Heinz Beck

Summary

Affiliation: University of Bonn
Country: Germany

Publications

  1. ncbi request reprint Molecular and cellular mechanisms of pharmacoresistance in epilepsy
    Stefan Remy
    Department of Epileptology, University of Bonn Medical Center, Bonn, Germany
    Brain 129:18-35. 2006
  2. doi request reprint Plasticity of intrinsic neuronal properties in CNS disorders
    Heinz Beck
    Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Str 25, 53105 Bonn, Germany
    Nat Rev Neurosci 9:357-69. 2008
  3. ncbi request reprint Plasticity of antiepileptic drug targets
    Heinz Beck
    Department of Epileptology, University of Bonn, Bonn, Germany
    Epilepsia 48:14-8. 2007
  4. ncbi request reprint Transcriptional upregulation of Cav3.2 mediates epileptogenesis in the pilocarpine model of epilepsy
    Albert J Becker
    Departments of Neuropathology, University of Bonn Medical Center, University of Bonn, Bonn, Germany
    J Neurosci 28:13341-53. 2008
  5. ncbi request reprint Functional properties of ES cell-derived neurons engrafted into the hippocampus of adult normal and chronically epileptic rats
    Christiane Rüschenschmidt
    Institute of Reconstructive Neurobiology, University of Bonn Medical Center and Hertie Foundation, Bonn, Germany
    Epilepsia 46:174-83. 2005
  6. ncbi request reprint Diminished response of CA1 neurons to antiepileptic drugs in chronic epilepsy
    Christina Schaub
    Department of Epileptology, University of Bonn Medical Center, Bonn, Germany
    Epilepsia 48:1339-50. 2007
  7. doi request reprint Impaired D-serine-mediated cotransmission mediates cognitive dysfunction in epilepsy
    Katharina Klatte
    Laboratory of Experimental Epileptology, Department of Epileptology and Institute of Molecular Psychiatry, University of Bonn, D 53127 Bonn, Germany
    J Neurosci 33:13066-80. 2013
  8. doi request reprint Efficacy loss of the anticonvulsant carbamazepine in mice lacking sodium channel beta subunits via paradoxical effects on persistent sodium currents
    Mischa Uebachs
    Department of Epileptology, University of Bonn Medical Center, 53105 Bonn, Germany
    J Neurosci 30:8489-501. 2010
  9. doi request reprint Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons
    Michel Royeck
    Department of Epileptology, University of Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    J Neurophysiol 100:2361-80. 2008
  10. ncbi request reprint Functional integration of embryonic stem cell-derived neurons in vivo
    Marius Wernig
    Institute of Reconstructive Neurobiology, University of Bonn Medical Center and Hertie Foundation, University of Bonn, D 53105 Bonn, Germany
    J Neurosci 24:5258-68. 2004

Detail Information

Publications51

  1. ncbi request reprint Molecular and cellular mechanisms of pharmacoresistance in epilepsy
    Stefan Remy
    Department of Epileptology, University of Bonn Medical Center, Bonn, Germany
    Brain 129:18-35. 2006
    ..An emerging understanding of these underlying molecular and cellular mechanisms is likely to provide important impetus for the development of new pharmacological treatment strategies...
  2. doi request reprint Plasticity of intrinsic neuronal properties in CNS disorders
    Heinz Beck
    Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Str 25, 53105 Bonn, Germany
    Nat Rev Neurosci 9:357-69. 2008
    ..The studies reviewed here show that intrinsic plasticity, in conjunction with synaptic plasticity, can fundamentally alter the input-output properties of neuronal networks in CNS disorders...
  3. ncbi request reprint Plasticity of antiepileptic drug targets
    Heinz Beck
    Department of Epileptology, University of Bonn, Bonn, Germany
    Epilepsia 48:14-8. 2007
    ....
