does not worsen disease progression
    Geraldine T Petr
    Department of Neurology and the FM Kirby Neurobiology Center, Children s Hospital Boston, Boston, MA, USA
    Eur J Neurosci 38:2477-90. 2013
    ..These results suggest that changes in GLT-1 expression or function per se are unlikely to potentiate or ameliorate the progression of HD...
  16. pmc Expression of EAAT2 in neurons and protoplasmic astrocytes during human cortical development
    Tara M Desilva
    Department of Neurology and the FM Kirby Neurobiology Center, Children s Hospital Boston and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Comp Neurol 520:3912-32. 2012
    ..In addition, by studying the expression of EAAT1 and EAAT2 glutamate transporters, it was possible to document the development of protoplasmic astrocytes...
  17. pmc Peroxynitrite generated by inducible nitric oxide synthase and NADPH oxidase mediates microglial toxicity to oligodendrocytes
    Jianrong Li
    Department of Neurology, Children s Hospital, and Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:9936-41. 2005
    ..Our results reveal a role for NADPH oxidase in LPS-induced OL death and suggest that peroxynitrite produced by iNOS and NADPH oxidase in activated microglia may play an important role in the pathogenesis of white matter disorders...
  18. pmc Hyperoxia causes maturation-dependent cell death in the developing white matter
    Bettina Gerstner
    Department of Neurology and the F M Kirby Neurobiology Center, Children s Hospital Boston, Boston, Massachusetts 02115, USA
    J Neurosci 28:1236-45. 2008
    ..These observations may be relevant to white matter injury observed in premature infants...
  19. ncbi request reprint Alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor subunit composition and cAMP-response element-binding protein regulate oligodendrocyte excitotoxicity
    Wenbin Deng
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 281:36004-11. 2006
    ..Overall, these data suggest that targeting GluR2-lacking AMPARs or CREB may be a useful strategy for treating nervous system disorders associated with OL excitotoxicity...
  20. ncbi request reprint The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter
    Tara M Desilva
    Neurobiology Program, Children s Hospital Boston, Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Comp Neurol 501:879-90. 2007
    ....
  21. ncbi request reprint 12-Lipoxygenase plays a key role in cell death caused by glutathione depletion and arachidonic acid in rat oligodendrocytes
    Hong Wang
    Department of Neurology, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Eur J Neurosci 20:2049-58. 2004
    ..These results suggest that 12-LOX activation plays a key role in oxidative stress-induced OL death...
  22. ncbi request reprint Nitric oxide-induced cell death in developing oligodendrocytes is associated with mitochondrial dysfunction and apoptosis-inducing factor translocation
    Olivier Baud
    Department of Neurology, Division of Neuroscience, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Eur J Neurosci 20:1713-26. 2004
    ..In conclusion, we suggest that the vulnerability of developing OLs to NO involves mitochondrial dysfunction and translocation of AIF from mitochondria to nuclei...
  23. ncbi request reprint Zaprinast stimulates extracellular adenosine accumulation in rat pontine slices
    Minou Le
    Department of Neurology and Program in Neuroscience, Enders Research Building, Room 349, Children s Hospital and Harvard Medical School, Longwood Avenue, Boston, MA 02115, USA
    Neurosci Lett 371:12-7. 2004
    ....
  24. ncbi request reprint Nitric oxide-induced adenosine inhibition of hippocampal synaptic transmission depends on adenosine kinase inhibition and is cyclic GMP independent
    Elda Arrigoni
    Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Eur J Neurosci 24:2471-80. 2006
    ..Although a direct block of adenosine kinase by nitric oxide can not be excluded, the depression of adenosine kinase activity may be due to inhibition by its own substrate adenosine...
  25. pmc The developing oligodendrocyte: key cellular target in brain injury in the premature infant
    Joseph J Volpe
    Department of Neurology, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Int J Dev Neurosci 29:423-40. 2011
    ..The critical next step, i.e., clinical trials in the living infant, is now on the horizon...
  26. ncbi request reprint Glutathione peroxidase-catalase cooperativity is required for resistance to hydrogen peroxide by mature rat oligodendrocytes
    Olivier Baud
    Department of Neurology, Division of Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 24:1531-40. 2004
    ..These data provide evidence for a key role for GPx-catalase cooperativity in the resistance of mature OLs to H2O2-induced cell death...
  27. ncbi request reprint Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons
    Jianrong Li
    Department of Neurology, Division of Neuroscience, Children s Hospital, Boston, MA 02115, USA
    J Neurosci 23:5816-26. 2003
    ....
  28. pmc Role of metabotropic glutamate receptors in oligodendrocyte excitotoxicity and oxidative stress
    Wenbin Deng
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 101:7751-6. 2004
    ....
