K. Shen

发表

Effects of temperature alterations on population and cellular activities in hippocampal slices from mature and immature rabbit

P. Schwartzkroin, K. Shen, 1988, Brain Research.

Modulation of opioid analgesia, tolerance and dependence by Gs-coupled, GM1 ganglioside-regulated opioid receptor functions.

K. Shen, S. Crain, S. Crain, 1998, Trends in pharmacological sciences.

Specific N- or C-terminus modified dynorphin and β-endorphin peptides can selectively block excitatory opioid receptor functions in sensory neurons and unmask potent inhibitory effects of opioid agonists

K. Shen, S. Crain, 1995, Brain Research.

Chronic morphine-treated sensory ganglion neurons remain supersensitive to the excitatory effects of naloxone for months after return to normal culture medium: an in vitro model of ‘protracted opioid dependence’

K. Shen, S. Crain, 1995, Brain Research.

Ultra-low concentrations of naloxone selectively antagonize excitatory effects of morphine on sensory neurons, thereby increasing its antinociceptive potency and attenuating tolerance/dependence during chronic cotreatment.

K. Shen, S. Crain, S. Crain, 1995, Proceedings of the National Academy of Sciences of the United States of America.

Chronic selective activation of excitatory opioid receptor functions in sensory neurons results in opioid ‘dependence’ without tolerance

K. Shen, S. Crain, 1992, Brain Research.

F11 neuroblastoma × DRG neuron hybrid cells express inhibitory μ- and δ-opioid receptors which increase voltage-dependent K+ currents upon activation

K. Shen, M. Scheideler, S. Crain, 1992, Brain Research.

Cholera toxin-B subunit blocks excitatory effects of opioids on sensory neuron action potentials indicating that GM1 ganglioside may regulate Gs-linked opioid receptor functions

K. Shen, S. Crain, 1990, Brain Research.

Dual opioid modulation of the action potential duration of mouse dorsal root ganglion neurons in culture

K. Shen, S. Crain, S. Crain, 1989, Brain Research.

Antagonists of excitatory opioid receptor functions enhance morphine's analgesic potency and attenuate opioid tolerance/dependence liability

K. Shen, S. Crain, 2000, PAIN®.

Inhibitor of cyclic AMP-dependent protein kinase blocks opioid-induced prolongation of the action potential of mouse sensory ganglion neurons in dissociated cell cultures

K. Shen, A. Chalazonitis, S. Crain, 1988, Brain Research.

Opioids excite rather than inhibit sensory neurons after chronic opioid exposure of spinal cord-ganglion cultures

K. Shen, A. Chalazonitis, S. Crain, 1988, Brain Research.

Low doses of cyclic AMP-phosphodiesterase inhibitors rapidly evoke opioid receptor-mediated thermal hyperalgesia in naïve mice which is converted to prominent analgesia by cotreatment with ultra-low-dose naltrexone

K. Shen, S. Crain, 2008, Brain Research.

Acute thermal hyperalgesia elicited by low-dose morphine in normal mice is blocked by ultra-low-dose naltrexone, unmasking potent opioid analgesia

K. Shen, S. Crain, 2001, Brain Research.

GM1 Ganglioside‐induced Modulation of Opioid Receptor‐mediated Functions

K. Shen, S. Crain, S. Crain, 1998, Annals of the New York Academy of Sciences.

Opioids can evoke direct receptor-mediated excitatory effects on sensory neurons.

K. Shen, S. Crain, S. Crain, 1990, Trends in pharmacological sciences.

Neuraminidase inhibitor, oseltamivir blocks GM1 ganglioside-regulated excitatory opioid receptor-mediated hyperalgesia, enhances opioid analgesia and attenuates tolerance in mice

K. Shen, S. Crain, 2004, Brain Research.

Ultra-low doses of naltrexone or etorphine increase morphine's antinociceptive potency and attenuate tolerance/dependence in mice

K. Shen, S. Crain, 1997, Brain Research.

Modulatory effects of Gs-coupled excitatory opioid receptor functions on opioid analgesia, tolerance, and dependence

K. Shen, S. Crain, 1996, Neurochemical Research.

Enhanced analgesic potency and reduced tolerance of morphine in 129/SvEv mice: evidence for a deficiency in GM1 ganglioside-regulated excitatory opioid receptor functions

K. Shen, S. Crain, 2000, Brain Research.

Etorphine elicits anomalous excitatory opioid effects on sensory neurons treated with GM1 ganglioside or pertussis toxin in contrast to its potent inhibitory effects on naive or chronic morphine-treated cells

K. Shen, S. Crain, 1996, Brain Research.

Biphalin, an enkephalin analog with unexpectedly high antinociceptive potency and low dependence liability in vivo, selectively antagonizes excitatory opioid receptor functions of sensory neurons in culture

K. Shen, S. Crain, 1995, Brain Research.

Antagonists at excitatory opioid receptors on sensory neurons in culture increase potency and specificity of opiate analgesics and attenuate development of tolerance/dependence

K. Shen, S. Crain, 1994, Brain Research.

Naloxone rapidly evokes endogenous kappa opioid receptor-mediated hyperalgesia in naïve mice pretreated briefly with GM1 ganglioside or in chronic morphine-dependent mice

K. Shen, S. Crain, 2007, Brain Research.

Cholera toxin-A subunit blocks opioid excitatory effects of sensory neuron action potentials indicating mediation by Gs-linked opioid receptors

K. Shen, S. Crain, 1990, Brain Research.

Dynorphin prolongs the action potential of mouse sensory ganglion neurons by decreasing a potassium conductance whereas another specific kappa opioid does so by increasing a calcium conductance

K. Shen, S. Crain, 1990, Neuropharmacology.

After chronic opioid exposure sensory neurons become supersensitive to the excitatory effects of opioid agonists and antagonists as occurs after acute elevation of GM1 ganglioside

K. Shen, S. Crain, 1992, Brain Research.

Cholera toxin-B subunit blocks excitatory opioid receptor-mediated hyperalgesic effects in mice, thereby unmasking potent opioid analgesia and attenuating opioid tolerance/dependence

K. Shen, S. Crain, 2001, Brain Research.

μ and δ opioid agonists at low concentrations decrease voltage-dependent K+ currents in F11 neuroblastoma × DRG neuron hybrid cells via cholera toxin-sensitive receptors

K. Shen, S. Crain, S. Fan, 1993, Brain Research.

After GM1 ganglioside treatment of sensory neurons naloxone paradoxically prolongs the action potential but still antagonizes opioid inhibition.

K. Shen, S. Crain, 1992, The Journal of pharmacology and experimental therapeutics.

Brief treatment of sensory ganglion neurons with GM1 ganglioside enhances the efficacy of opioid excitatory effects on the action potential

K. Shen, R. Ledeen, S. Crain, 1991, Brain Research.

Organization of synaptic transmission in the mammalian solitary complex, studied in vitro.

K. Grant, J. Champagnat, M. Denavit-Saubié, 1986, The Journal of physiology.

Effect of stimulation of bulbar reticular formation on long latency discharges in the region of nucleus centralis lateralis of thalamus.

K. Shen, S. Ho, 1977, Scientia Sinica.

Etorphine elicits unique dose-dependent inhibitory effects on the action potential duration of sensory neurons even at low concentrations where other opioids elicit excitatory effects

K. Shen, S. Crain, 1994, Regulatory Peptides.

Opioids at low concentration decrease openings of K+ channels in sensory ganglion neurons

K. Shen, S. Crain, S. Fan, 1991, Brain Research.