J R Clay

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. doi request reprint A comparative analysis of models of Na+ channel gating for mammalian and invertebrate nonmyelinated axons: relationship to energy efficient action potentials
    John R Clay
    Ion Channel Biophysics Group, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 5625 Fishers Lane, Rockville, MD 20852, USA
    Prog Biophys Mol Biol 111:1-7. 2013
  2. pmc Ionic mechanism underlying optimal stimuli for neuronal excitation: role of Na+ channel inactivation
    John R Clay
    National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA
    PLoS ONE 7:e45983. 2012
  3. pmc A simple modification of the Hodgkin and Huxley equations explains type 3 excitability in squid giant axons
    John R Clay
    National Institute of Neurological Disorders and Stroke, National Institutes of Health, Twinbrook Building, Rm TN 41, 5625 Fishers Lane, Bethesda, MD 20892, USA
    J R Soc Interface 5:1421-8. 2008
  4. ncbi request reprint Axonal excitability revisited
    John R Clay
    Ion Channel Biophysics Group, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 36 Room 4A21, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Prog Biophys Mol Biol 88:59-90. 2005
  5. ncbi request reprint A novel mechanism for irregular firing of a neuron in response to periodic stimulation: irregularity in the absence of noise
    John R Clay
    Ion Channel Biophysics Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
    J Comput Neurosci 15:43-51. 2003
  6. ncbi request reprint On the persistent sodium current in squid giant axons
    John R Clay
    Ion Channel Biophysics Unit, Basic Neurosciences Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurophysiol 89:640-4. 2003
  7. ncbi request reprint Temperature dependence of bistability in squid giant axons with alkaline intracellular pH
    J R Clay
    Ion Channel Biophysics Unit, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
    J Membr Biol 187:213-23. 2002
  8. ncbi request reprint Trafficking of axonal K+ channels: potential role of Hsc70
    John R Clay
    Ion Channel Biophysics Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurosci Res 67:745-52. 2002
  9. ncbi request reprint Action potentials occur spontaneously in squid giant axons with moderately alkaline intracellular pH
    J R Clay
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biol Bull 201:186-92. 2001
  10. ncbi request reprint Localization of voltage-gated K(+) channels in squid giant axons
    J R Clay
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurobiol 45:172-84. 2000

Detail Information

Publications16

  1. doi request reprint A comparative analysis of models of Na+ channel gating for mammalian and invertebrate nonmyelinated axons: relationship to energy efficient action potentials
    John R Clay
    Ion Channel Biophysics Group, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 5625 Fishers Lane, Rockville, MD 20852, USA
    Prog Biophys Mol Biol 111:1-7. 2013
    ....
  2. pmc Ionic mechanism underlying optimal stimuli for neuronal excitation: role of Na+ channel inactivation
    John R Clay
    National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA
    PLoS ONE 7:e45983. 2012
    ..This result demonstrates how an optimal stimulus waveform relates to ionic dynamics and may have implications for energy efficiency of neural excitation in many systems including the mammalian brain...
  3. pmc A simple modification of the Hodgkin and Huxley equations explains type 3 excitability in squid giant axons
    John R Clay
    National Institute of Neurological Disorders and Stroke, National Institutes of Health, Twinbrook Building, Rm TN 41, 5625 Fishers Lane, Bethesda, MD 20892, USA
    J R Soc Interface 5:1421-8. 2008
    ..Our analysis may have broad significance given the use of IK=gK(V-EK) to describe K+ currents in a wide variety of biological preparations...
  4. ncbi request reprint Axonal excitability revisited
    John R Clay
    Ion Channel Biophysics Group, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 36 Room 4A21, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Prog Biophys Mol Biol 88:59-90. 2005
    ..Physiol. 117 (1952d) 500) model previously described (Clay, J. Neurophysiol. 80 (1998) 903)...
  5. ncbi request reprint A novel mechanism for irregular firing of a neuron in response to periodic stimulation: irregularity in the absence of noise
    John R Clay
    Ion Channel Biophysics Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
    J Comput Neurosci 15:43-51. 2003
    ..The emphasis is not as much on events prior to an AP as it is on the AP's themselves...
  6. ncbi request reprint On the persistent sodium current in squid giant axons
    John R Clay
    Ion Channel Biophysics Unit, Basic Neurosciences Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurophysiol 89:640-4. 2003
    ..Subtraction of this current from the I(NaP) measurements yields the portion of I(NaP) that appears to be attributable to an ion channel mechanism distinct from I(Na)...
  7. ncbi request reprint Temperature dependence of bistability in squid giant axons with alkaline intracellular pH
    J R Clay
    Ion Channel Biophysics Unit, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
    J Membr Biol 187:213-23. 2002
    ....
  8. ncbi request reprint Trafficking of axonal K+ channels: potential role of Hsc70
    John R Clay
    Ion Channel Biophysics Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurosci Res 67:745-52. 2002
    ..The addition of MgATP to the solution appears to release a significant amount of kinesin from the vesicles, possibly by the Hsc70-MgATP catalysis mechanism recently proposed by Tsai et al...
  9. ncbi request reprint Action potentials occur spontaneously in squid giant axons with moderately alkaline intracellular pH
    J R Clay
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biol Bull 201:186-92. 2001
    ..5. In other words, the effect has a threshold at a pH(i) of about 7.7. A mathematical model that is sufficient to mimic these results is provided using a modified version of the Clay (1998) description of the axonal ionic currents...
  10. ncbi request reprint Localization of voltage-gated K(+) channels in squid giant axons
    J R Clay
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurobiol 45:172-84. 2000
    ..We have also isolated an axoplasmic fraction containing approximately 150-nm-diameter vesicles that may transport K(+) channels back to the cell body...
  11. ncbi request reprint On the role of subthreshold dynamics in neuronal signaling
    J R Clay
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
    J Theor Biol 197:207-16. 1999
    ..We conclude that this mechanism may contribute to multimodal interspike interval histograms which have been observed from individual neurons throughout the nervous system...
  12. pmc Effects of intracellular K+ and Rb+ on gating of embryonic rat telencephalon Ca(2+)-activated K+ channels
    J M Mienville
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biophys J 70:778-85. 1996
    ..Substitution of Rbi+ for Ki+ also increased the mean burst duration for V > or = -30 mV. Both effects of Rbi+ were removed by membrane hyperpolarization...
  13. pmc A quantitative description of the E-4031-sensitive repolarization current in rabbit ventricular myocytes
    J R Clay
    Laboratory of Neurophysiology, National Institutes of Health, Bethesda, Maryland 20897, USA
    Biophys J 69:1830-7. 1995
    ....
  14. pmc Ion conductance of the Ca(2+)-activated maxi-K+ channel from the embryonic rat brain
    J M Mienville
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biophys J 72:188-92. 1997
    ..The gK versus [K+] relationship is described, theoretically, by a three-barrier, two-binding-site model in which the barrier that an ion must cross to leave the channel is decreased as [K+] is increased...
  15. ncbi request reprint Determining K+ channel activation curves from K+ channel currents
    J R Clay
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA
    Eur Biophys J 29:555-7. 2000
    ..Novel insights into the voltage dependence of the rapidly inactivating I(A) channels Kv1.4 and Kv4.2 have been obtained when this procedure was applied to recently published results...
  16. ncbi request reprint Noisy inputs and the induction of on-off switching behavior in a neuronal pacemaker
    David Paydarfar
    Department of Neurology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
    J Neurophysiol 96:3338-48. 2006
    ....