T Kleppisch

Summary

Affiliation: Klinikum rechts der Isar
Country: Germany

Publications

  1. ncbi ATP-sensitive potassium channels in cultured arterial segments
    T Kleppisch
    Department of Pharmacology, University of Vermont, Colchester 05446 2500, USA
    Am J Physiol 271:H2462-8. 1996
  2. ncbi G(alpha)q-deficient mice lack metabotropic glutamate receptor-dependent long-term depression but show normal long-term potentiation in the hippocampal CA1 region
    T Kleppisch
    Institut fur Pharmakologie und Toxikologie, Technische Universitat Munchen, 80802 Munchen, Germany
    J Neurosci 21:4943-8. 2001
  3. ncbi Hippocampal cGMP-dependent protein kinase I supports an age- and protein synthesis-dependent component of long-term potentiation but is not essential for spatial reference and contextual memory
    Thomas Kleppisch
    Institut fur Pharmakologie und Toxikologie, 80802 Munchen, Germany, Max Planck Institut fur Psychiatrie, 80804 München, Germany
    J Neurosci 23:6005-12. 2003
  4. ncbi Signaling through cGMP-dependent protein kinase I in the amygdala is critical for auditory-cued fear memory and long-term potentiation
    Cindy Paul
    Institut fur Pharmakologie und Toxikologie, 80802 Munich, Germany
    J Neurosci 28:14202-12. 2008
  5. ncbi Long-term potentiation in the hippocampal CA1 region of mice lacking cGMP-dependent kinases is normal and susceptible to inhibition of nitric oxide synthase
    T Kleppisch
    Institut fur Pharmakologie und Toxikologie, 80802 Munchen, Germany
    J Neurosci 19:48-55. 1999
  6. ncbi Role of hippocampal Cav1.2 Ca2+ channels in NMDA receptor-independent synaptic plasticity and spatial memory
    Sven Moosmang
    Institut fur Pharmakologie und Toxikologie, Technische Universitat Munchen, 80802 Munich, Germany
    J Neurosci 25:9883-92. 2005
  7. ncbi An essential role of Cav1.2 L-type calcium channel for urinary bladder function
    Jörg W Wegener
    Institut fur Pharmakologie und Toxikologie, Technische Universitat Munchen, Biedersteiner Str 29, D 80802 München, Germany
    FASEB J 18:1159-61. 2004
  8. ncbi cGMP-dependent protein kinase type I promotes CREB/CRE-mediated gene expression in neurons of the lateral amygdala
    Cindy Paul
    Institut fur Pharmakologie und Toxikologie der Technischen Universitat Munchen, Biedersteiner Strasse 29, 80802 Munchen, Germany
    Neurosci Lett 473:82-6. 2010
  9. ncbi Calmodulin kinase II is involved in voltage-dependent facilitation of the L-type Cav1.2 calcium channel: Identification of the phosphorylation sites
    Tae Seong Lee
    Institut fur Pharmakologie und Toxikologie, Technische Universitat Munchen, Munchen, Germany
    J Biol Chem 281:25560-7. 2006
  10. ncbi Function of cGMP-dependent protein kinases as revealed by gene deletion
    F Hofmann
    Institut für Pharmakologie und Toxicologie, Technische Universitat Munchen, Biedersteiner Strasse 29, D 80802 Munich, Germany
    Physiol Rev 86:1-23. 2006