  29. pmc 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
    Geraldine T Petr
    Department of Neurology and the F M Kirby Neurobiology Center, Boston Children s Hospital, Boston, Massachusetts 02115, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115
    J Neurosci 35:5187-201. 2015
    ..These results have important implications for the interpretation of the many previous studies assessing glutamate uptake capacity by measuring synaptosomal uptake. ..
  30. pmc NMDA receptor-mediated extracellular adenosine accumulation is blocked by phosphatase 1/2A inhibitors
    Yin Lu
    Enders Research Building, Department of Neurology, Neurobiology Program, Children s Hospital, Boston, MA 02115, USA
    Brain Res 1155:116-24. 2007
    ....
  31. pmc Ceftriaxone treatment after traumatic brain injury restores expression of the glutamate transporter, GLT-1, reduces regional gliosis, and reduces post-traumatic seizures in the rat
    Grant S Goodrich
    Department of Neurology, Boston Children s Hospital, Harvard Medical School, Boston, MA 02215, USA
    J Neurotrauma 30:1434-41. 2013
    ..001). We cautiously conclude that our data suggest a potential role for ceftriaxone in treatment of epileptogenic TBI...
  32. pmc Calcium-permeable AMPA/kainate receptors mediate toxicity and preconditioning by oxygen-glucose deprivation in oligodendrocyte precursors
    Wenbin Deng
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 100:6801-6. 2003
    ....
  33. pmc Interaction between the glutamate transporter GLT1b and the synaptic PDZ domain protein PICK1
    Merav Bassan
    Department of Neurology, Children s Hospital, Boston, MA 02115, USA
    Eur J Neurosci 27:66-82. 2008
    ..These results suggest that the PICK1-GLT1b interaction regulates the modulation of GLT1 function by PKC...
  34. ncbi request reprint Caspase-1 and poly (ADP-ribose) polymerase inhibitors may protect against peroxynitrite-induced neurotoxicity independent of their enzyme inhibitor activity
    Yumin Zhang
    Department of Neurology, Children s Hospital, Harvard Medical School, 300 Longwood Ave, Boston, Massachusetts 02115, USA
    Eur J Neurosci 20:1727-36. 2004
    ..Taken together, these results suggest that in the model system used here peroxynitrite neurotoxicity is independent of caspase and PARP activation, and therefore implicate a novel mechanism...
  35. pmc Evidence for change in current-flux coupling of GLT1 at high glutamate concentrations in rat primary forebrain neurons and GLT1a-expressing COS-7 cells
    Anatoli Y Kabakov
    FM Kirby Neurobiology Center and Department of Neurology, Children s Hospital Boston, Boston, MA, USA
    Eur J Neurosci 30:186-95. 2009
    ..This property is intrinsic to the protein because it was also observed in GLT1a-transfected COS-7 cells...
  36. ncbi request reprint Nitrosative and oxidative injury to premyelinating oligodendrocytes in periventricular leukomalacia
    Robin L Haynes
    Department of Neurology, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neuropathol Exp Neurol 62:441-50. 2003
    ..Agents that prevent nitrosative and oxidative stress may play a key role in ameliorating PVL in premature infants in the intensive care nursery...
  37. ncbi request reprint NMDA receptor-mediated extracellular adenosine accumulation in rat forebrain neurons in culture is associated with inhibition of adenosine kinase
    Yin Lu
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Eur J Neurosci 17:1213-22. 2003
    ..These studies suggest that several possible mechanisms are likely to be involved in NMDA-evoked extracellular adenosine accumulation...
  38. pmc Novel lipoxygenase inhibitors as neuroprotective reagents
    Klaus van Leyen
    Neuroprotection Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci Res 86:904-9. 2008
    ..Future studies of these novel neuroprotective inhibitors of 12/15-LOX may provide new therapeutic opportunities to combat stroke and other neurodegenerative diseases...
  39. pmc Dysregulation of system xc(-) expression induced by mutant huntingtin in a striatal neuronal cell line and in R6/2 mice
    Natalie M Frederick
    Department of Neurology and F M Kirby Neurobiology Center, Children s Hospital Boston and Harvard Medical School, Boston, MA 02115, USA
    Neurochem Int 76:59-69. 2014
    ..These results suggest that a defect in the regulation of xCT may be involved in the pathogenesis of HD by compromising xCT expression and increasing susceptibility to oxidative stress. ..
  40. pmc Glutamate transporter expression and function in a striatal neuronal model of Huntington's disease
    Geraldine T Petr
    Department of Neurology and the F M Kirby Neurobiology Center, Children s Hospital Boston, Boston, MA 02115, USA
    Neurochem Int 62:973-81. 2013
    ..We found no difference in Akt activation between the two cell lines under our conditions of culture. Therefore a difference in Akt activation does not seem to explain the increase in EAAC1 mediated uptake in the STHdh(Q111/Q111) cells...
