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Review

An assessment of the present and future roles of non-ligand gated ion channel modulators as CNS therapeutics

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Pages 61-70 | Published online: 24 Feb 2005

Bibliography

  • GOLDSTEIN S: A structural vignette common to voltage sensors and conduction pores: canaliculi. Neurone (1996) 16:717–722.
  • ••A brief general review of ion channel structure.
  • WANNER SG, KOCH RO, KOSCHAK A et al.: High-conductance calcium-activated potassium channels in rat brain: pharmacology, distribution, and subunit composition. Biochemistry (1999) 38:5392–5400.
  • •A good recent review of the pharmacology and molecular biology of BK channels.
  • MEIR A, GINSBURG S, BUTKEVITCH A etal.: Ion channels in presynaptic nerve terminals and control of transmitter release. Physiol. Rev. (1999) 79:1019–1088.
  • ••A review of the role of ion channels in the release ofneurotransmitters.
  • CHITTAJALLU R, ALFORD S, COLLINGRIDGE GL: Caz+ and synaptic plasticity. Cell Calcium (1998) 24:377–385.
  • •A discussion of the roles of Ca2+ in the synaptic plasticity that underlies learning and memory.
  • SCHIFFMANN SN, CHERON G, LOHOF A et al.: Impairedmotor coordination and Purkinje cell excitability in mice lacking calretinin. Proc. Nati Acad. Sci. USA (1999) 96:5257–5262.
  • KRISTIAN T, SIESJO BK: Calcium in ischemic cell death. Stroke (1998) 29:705–718.
  • ••A review of the importance of intracellular Ca2+ in thecascade leading to neuronal death in ischaemia.
  • UN Z, HANS S, EDGERTON J et al.: Identification of functionally distinct isoforms of the N-type Ca2+ channel in rat sympathetic ganglia and brain. Neuron (1997) 18:153–166.
  • •Article describing the diversity of N-type Ca2+ channels in rat neurones.
  • MINTZ I, ADAMS ME, BEAN BP: P type calcium channelsin rat central and peripheral neurons. Neuron (1992) 9:85–95.
  • RANDALL A, TSIEN R: Contrasting biophysical andpharmacological properties of T type and R type calcium channels. Neuropharmacology (1 9 9 7) 36:879–893.
  • •Comparing and contrasting the properties of these two species of voltage-dependent Ca2+ channels.
  • PEREZ-REYES E, CRIBBS LL, DAUD A et al.: Molecular characterization of a neuronal low voltage activated T type calcium channel. Nature (1998) 391:896–900.
  • •Article describing the structure of the T-type calcium channel.
  • DAVILA HM: Molecular and functional diversity of voltage-gated calcium channels. Ann. NY Acad. Sci. (1999) 868:102–117.
  • •A good recent review of the structure and function of voltage-dependent Ca2+ channels.
  • GOLDIN AL: Voltage-gated sodium channels. In: Ligand-and Voltage-Gated Ion Channels (Volume 2). North RA (Ed.), CRC Press, Boca Raton, USA (1995):73–112.
  • GOLDIN AL: Diversity of mammalian voltage-gated sodium channels. Ann. NY Acad. Sci. (1999) 868:38–50.
  • •Two recent reviews stressing the structural diversity and distributions of voltage-dependent Na + channels.
  • JAN LY, JAN YN: Voltage-gated and inwardly rectifying potassium channels. J. Physiol. (1997) 505:267–282.
  • DOLLY JO, PARCEJ DN: Molecular properties of voltage-gated IC channels. J. Bioen erg. Biomembr. (1996) 28:231–253.
  • •Two reviews of the molecular biology and functions of voltage-dependent and inward rectifier K.+ channels.
  • GOLDSTEIN S, WANG KW, ILAN N, et al.: Sequence and function of the two-P domain potassium channels: Implication of an emerging superfamily. J. Mot. Merl. (1998) 76:13–20.
  • •Recent review of the structure and function of two-pore domain leak' K+ channels.
  • TAYLOR CP: Voltage-gated channels as targets for anticonvulsant, analgesic and neuroprotective drugs. Curr. Pharm. Design (1996) 2:375–388.
  • ••Review of the appropriateness of neuronal voltage-dependent ion channels as targets for drug discovery.
  • RALL TW, SCHLEIFER LS: Drugs effective in the therapy of the epilepsies. In: The Pharmacological Basis of Therapeutics (Eighth Edition). Gilman AG, Rail TW, Nies AS, Taylor P (Eds.), Pergamon Press, Elsmford, New York, USA (1993):436–462.
  • •Standard reference review of anti-epileptic drugs and their actions.
  • SEVERT L, COULTER DA, SOMBARTI S et al.: Topiramate selectively blocks kainate currents in cultured hippocampal neurons. Epilepsia (1995) 36\(Suppl. 4):38.
  • WHITE HS, BRWON SD, SKEEN GA et al.: The investiga-tional anticonvulsant topiramate potentiates GABA-evoked currents in mouse cortical neurons. Epilepsia (1995) 36\(Suppl. 4):34.
  • PISANI A, STEFANI A, SINICHALCHI A et al.: Electro-physiological actions of felbamate on rat striatal neurones. Br. J. Pharmacol. (1995) 116(3):2053–2061.
  • SUBRAMANIAM S, RHOJ M, PENIX L et al.: Felbamate block of the N-methyl-D-aspartate receptor. J. Pharmacol. Exp. Ther. (1995) 273:878–886.
  • KELLY KM, GROSS RA, MACDONALD R: Valproic acid selectively reduces the low-threshold (T) calcium current in rat nodose neurons. Neurosci. Letts. (1990) 116:233–238