Collaborators

Detail Information

Publications12

  1. ncbi ATP-sensitive potassium channels in cultured arterial segments
    T Kleppisch
    Department of Pharmacology, University of Vermont, Colchester 05446 2500, USA
    Am J Physiol 271:H2462-8. 1996
    ..These results suggest that this approach can be used to study either long-term regulation of KATP channels or the role of this channel type in growth responses...
  2. ncbi G(alpha)q-deficient mice lack metabotropic glutamate receptor-dependent long-term depression but show normal long-term potentiation in the hippocampal CA1 region
    T Kleppisch
    Institut fur Pharmakologie und Toxikologie, Technische Universitat Munchen, 80802 Munchen, Germany
    J Neurosci 21:4943-8. 2001
    ..These results show that G(q) plays a crucial role in the mGluR-dependent LTD, whereas hippocampal LTP is not affected by the lack of a single member of the G(q) family...
  3. ncbi Hippocampal cGMP-dependent protein kinase I supports an age- and protein synthesis-dependent component of long-term potentiation but is not essential for spatial reference and contextual memory
    Thomas Kleppisch
    Institut fur Pharmakologie und Toxikologie, 80802 Munchen, Germany, Max Planck Institut fur Psychiatrie, 80804 München, Germany
    J Neurosci 23:6005-12. 2003
    ..These results suggest that hippocampal cGKI supports an age- and protein synthesis-dependent form of hippocampal LTP, whereas it is dispensable for hippocampus-dependent spatial reference and contextual memory...
  4. ncbi Signaling through cGMP-dependent protein kinase I in the amygdala is critical for auditory-cued fear memory and long-term potentiation
    Cindy Paul
    Institut fur Pharmakologie und Toxikologie, 80802 Munich, Germany
    J Neurosci 28:14202-12. 2008
    ..In contrast, cGKII null mutants lack these phenotypes. Our data suggest a function of cGKI, likely the beta isoform, in the LA, supporting synaptic plasticity and consolidation of fear memory...
  5. ncbi Long-term potentiation in the hippocampal CA1 region of mice lacking cGMP-dependent kinases is normal and susceptible to inhibition of nitric oxide synthase
    T Kleppisch
    Institut fur Pharmakologie und Toxikologie, 80802 Munchen, Germany
    J Neurosci 19:48-55. 1999
    ..These results show that cGKs are not involved in LTP in mice and that NO induces LTP through an alternative cGMP-independent pathway, possibly ADP-ribosylation...
  6. ncbi Role of hippocampal Cav1.2 Ca2+ channels in NMDA receptor-independent synaptic plasticity and spatial memory
    Sven Moosmang
    Institut fur Pharmakologie und Toxikologie, Technische Universitat Munchen, 80802 Munich, Germany
    J Neurosci 25:9883-92. 2005
    ..2 channel-mediated Ca2+ influx to either process...
  7. ncbi An essential role of Cav1.2 L-type calcium channel for urinary bladder function
    Jörg W Wegener
    Institut fur Pharmakologie und Toxikologie, Technische Universitat Munchen, Biedersteiner Str 29, D 80802 München, Germany
    FASEB J 18:1159-61. 2004
    ..These results show that the Cav1.2 Ca2+ channel is essential for normal bladder function. The Rho-kinase and Ca2+-release pathways cannot compensate the lack of the L-type Ca2+ channel...
  8. ncbi cGMP-dependent protein kinase type I promotes CREB/CRE-mediated gene expression in neurons of the lateral amygdala
    Cindy Paul
    Institut fur Pharmakologie und Toxikologie der Technischen Universitat Munchen, Biedersteiner Strasse 29, 80802 Munchen, Germany
    Neurosci Lett 473:82-6. 2010
    ..In summary, we provide evidence that cytosolic cGKI can support fear memory consolidation and LTP in neurons of the lateral amygdala via activation of CREB and CRE-dependent transcription...
  9. ncbi Calmodulin kinase II is involved in voltage-dependent facilitation of the L-type Cav1.2 calcium channel: Identification of the phosphorylation sites
    Tae Seong Lee
    Institut fur Pharmakologie und Toxikologie, Technische Universitat Munchen, Munchen, Germany
    J Biol Chem 281:25560-7. 2006
    ..2 protein was strongly decreased in the S1512A/S1570A double mutant. These results suggest that voltage-dependent facilitation of the Ca(v)1.2 channel depends on the phosphorylation of Ser1512/Ser1570 by calmodulin kinase II...
  10. ncbi Function of cGMP-dependent protein kinases as revealed by gene deletion
    F Hofmann
    Institut für Pharmakologie und Toxicologie, Technische Universitat Munchen, Biedersteiner Strasse 29, D 80802 Munich, Germany
    Physiol Rev 86:1-23. 2006
    ..These data show that cGKs are signaling molecules involved in many biological functions...
  11. ncbi Function of cGMP-dependent protein kinases in the nervous system
    Robert Feil
    , , , Germany
    Rev Neurosci 16:23-41. 2005
    ..Thus, cGKs serve key functions in the transduction of cGMP signals into cellular responses in distinct regions of the nervous system.-..
  12. ncbi Cav1.2 calcium channels modulate the spiking pattern of hippocampal pyramidal cells
    Lubica Lacinova
    Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, Vlarska 5, 833 34 Bratislava, Slovakia
    Life Sci 82:41-9. 2008
    ..2 channels are involved in regulating the intrinsic excitability of CA1 pyramidal neurons. This cellular mechanism may contribute to the known function of Ca(v)1.2 channels in supporting synaptic plasticity and memory...