  4. ncbi request reprint Transcriptional upregulation of Cav3.2 mediates epileptogenesis in the pilocarpine model of epilepsy
    Albert J Becker
    Departments of Neuropathology, University of Bonn Medical Center, University of Bonn, Bonn, Germany
    J Neurosci 28:13341-53. 2008
    ..In addition, the appearance of spontaneous seizures was dramatically reduced in these mice. Together, these data establish transcriptional induction of Ca(v)3.2 as a critical step in epileptogenesis and neuronal vulnerability...
  5. ncbi request reprint Functional properties of ES cell-derived neurons engrafted into the hippocampus of adult normal and chronically epileptic rats
    Christiane Rüschenschmidt
    Institute of Reconstructive Neurobiology, University of Bonn Medical Center and Hertie Foundation, Bonn, Germany
    Epilepsia 46:174-83. 2005
    ..Nonetheless, studies addressing the functional properties of ES cell-derived progeny after transplantation into the adult, pathologically modified CNS are scarce...
  6. ncbi request reprint Diminished response of CA1 neurons to antiepileptic drugs in chronic epilepsy
    Christina Schaub
    Department of Epileptology, University of Bonn Medical Center, Bonn, Germany
    Epilepsia 48:1339-50. 2007
    ..These changes then contribute to drug-resistance on a clinical level. We have tested this hypothesis in hippocampal CA1 neurons in experimental epilepsy...
  7. doi request reprint Impaired D-serine-mediated cotransmission mediates cognitive dysfunction in epilepsy
    Katharina Klatte
    Laboratory of Experimental Epileptology, Department of Epileptology and Institute of Molecular Psychiatry, University of Bonn, D 53127 Bonn, Germany
    J Neurosci 33:13066-80. 2013
    ..These results strongly suggest that d-serine deficiency is important in the amnestic symptoms of temporal lobe epilepsy. Our results point to a possible clinical utility of d-serine to alleviate these disease manifestations. ..
  8. doi request reprint Efficacy loss of the anticonvulsant carbamazepine in mice lacking sodium channel beta subunits via paradoxical effects on persistent sodium currents
    Mischa Uebachs
    Department of Epileptology, University of Bonn Medical Center, 53105 Bonn, Germany
    J Neurosci 30:8489-501. 2010
    ..Consequently, altered expression of beta subunits in other neurological disorders may cause altered neuronal sensitivity to drugs targeting Na(+) channels...
  9. doi request reprint Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons
    Michel Royeck
    Department of Epileptology, University of Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    J Neurophysiol 100:2361-80. 2008
    ..These results suggest that NaV1.6 subunits at the AIS contribute significantly to its role as spike trigger zone and shape repetitive discharge properties of CA1 neurons...
  10. ncbi request reprint Functional integration of embryonic stem cell-derived neurons in vivo
    Marius Wernig
    Institute of Reconstructive Neurobiology, University of Bonn Medical Center and Hertie Foundation, University of Bonn, D 53105 Bonn, Germany
    J Neurosci 24:5258-68. 2004
    ..Thus, the lack of an appropriate regional "code" does not preclude morphological and synaptic integration of ES cell-derived neurons...
  11. doi request reprint Stable mossy fiber long-term potentiation requires calcium influx at the granule cell soma, protein synthesis, and microtubule-dependent axonal transport
    Steven J Barnes
    Department of Epileptology, University of Bonn, D 53105 Bonn, Germany
    J Neurosci 30:12996-3004. 2010
    ..Finally, the present data imply that synaptic plasticity at the MF-CA3 synapse can be affected by local modulation of somatic and presynaptic Ca(2+) channel activity...
  12. doi request reprint RIM3γ and RIM4γ are key regulators of neuronal arborization
    Elena Alvaréz-Baron
    Department of Neuropathology, Department of Epileptology, Laboratory for Experimental Epileptology and Cognition Research, University of Bonn, 53105 Bonn, Germany
    J Neurosci 33:824-39. 2013
    ....
