Thomas Blank

Summary

Affiliation: Max Planck Institute for Experimental Medicine
Country: Germany

Publications

  1. ncbi request reprint Priming of long-term potentiation in mouse hippocampus by corticotropin-releasing factor and acute stress: implications for hippocampus-dependent learning
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    J Neurosci 22:3788-94. 2002
  2. ncbi request reprint Corticotropin-releasing factor receptors couple to multiple G-proteins to activate diverse intracellular signaling pathways in mouse hippocampus: role in neuronal excitability and associative learning
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    J Neurosci 23:700-7. 2003
  3. ncbi request reprint Small conductance Ca2+-activated K+ channels as targets of CNS drug development
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    Curr Drug Targets CNS Neurol Disord 3:161-7. 2004
  4. ncbi request reprint The corticotropin-releasing factor receptor 1 antagonist CP-154,526 reverses stress-induced learning deficits in mice
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Hermann Rein Street 3, D 37075 Goettingen, Germany
    Behav Brain Res 138:207-13. 2003
  5. ncbi request reprint Molecular determinants mediating effects of acute stress on hippocampus-dependent synaptic plasticity and learning
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    Mol Neurobiol 29:131-8. 2004
  6. ncbi request reprint Small-conductance, Ca2+-activated K+ channel SK3 generates age-related memory and LTP deficits
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    Nat Neurosci 6:911-2. 2003
  7. ncbi request reprint In vivo CREB phosphorylation mediated by dopamine and NMDA receptor activation in mouse hippocampus and caudate nucleus
    Ingrid Nijholt
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Hermann Rein Strasse 3, D 37075 Goettingen, Germany
    Brain Res Gene Expr Patterns 1:101-6. 2002
  8. ncbi request reprint Transcriptional regulation of intronic calcium-activated potassium channel SK2 promoters by nuclear factor-kappa B and glucocorticoids
    Min Jeong Kye
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Goettingen, Germany
    Mol Cell Biochem 300:9-17. 2007
  9. doi request reprint Identification and characterization of a novel, shorter isoform of the small conductance Ca2+ -activated K+ channel SK2
    Saravana R K Murthy
    Max Planck Institute for Experimental Medicine, John A Burns School of Medicine, University of Hawaii, Honolulu, Hawaii 96813, USA
    J Neurochem 106:2312-21. 2008

Collaborators

Detail Information

Publications9

  1. ncbi request reprint Priming of long-term potentiation in mouse hippocampus by corticotropin-releasing factor and acute stress: implications for hippocampus-dependent learning
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    J Neurosci 22:3788-94. 2002
    ..This observation suggests that priming of PS-LTP and activation of CaMKII represent two essential mechanisms that may contribute independently to long-term memory...
  2. ncbi request reprint Corticotropin-releasing factor receptors couple to multiple G-proteins to activate diverse intracellular signaling pathways in mouse hippocampus: role in neuronal excitability and associative learning
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    J Neurosci 23:700-7. 2003
    ..These results indicate that the CRF system activates different intracellular signaling pathways in mouse hippocampus and may have distinct effects on associative learning depending on the mouse strain investigated...
  3. ncbi request reprint Small conductance Ca2+-activated K+ channels as targets of CNS drug development
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    Curr Drug Targets CNS Neurol Disord 3:161-7. 2004
    ..The potential value of pharmacological SK channel modulation in various pathological states such as increased epileptiform activity, cognitive impairment, pain, mood disorders and schizophrenia will be discussed...
  4. ncbi request reprint The corticotropin-releasing factor receptor 1 antagonist CP-154,526 reverses stress-induced learning deficits in mice
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Hermann Rein Street 3, D 37075 Goettingen, Germany
    Behav Brain Res 138:207-13. 2003
    ..The CP-154,526-induced enhancements in fear conditioning and PPF could be prevented by the selective CaMKII inhibitor KN-62. Our results demonstrated that learning impairment after acute stress was antagonized by CP-154,526 pretreatment...
  5. ncbi request reprint Molecular determinants mediating effects of acute stress on hippocampus-dependent synaptic plasticity and learning
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    Mol Neurobiol 29:131-8. 2004
    ..The relative contribution of these molecular targets to the stress response, the relation to hippocampal synaptic plasticity and memory formation, and the possible interaction of the underlying processes are discussed...
  6. ncbi request reprint Small-conductance, Ca2+-activated K+ channel SK3 generates age-related memory and LTP deficits
    Thomas Blank
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, D 37075 Goettingen, Germany
    Nat Neurosci 6:911-2. 2003
    ....
  7. ncbi request reprint In vivo CREB phosphorylation mediated by dopamine and NMDA receptor activation in mouse hippocampus and caudate nucleus
    Ingrid Nijholt
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Hermann Rein Strasse 3, D 37075 Goettingen, Germany
    Brain Res Gene Expr Patterns 1:101-6. 2002
    ..The results demonstrated that NMDA and dopamine receptors modulate pCREB levels in the caudate nucleus and suggest mutual permissive roles for both receptors...
  8. ncbi request reprint Transcriptional regulation of intronic calcium-activated potassium channel SK2 promoters by nuclear factor-kappa B and glucocorticoids
    Min Jeong Kye
    Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Goettingen, Germany
    Mol Cell Biochem 300:9-17. 2007
    ..These findings suggest a possible transcriptional cross talk between GRs and NF-kappaB in the intronic promoter regulation of SK2-S channel gene transcription...
  9. doi request reprint Identification and characterization of a novel, shorter isoform of the small conductance Ca2+ -activated K+ channel SK2
    Saravana R K Murthy
    Max Planck Institute for Experimental Medicine, John A Burns School of Medicine, University of Hawaii, Honolulu, Hawaii 96813, USA
    J Neurochem 106:2312-21. 2008
    ..Thus, SK2-sh as a downstream target of cytokines, provide a promising target for additional investigation regarding potential therapeutic intervention...