  • CHEUNG H, KAMP D, HARRIS E: An in vitro investigationof the action of lamotrigine on neuronal voltage-activated sodium channels. Epilepsy Res. (1992) 13:107–112.
  • LEES G, LEACH MJ: Studies on the mechanism of actionof the novel anticonvulsant lamotrigine (Lamictal) using primary neuroglial cultures from rat cortex. Brain Res. (1993) 612:190–199.
  • SCHAUF CL: Zonisamide enhances slow sodium inacti-vation in Myxicola. Brain Res. (1987) 413:185–189
  • SUZUKI S, KAWAKAMI K, NISHIMURA S et al.:Zonisamide blocks T-type calcium channel in cultured neurons of rat cerebral cortex. Epilepsy Res. (1992) 12:21–27.
  • ERDO SL, MOLNAR P, LAKICS V et al.: Vincamine andvincanol are potent blockers of voltage-gated Na+ channels. Eur. j Pharmacol (1996) 314(1/2):69–73.
  • KISS B, KARPATI E: The mechanism of action ofvinpocetine. Acta Pharm. Hung. (1996) 66(5):213–224.
  • COULTER DA, HUGUENARD JR, PRINCE DA: Characteri-zation of ethosuximide reduction of low-threshold calcium current in thalamic neurons. Ann. Neurol (1989) 25:582–593.
  • COULTER DA, HUGUENARD JR, PRINCE DA: Differentialeffects of petit mal anticonvulsants and convulsants on thalamic neurones: GABA current blockade. (1990) 100:807–813.
  • FOX JA: Irreversible and reversible blockade of IMR32calcium channel currents by synthetic MVIIA and iodinated MVIIC w-conopeptides. Pflug Arch. Eur. J. Physiol. (1995) 429(6):873–875.
  • MARWICK C: Nature's agents help heal humans- somenow take steps to reciprocate: complex cone snail venom. JAMA (1998) 279(20:1678–1679.
  • MCGUIRE D, BOWERBOX S, FELLMAN JD et al.: Sympatholysis after neuron-specific, N-type, voltage-sensitive calcium channel blockade: first demonstra-tion of N-channel function in humans. J. Cardiovas. Pharmacol. (1997) 30(3):400–403.
  • DIENNER H, KAUBE H, LIMMROTH V: A practical guideto the management and prevention of migraine. Drugs (1998) 56:811–824.
  • EDWARDS KR, GOODMAN WA, NORTON JA et al.: Intravenous Valproate (Depacon) for acute treatment of migraine headache. 41st Annual Meeting of the American Association for the Study of Headache. Boston, USA (1999). Abstract 201.
  • BARCHI RL: Ion channel mutations affecting muscleand brain. Curr. Opin. Neurol. (1998) 11:461–468.
  • •Discussion of the known mutations in ion channels producing neuromuscular syndromes.
  • DENYER J et al.: HTS approaches to voltage-gated ion channel drug discovery. Drug Discov. Today (1998) 3:323–332.
  • ••Good discussion of the technology and potential forhigh-throughput screening at ion channel targets.
  • STARRETT JE, JR., DWORETZKY SI, GRIBKOFF VK: Modulators of large-conductance calcium-activated potassium (BK) channels as potential therapeutic targets. Curr. Pharm. Design (1996) 2:413–428.
  • ••Recent review of the potential for BK channels as drugdiscovery targets in both brain and periphery.
  • WANG Q, BOWLES NE, TOWBIN JA: The molecular basis of long QT syndrome and prospects for therapy. Mol. Med. Today (1998) 4:382–388.
  • •Brief review of the several molecular bases of long QT syndrome in the heart, involving K.+ channel mutations.
  • SINGH NA, CHARLIER C, STAUFFER D et al.: A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns. Nature Genetics (1998) 18:25–29.
  • BIEVERT C et al: A potassium channel mutation in neonatal human epilepsy. Science (1998) 279:403–406.
  • •Two articles that described new members of a class of brain voltage-dependent K+ channels and demonstrated their involvement in a type of inherited epilepsy of new-borns.
  • KRALL WJ, SRAMEK JJ, CUTLER NR: Cholinesterase inhibitors: a therapeutic strategy for Alzheimer's disease. Ann. Pharmacother. (1999) 33:441–450
  • •Review of the rationale for targeting cholinesterase inhibi-tion for Alzheimer's disease. Both compounds approved to date for cognition enhancement have been of this class.
  • EID CN, ROSE GM: Cognition enhancement strategies by ion channel modulation of neurotransmission. Curr. Pharm. Design (1999) 5:345–361.
  • ••A recent review of ion channel targeting for cognitionenhancement, includes ligand-gated ion channel discussion.
  • WANG HS, PAN Z, SHI W et al.: KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel. Science (1998) 282: 1890-1893.
  • ••Landmark recent paper identifying the molecular substratesof the M-channel, a K.+ channel that mediates many of the effects of activation of muscarinic acetylcholine receptors. These channels may be particularly well suited for targeting in cognition enhancement.
  • DOBLE A. The role of excitotoxicity in neurodegenera- tive disease: implications for therapy. Pharmacol. Ther. (1999) 81:163–221.
  • ••Discussion of involvement of excitotoxicity in andapproaches to treatment of neurodegenerative disorders.
  • YU SP, YEH C, GOTTRON F et al: Role of the outward delayed rectifier IC current in ceramide-induced caspase activation and apoptosis in cultured cortical neurons. J. Neurochem. (1999) 73:933–941.
  • •Recent article demonstrating the involvement of K.+ currents in one form of neuronal apoptosis.

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