1. Nonmigraine-associated TRESK K+ channel variant C110R does not increase the excitability of trigeminal ganglion neurons.

    Journal of Neurophysiology 112(3):568 (2014) PMID 24805079 PMCID PMC4122697

    Recent genetic studies suggest that dysfunction of ion channels and transporters may contribute to migraine pathophysiology. A migraine-associated frameshift mutation in the TWIK-related spinal cord K+ (TRESK) channel results in nonfunctional channels. Moreover, mutant TRESK subunits exert a dom...
  2. Left ventricular noncompaction cardiomyopathy: a case report and literature review.

    International journal of clinical and experimen... 7(12):5130 (2014) PMID 25664015 PMCID PMC4307462

    Left ventricular noncompaction cardiomyopathy (LVNC) is a relatively rare congenital disorder prominently characterized by prominent trabeculations and intertrabecular recesses that communicate with the ventricular cavity rather than the coronary circulation. LVNC can occur in isolation or coexi...
  3. Over-expression of TRESK K(+) channels reduces the excitability of trigeminal ganglion nociceptors.

    PLoS ONE 9(1):e87029 (2014) PMID 24466320 PMCID PMC3900698

    TWIK-related spinal cord K(+) (TRESK) channel is abundantly expressed in trigeminal ganglion (TG) and dorsal root ganglion neurons and is one of the major background K(+) channels in primary afferent neurons. Mutations in TRESK channels are associated with familial and sporadic migraine. In rats...
  4. Left ventricular noncompaction cardiomyopathy: a case report and literature review.

    International journal of clinical and experimen... 7(12):5130 (2014) PMID 25664015

    Left ventricular noncompaction cardiomyopathy (LVNC) is a relatively rare congenital disorder prominently characterized by prominent trabeculations and intertrabecular recesses that communicate with the ventricular cavity rather than the coronary circulation. LVNC can occur in isolation or coexi...
  5. Functional analysis of a migraine-associated TRESK K+ channel mutation.

    Journal of Neuroscience 33(31):12810 (2013) PMID 23904616 PMCID PMC3728689

    Recent genetic and functional studies suggest that migraine may result from abnormal activities of ion channels and transporters. A frameshift mutation in the human TWIK-related spinal cord K(+) (TRESK) channel has been identified in migraine with aura patients in a large pedigree. In Xenopus oo...
  6. Serine 363 is required for nociceptin/orphanin FQ opioid receptor (NOPR) desensitization, internalization, and arrestin signaling.

    Journal of Biological Chemistry 287(50):42019 (2012) PMID 23086955 PMCID PMC3516748

    We determined the role of carboxyl-terminal regulation of NOPR (nociceptin, orphanin FQ receptor) signaling and function. We mutated C-terminal serine and threonine residues and examined their role in NOPR trafficking, homologous desensitization, and arrestin-dependent MAPK signaling. The NOPR a...
  7. Effects of familial hemiplegic migraine type 1 mutation T666M on voltage-gated calcium channel activities in trigeminal ganglion neurons.

    Journal of Neurophysiology 107(6):1666 (2012) PMID 22190617 PMCID PMC3311679

    Familial hemiplegic migraine type 1 (FHM-1), a rare hereditary form of migraine with aura and hemiparesis, serves as a good model for exploring migraine pathophysiology. The FHM-1 gene encodes the pore-forming Ca(V)2.1 subunit of human P/Q-type voltage-gated Ca(2+) channels (VGCCs). Some FHM-1 m...
  8. Expression of the transient receptor potential channels TRPV1, TRPA1 and TRPM8 in mouse trigeminal primary afferent neurons innervating the dura.

    Molecular Pain 8:66 (2012) PMID 22971321 PMCID PMC3489865

    Migraine and other headache disorders affect a large percentage of the population and cause debilitating pain. Activation and sensitization of the trigeminal primary afferent neurons innervating the dura and cerebral vessels is a crucial step in the "headache circuit". Many dural afferent neuron...
  9. Different relationship of N- and P/Q-type Ca2+ channels to channel-interacting slots in controlling neurotransmission at cultured hippocampal synapses.