  13. ncbi request reprint Anticonvulsant pharmacology of voltage-gated Na+ channels in hippocampal neurons of control and chronically epileptic rats
    Stefan Remy
    Department of Epileptology, University of Bonn Medical Center, Siegmund Freud Str 25, 53105 Bonn, Germany
    Eur J Neurosci 17:2648-58. 2003
    ....
  14. ncbi request reprint Loss of metabotropic glutamate receptor-dependent long-term depression via downregulation of mGluR5 after status epilepticus
    Timo Kirschstein
    Department of Epileptology, University of Bonn, D 53105 Bonn, Germany
    J Neurosci 27:7696-704. 2007
    ..Thus, we conclude that the reduction of mGluR LTD after pilocarpine-induced status epilepticus is the result of the subtype-specific downregulation of mGluR5 and associated downstream signaling components...
  15. ncbi request reprint Impaired synaptic plasticity in a rat model of tuberous sclerosis
    Christian von der Brelie
    Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Eur J Neurosci 23:686-92. 2006
    ..An understanding of the underlying molecular pathways may suggest new therapeutic approaches aimed at inhibiting the development of the profound mental retardation in TSC...
  16. ncbi request reprint A novel mechanism underlying drug resistance in chronic epilepsy
    Stefan Remy
    Department of Epileptology, University of Bonn Medical Center, Bonn, Germany
    Ann Neurol 53:469-79. 2003
    ..Taken together, these data suggest that a loss of Na(+) channel drug sensitivity may constitute a novel mechanism underlying the development of drug-resistant epilepsy...
  17. ncbi request reprint The presynaptic active zone protein RIM1α controls epileptogenesis following status epilepticus
    Julika Pitsch
    Department of Neuropathology, University of Bonn, 53105 Bonn, Germany
    J Neurosci 32:12384-95. 2012
    ..In summary, our results suggest that presynaptic plasticity and proper function of RIM1α play an important part in a neuron's adaptive response to aberrant electrical activity...
  18. ncbi request reprint Dendritic integration in hippocampal dentate granule cells
    Roland Krueppel
    Laboratory for Cognition Research and Experimental Epileptology, Department of Epileptology, University of Bonn, Sigmund Freud Strase 25, 53105 Bonn, Germany
    Neuron 71:512-28. 2011
    ....
  19. ncbi request reprint Functional integration of embryonic stem cell-derived neurons in hippocampal slice cultures
    Felix Benninger
    Institute of Reconstructive Neurobiology, University of Bonn Medical Center, D 53105 Bonn, Germany
    J Neurosci 23:7075-83. 2003
    ..Thus, ES cell-derived neural precursors generate functionally active neurons capable of integrating into the brain circuitry...
  20. doi request reprint Activity-dependent control of neuronal output by local and global dendritic spike attenuation
    Stefan Remy
    Laboratory for Cognition Research and Experimental Epileptology, Department of Epileptology, University of Bonn, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
    Neuron 61:906-16. 2009
    ..They are invoked at frequencies encountered during learning, and impose limits on the storage and retrieval rates of information encoded as branch excitability...
  21. pmc Transcriptional regulation of T-type calcium channel CaV3.2: bi-directionality by early growth response 1 (Egr1) and repressor element 1 (RE-1) protein-silencing transcription factor (REST)
    Karen M J Van Loo
    Department of Neuropathology, University of Bonn Medical Center, D 53105 Bonn, Germany
    J Biol Chem 287:15489-501. 2012
    ..This mechanism has critical implications for the regulation of neuronal and cardiac Ca(2+) homeostasis under physiological conditions and in episodic disorders such as arrhythmias and epilepsy...