  41. doi request reprint Reprint of "The developing oligodendrocyte: key cellular target in brain injury in the premature infant"
    Joseph J Volpe
    Department of Neurology, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Int J Dev Neurosci 29:565-82. 2011
    ..The critical next step, i.e., clinical trials in the living infant, is now on the horizon...
  42. ncbi request reprint The toll-like receptor TLR4 is necessary for lipopolysaccharide-induced oligodendrocyte injury in the CNS
    Seija Lehnardt
    Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
    J Neurosci 22:2478-86. 2002
    ..Our data provide a general mechanistic link between (1) lipopolysaccharide and similar microbial molecular motifs and (2) injury to oligodendrocytes and myelin as occurs in periventricular leukomalacia and multiple sclerosis...
  43. pmc GLT-1 Transport Stoichiometry Is Constant at Low and High Glutamate Concentrations when Chloride Is Substituted by Gluconate
    Anatoli Y Kabakov
    F M Kirby Neurobiology Center and Department of Neurology, Children s Hospital and Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 10:e0136111. 2015
    ..Therefore, only in the absence of chloride, GLT-1 GTS remains constant at all glutamate concentrations. Possible explanations for why apparent GTS might vary in the presence of chloride are discussed. ..
  44. ncbi request reprint The essential nutrient pyrroloquinoline quinone may act as a neuroprotectant by suppressing peroxynitrite formation
    Yumin Zhang
    Department of Neurology and Program in Neuroscience, Children s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    Eur J Neurosci 16:1015-24. 2002
    ..These results suggest that PQQ scavenges superoxide without forming toxic levels of H2O2. Therefore, the protective effect of PQQ on stroke might be due, at least in part, to the suppression of peroxynitrite formation...
  45. pmc The glutamate transporter GLT1a is expressed in excitatory axon terminals of mature hippocampal neurons
    Weizhi Chen
    Department of Neurology, Children s Hospital, Boston, Massachusetts 02115, USA
    J Neurosci 24:1136-48. 2004
    ..Thus, the originally cloned form of GLT1, GLT1a, is expressed as protein in neurons in the mature hippocampus and may contribute significantly to glutamate uptake into excitatory terminals...
  46. pmc Expression of a variant form of the glutamate transporter GLT1 in neuronal cultures and in neurons and astrocytes in the rat brain
    Weizhi Chen
    Department of Neurology, Children s Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Neurosci 22:2142-52. 2002
    ....
  47. pmc Intracellular zinc release, 12-lipoxygenase activation and MAPK dependent neuronal and oligodendroglial death
    Yumin Zhang
    Department of Anatomy, Physiology and Genetics and Program in Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    Mol Med 13:350-5. 2007
    ..In this review, we describe how the activation of 12-lipoxygenase and mitogen-activated protein kinase (MAPK) contribute to the toxicity of liberated zinc to neurons and oligodendrocytes...
  48. ncbi request reprint Estradiol attenuates hyperoxia-induced cell death in the developing white matter
    Bettina Gerstner
    Department of Neonatology, Charite Campus Virchow Klinikum, Berlin, Germany
    Ann Neurol 61:562-73. 2007
    ..Furthermore, neuroprotective properties have been attributed to estrogens. We examined the effect of E2 on hyperoxia-induced cell death in the developing white matter in the rat brain...
  49. pmc Apoptotic surge of potassium currents is mediated by p38 phosphorylation of Kv2.1
    Patrick T Redman
    Department of Neurobiology and Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA
    Proc Natl Acad Sci U S A 104:3568-73. 2007
    ..Consequently, phosphorylation of Kv2.1 residue S800 by p38 leads to trafficking and membrane insertion during apoptosis, and remarkably, the absence of S800 phosphorylation is sufficient to prevent completion of the cell death program...
  50. ncbi request reprint Epilepsy and dental procedures. A review
    Charles K Vorkas
    Comprehensive Epilepsy Center, New York University School of Medicine, New York City, New York, USA
    N Y State Dent J 74:39-43. 2008
    ..A clinical case photo is presented to show gingival hyperplasia, along with four tables on which common antiepileptic medications are enumerated...
  51. pmc Cellular and subcellular mRNA localization of glutamate transporter isoforms GLT1a and GLT1b in rat brain by in situ hybridization
    Urs V Berger
    UB In Situ, Natick, Massachusetts 01760
    J Comp Neurol 492:78-89. 2005
    ..These findings suggest that the expression of the two GLT1 isoforms is regulated by different mechanisms. Moreover, the function of the two isoforms may be subject to different regulatory processes...