    Journal of Neuroscience 30(13):4536 (2010) PMID 20357104 PMCID PMC3842455

    Synaptic transmission at CNS synapses is often mediated by joint actions of multiple Ca(2+) channel subtypes, most prominently, P/Q- and N-type. We have proposed that P/Q-type Ca(2+) channels saturate type-preferring slots at presynaptic terminals, which impose a ceiling on the synaptic efficacy...
  10. Dissociation of the opioid receptor mechanisms that control mechanical and heat pain.

    Cell 137(6):1148 (2009) PMID 19524516 PMCID PMC3683597

    Delta and mu opioid receptors (DORs and MORs) are inhibitory G protein-coupled receptors that reportedly cooperatively regulate the transmission of pain messages by substance P and TRPV1-expressing pain fibers. Using a DOReGFP reporter mouse we now show that the DOR and MOR are, in fact, express...
  11. Dissociation of the Opioid Receptor Mechanisms that Control Mechanical and Heat Pain

    Cell 137(6):1148 (2009)

    Delta and mu opioid receptors (DORs and MORs) are inhibitory G protein-coupled receptors that reportedly cooperatively regulate the transmission of pain messages by substance P and TRPV1-expressing pain fibers. Using a DOReGFP reporter mouse we now show that the DOR and MOR are, in fact, ex...
  12. Quantum dots provide an optical signal specific to full collapse fusion of synaptic vesicles.

    PNAS 104(45):17843 (2007) PMID 17968015 PMCID PMC2077028

    Synaptic vesicles are responsible for releasing neurotransmitters and are thus essential to brain function. The classical mode of vesicle recycling includes full collapse of the vesicle into the plasma membrane and clathrin-mediated regeneration of a new vesicle. In contrast, a nonclassical mode...
  13. Voltage-gated calcium channels, calcium signaling, and channelopathies

    New Comprehensive Biochemistry 41:127 (2007)

    Voltage-gated calcium channels mediate intracellular Ca2+ influx and are absolutely critical for the physiological function of excitable cells in brain, skeletal, cardiac and smooth muscle, endocrine glands, and other tissues. These membrane proteins translate membrane depolarization s...
  14. Voltage-gated calcium channels and pain.

    PAIN® 126(1-3):5 (2006) PMID 17084979

  15. Voltage-gated calcium channels and pain

    PAIN® 126(1):5 (2006)

  16. Gating deficiency in a familial hemiplegic migraine type 1 mutant P/Q-type calcium channel.

    Journal of Biological Chemistry 280(25):24064 (2005) PMID 15795222

    Familial hemiplegic migraine type 1 (FHM1) arises from missense mutations in the gene encoding alpha1A, the pore-forming subunit of P/Q-type calcium channels. The nature of the channel disorder is fundamental to the disease, yet is not well understood. We studied how the most prevalent FHM1 muta...
    PDF not found
  17. Effects of familial hemiplegic migraine type 1 mutations on neuronal P/Q-type Ca2+ channel activity and inhibitory synaptic transmission.

    PNAS 102(7):2590 (2005) PMID 15699344 PMCID PMC548328

    Inhibitory synapses play key roles in the modulatory circuitry that regulates pain signaling and generation of migraine headache. A rare, dominant form of this common disease, familial hemiplegic migraine type 1 (FHM1), arises from missense mutations in the pore-forming alpha1A subunit of P/Q-ty...
  18. Presynaptic Ca2+ channels compete for channel type-preferring slots in altered neurotransmission arising from Ca2+ channelopathy.

    Neuron 43(3):387 (2004) PMID 15294146

    Several human channelopathies result from mutations in alpha1A, the pore-forming subunit of P/Q-type Ca2+ channels, conduits of presynaptic Ca2+ entry for evoked neurotransmission. We found that wild-type human alpha1A subunits supported transmission between cultured mouse hippocampal neurons eq...
  19. Presynaptic Ca2+Channels Compete for Channel Type-Preferring Slots in Altered Neurotransmission Arising from Ca2+Channelopathy

    Neuron 43(3):387 (2004)

    Several human channelopathies result from mutations in α 1A, the pore-forming subunit of P/Q-type Ca 2+ channels, conduits of presynaptic Ca 2+ entry for evoked neurotransmission. We found that wild-type human α 1A subunits supported transmission between cultured mou...