  22. ncbi request reprint Hippocampal synaptic metaplasticity requires inhibitory autophosphorylation of Ca2+/calmodulin-dependent kinase II
    Lian Zhang
    Department of Epileptology, University of Bonn, D 53105 Bonn, Germany
    J Neurosci 25:7697-707. 2005
    ..Thus, modulation of alphaCaMKII activity via autophosphorylation at Thr305/Thr306 is a key mechanism for metaplasticity that may be of importance in the integration of temporally separated episodes of activity...
  23. ncbi request reprint Inhibitory control of linear and supralinear dendritic excitation in CA1 pyramidal neurons
    Christina Müller
    NRW Research Group Dendritic Integration in the CNS, Department of Epileptology, University of Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Neuron 75:851-64. 2012
    ..Our findings suggest that dendritic spikes may serve to transform correlated branch input into reliable and temporally precise output even in the presence of inhibition...
  24. pmc Hyperpolarization-activated cation current Ih of dentate gyrus granule cells is upregulated in human and rat temporal lobe epilepsy
    Rainer Surges
    Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Str 25, 53105 Bonn, Germany
    Biochem Biophys Res Commun 420:156-60. 2012
    ....
  25. ncbi request reprint Functional specialization of presynaptic Cav2.3 Ca2+ channels
    Dirk Dietrich
    Department of Neurosurgery, University Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    Neuron 39:483-96. 2003
    ....
  26. ncbi request reprint L-CCG-I activates group III metabotropic glutamate receptors in the hippocampal CA3 region
    Timo Kirschstein
    Department of Epileptology, University of Bonn, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
    Neuropharmacology 47:157-62. 2004
    ..For this reason, DCG-IV should be the drug of choice when aiming to discriminate between mossy fiber and A/C input to CA3 pyramidal cells...
  27. ncbi request reprint Nanodomains of single Ca2+ channels contribute to action potential repolarization in cortical neurons
    Andreas Muller
    Department of Neurosurgery, University Clinic Bonn, 53105 Bonn, Germany
    J Neurosci 27:483-95. 2007
    ....
  28. doi request reprint Chronic homocysteine exposure causes changes in the intrinsic electrophysiological properties of cultured hippocampal neurons
    Christina Schaub
    Department of Neurology, University of Bonn, Bonn, Germany
    Exp Brain Res 225:527-34. 2013
    ..We conclude that homocysteine exposure causes changes in the intrinsic electrophysiological properties of cultured hippocampal neurons as a mechanism of neurological symptoms of hyperhomocysteinemia...
  29. doi request reprint Loss of β1 accessory Na+ channel subunits causes failure of carbamazepine, but not of lacosamide, in blocking high-frequency firing via differential effects on persistent Na+ currents
    Mischa Uebachs
    Department of Epileptology, University of Bonn, Sigmund Freud Strasse 25, Bonn, Germany
    Epilepsia 53:1959-67. 2012
    ....
  30. pmc N-acetyl cysteine treatment rescues cognitive deficits induced by mitochondrial dysfunction in G72/G30 transgenic mice
    David Marian Otte
    Institute of Molecular Psychiatry, University of Bonn, Bonn, Germany
    Neuropsychopharmacology 36:2233-43. 2011
    ..Our results implicate LG72-induced mitochondrial and synaptic defects as a possible pathomechanism of psychiatric disorders...
  31. pmc Epilepsy research: a window onto function to and dysfunction of the human brain
    Heinz Beck
    Department of Epileptology, University of Bonn Medical Center, Bonn, Germany
    Dialogues Clin Neurosci 10:7-15. 2008
    ..In addition, the study of epilepsy has frequently shed light on basic mechanisms underlying the function and dysfunction of the human brain,..
  32. ncbi request reprint Modulation of voltage-dependent sodium channels by the delta-agonist SNC80 in acutely isolated rat hippocampal neurons
    Christina Remy
    Institute of Physiology, University of Bonn, Wilhelmstr 31, 53111 Bonn, Germany
    Neuropharmacology 47:1102-12. 2004
    ..SNC80 is to our knowledge hitherto the only substance that selectively influences slow but not fast inactivation processes and could provide an important tool in unraveling the mechanism underlying these distinct biophysical processes...
  33. ncbi request reprint Functional network integration of embryonic stem cell-derived astrocytes in hippocampal slice cultures
    Bjorn Scheffler
    Department of Neuropathology, University of Bonn Medical Center, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
    Development 130:5533-41. 2003
    ..Our findings provide the first evidence of functional integration of grafted astrocytes, and depict glial network integration as a potential route for widespread transcellular delivery of small molecules to the CNS...
  34. ncbi request reprint Long-lasting modification of intrinsic discharge properties in subicular neurons following status epilepticus
    Jörg Wellmer
    Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Str 25, 53105 Bonn, Germany
    Eur J Neurosci 16:259-66. 2002
    ..The persistent up-regulation of intrinsic bursting in the subiculum, in concert with similar changes in the hippocampus, undoubtedly contributes to epileptogenesis following pilocarpine-induced SE...
  35. ncbi request reprint Sulfatide storage in neurons causes hyperexcitability and axonal degeneration in a mouse model of metachromatic leukodystrophy
    Matthias Eckhardt
    Institute of Physiological Chemistry, University of Bonn, 53115 Bonn, Germany
    J Neurosci 27:9009-21. 2007
    ..These observations suggest that SGalCer accumulation in neurons contributes to disease phenotype...
  36. ncbi request reprint Seizure-dependent modulation of mitochondrial oxidative phosphorylation in rat hippocampus
    Alexei P Kudin
    Department of Epileptology, University of Bonn Medical Centre, Sigmund Freud Str 25, D 53105 Bonn, Germany
    Eur J Neurosci 15:1105-14. 2002
    ..This mechanism could be invoked during diverse forms of pathological neuronal activity and could severely affect both excitability and viability of hippocampal pyramidal neurons...
  37. ncbi request reprint Transcriptional profiling in human epilepsy: expression array and single cell real-time qRT-PCR analysis reveal distinct cellular gene regulation
    Albert J Becker
    Department of Neuropathology, University of Bonn Medical Center, Sigmund Freud Str 25, 53105 Bonn, Germany
    Neuroreport 13:1327-33. 2002
    ..Ataxin-3 has been related to neuronal maintenance. Its functional role for TLE has to be further evaluated...
  38. doi request reprint Behavioral changes in G72/G30 transgenic mice
    David M Otte
    Institute of Molecular Psychiatry, University of Bonn, Sigmund Freud Strasse 25, Bonn, Germany
    Eur Neuropsychopharmacol 19:339-48. 2009
    ..These results demonstrate that expression of the human G72/G30 gene locus in mice produces behavioral phenotypes that are relevant to psychiatric disorders...
  39. pmc The Ca(V)2.3 Ca(2+) channel subunit contributes to R-type Ca(2+) currents in murine hippocampal and neocortical neurones
    Dmitry Sochivko
    Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Str 25, 53105 Bonn, Germany
    J Physiol 542:699-710. 2002
    ..3 subunits underlie a significant fraction of I(Ca,R) in different types of central neurones. They also indicate that Ca(V)2.3 subunits may give rise to Ca(2+) currents with differing pharmacological properties in native neurones...
  40. doi request reprint The effects of eslicarbazepine on persistent Na⁺ current and the role of the Na⁺ channel β subunits
    Anna Doeser
    University of Bonn, Department of Epileptology, Laboratory for Experimental Epileptology and Cognition Research, Bonn, Germany
    Epilepsy Res 108:202-11. 2014
    ..Therefore, eslicarbazepine potentially overcomes a previously described putative mechanism of resistance to established Na(+) channel acting antiepileptic drugs...
  41. doi request reprint The transcription factor Smad-interacting protein 1 controls pain sensitivity via modulation of DRG neuron excitability
    Monika Jeub
    Department of Neurology, University of Bonn Medical Center, Bonn, Germany
    Pain 152:2384-98. 2011
    ..These data suggest that Sip1 controls the transduction properties of heat-sensitive primary sensory neurons and thus thermal pain sensitivity in a novel manner via coordinated changes in DRG-neuron voltage-gated ion channels...
  42. ncbi request reprint Differential regulation of cadherins and catenins during axonal reorganization in the adult rat CNS
    Katrin Fasen
    Department of Epileptology, University of Bonn Medical Center, Germany
    J Neuropathol Exp Neurol 61:903-13. 2002
    ..Our results imply that members of the cadherin/catenin families undergo specific spatiotemporal patterns of regulation, which may be important in axon target recognition and synapse formation during lesion-induced sprouting...
  43. ncbi request reprint Upregulation of a T-type Ca2+ channel causes a long-lasting modification of neuronal firing mode after status epilepticus
    Hailing Su
    Department of Physiology, Hebrew University Hadassah School of Medicine, 91120 Jerusalem, Israel
    J Neurosci 22:3645-55. 2002
    ..This nonsynaptic plasticity considerably amplifies the output of CA1 pyramidal neurons to synaptic inputs and most probably contributes to the development and expression of an epileptic condition after SE...
  44. pmc Enhanced expression of a specific hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN) in surviving dentate gyrus granule cells of human and experimental epileptic hippocampus
    Roland A Bender
    Department of Anatomy, University of California, Irvine, Irvine, California 92697, USA
    J Neurosci 23:6826-36. 2003
    ....
  45. pmc Localization of HCN1 channels to presynaptic compartments: novel plasticity that may contribute to hippocampal maturation
    Roland A Bender
    Department of Anatomy, University of California, Irvine, Irvine, California 92697 4475, USA
    J Neurosci 27:4697-706. 2007
    ..These findings support a novel developmentally regulated axonal transport of functional ion channels and suggest a role for HCN1 channel-mediated presynaptic I(h) in hippocampal maturation...
  46. ncbi request reprint Endogenous Ca2+ buffer concentration and Ca2+ microdomains in hippocampal neurons
    Andreas Muller
    Department of Neurosurgery, University Clinic Bonn, D 53105 Bonn, Germany
    J Neurosci 25:558-65. 2005
    ....
  47. ncbi request reprint Novel mechanisms underlying drug resistance in temporal lobe epilepsy
    Uwe Heinemann
    Institute of Physiology, Charite University, Berlin, Germany
    Adv Neurol 97:85-95. 2006
  48. ncbi request reprint "Epileptic neurons" in temporal lobe epilepsy
    Yoel Yaari
    Department of Physiology, Hebrew University Hadassah, Faculty of Medicine, Jerusalem, Israel
    Brain Pathol 12:234-9. 2002
  49. ncbi request reprint Acquired dendritic channelopathy in temporal lobe epilepsy
    Christophe Bernard
    Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA
    Science 305:532-5. 2004
    ..Kinase inhibition partly reversed dendritic excitability to control levels. Such acquired channelopathy is likely to amplify neuronal activity and may contribute to the initiation and/or propagation of seizures in TLE...
  50. pmc Regulated expression of HCN channels and cAMP levels shape the properties of the h current in developing rat hippocampus
    Rainer Surges
    Department of Neurology, University Clinics Freiburg, Breisacher Strasse 64, 79106 Freiburg, Germany
    Eur J Neurosci 24:94-104. 2006
    ....
  51. ncbi request reprint Proximal persistent Na+ channels drive spike afterdepolarizations and associated bursting in adult CA1 pyramidal cells
    Cuiyong Yue
    Department of Physiology, Institute of Medical Sciences, Hebrew University Hadassah Faculty of Medicine, Jerusalem 91120, Israel
    J Neurosci 25:9704-20. 2005
    ..Through this action, proximal INaP critically determines the firing mode and spike output of adult CA1 pyramidal cells...