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Research Article

Mechanical and Temperature Stressor–Induced Seizure-and-Paralysis Behaviors in Drosophila Bang-Sensitive Mutants

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Pages 189-197 | Received 09 Apr 2012, Accepted 27 Apr 2012, Published online: 20 Jun 2012

REFERENCES

  • Bannister, R. (1985). Brain's clinical neurology (6th ed.). London: Oxford University Press.
  • Benzer, S. (1971). From the gene to behavior. JAMA, 218, 1015–1022.
  • Buchner, E. (1991). Genes expressed in the adult brain of Drosophila and effects of their mutations on behavior: A survey of transmitter- and second messenger-related genes. J Neurogenet, 7, 153–192.
  • Burg, M. G. (1987). Genetic and mosaic analysis of mutations which alter never and muscle excitability in Drosophila melanogaster: Effects on development and behavior. PhD thesis, University of Iowa, Iowa City, Iowa, USA.
  • Burg, M. G., & Wu, C.-F. (1986). Differentiation and central projections of peripheral sensory cells with action-potential block in Drosophila mosaics. J Neurosci, 6, 2968–2976.
  • Burg, M. G., & Wu, C.-F. (1989). Central projections of peripheral mechanosensory cells with increased excitability in Drosophila mosaics. Dev Biol, 131, 505–514.
  • Clases, L., Ceulemans, B., Audenaert, D., Smets, K., Lofgren, A., Del-Favero, J., Ala-Mello, S., Basel-Vanagaite, L., Plecko, B., Raskin, S., Thiry, P., Wolf, N., Van Broeckhoven C., & DeJonghe, P. (2001). De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy. Am J Hum Genet, 68, 1327–1332.
  • Engel, J. E. (1995). Effects of second messenger and excitability mutations upon identified neural circuits underlying activity-dependent plasticity of behavior in Drosophila. PhD thesis, University of Iowa, Iowa City, Iowa, USA.
  • Engel, J., & Wu, C.-F. (1994). Altered mechanoreceptor response in Drosophila bang-sensitive mutants. J Comp Physiol A, 175, 267–278.
  • Escayg, A., MacDonald, B., Meisler, M., Baulac, S., Huberfeld, G., An-Gourfinkel, I., Brice, A., Leguern, E., Moulard, B., Chaigne, D., Bruesi, C., & Malafosse, A. (2000). Mutations of SCN1A encoding a neuronal sodium channel, in two families with GEFS +2. Nat Genet, 24, 343–345.
  • Fergestad, T., Bostwick, B., & Ganetzky, B. (2006). Metabolic disruption in Drosophila bang-sensitive mutants. Genetics, 173, 1357–1364.
  • Fergestad, T., Olson, L., Patel, K. P., Miller, R., Palladino, M., & Ganetzky, B. (2008). Neuropathology in Drosophila mutants with increased seizure susceptibility. Genetics, 178, 947–956.
  • Fox, L., Ueda, A., Berke, B., Peng, I.-F., & Wu, C.-F. (2005). Movement disorders in Drosophila mutants of potassium channels and biogenic amine pathways. In M. S. LeDoux (Ed.), Animal models of movement disorders (pp. 487–504). San Diego: Academic Press/Elsevier.
  • Ganetzky, B., & Wu, C.-F. (1982). Indirect suppression involving behavioral mutants with altered nerve excitability in Drosophila melanogaster. Genetics, 100, 597–614.
  • Glasscock, E., Qian, J., Yoo, J. W., & Noebels, J. L. (2007). Masking epilepsy by combining two epilepsy genes. Nat Neurosci, 10, 1554–1558.
  • Gordon, H. W., Bogen, J. E., & Sperry, R. W. (1971). Absence of deconnexion syndrome in two patients with partial section of the neocommissures. Brain, 94, 327–336.
  • Grigliatti, T., Hall, L., Rosenbluth, R., & Suzuki, D. T. (1973). Temperature-sensitive mutations in Drosophila melanogaster. Mol Gen Genet, 120, 107–114.
  • Heinemann, U., & Gutnick, M. J. (1979). Relation between extracellular potassium concentration and neuronal activities in cat thalamus (VPL) during projection of cortical epileptiform discharge. Electroencephalogr Clin Neurophysiol, 47, 345–347.
  • Hinton, C. W. (1955). The behavior of an unstable ring chromosome of Drosophila melanogaster. Genetics, 40, 951–961.
  • Hotta, Y., & Benzer, S. (1972). Mapping of behaviour in Drosophila mosaics. Nature, 240, 527–535.
  • Jan, Y. N., & Jan, L. Y. (1978). Genetic dissection of short-term and long-term facilitation in Drosophila. Proc Nat Acad Sci USA, 75, 515–519.
  • Judd, B. H., Shen, M. W., & Kaufman, T. C. (1972). The anatomy and function of a segment of the X chromosome of Drosophila melanogaster. Genetics, 71, 139–156.
  • Kernan, M. J., Kuroda, M. I., Kreber, R., Baker, B. S., & Ganetzky, B. (1991). napts, a mutation affecting sodium channel activity in Drosophila, is an allele of mle a regulator of X chromosome transcription. Cell, 66, 949–959.
  • Klassen, T., Davis, C., Goldman, A., Burgess, D., Chen, T., Wheeler, D., McPherson, J., Bourquin, T., Lewis, L., Villasana, D., Morgan, M., Muzny, D., Gibbs, R., & Noebels, J. (2011). Exome sequencing of ion channel genes reveals complex profiles confounding personal risk assessment in epilepsy. Cell,145, 1036–1048.
  • Kuebler, D., & Tanouye, M. (2000). Modifications of seizure susceptibility in Drosophila. J Neurophysiol, 83, 998–1009.
  • Kuebler, D., & Tanouye, M. (2001). Genetic suppression of seizure susceptibility in Drosophila. J Neurophysiol, 86, 1211–1225.
  • Lee, J., & Wu, C. F. (2002). Electroconvulsive seizure behavior in Drosophila: Analysis of the physiological repertoire underlying a stereotyped action pattern in bang-sensitive mutants. J Neurosci, 22, 11065–11079.
  • Lee, J., & Wu, C.-F. (2006). Genetic modifications of seizure susceptibility and expression by altered excitability in Drosophila Na + and K + channel mutants. J Neurophysiol, 96, 2465–2478.
  • Marley, R., & Baines, R. A. (2011). Increased persistent Na + current contributes to seizure in the slamdance bang-sensitive Drosophila mutant. J Neurophysiol, 106, 18–29.
  • McNamara, J. O. (1994). Cellular and molecular basis of epilepsy. J Neurosci, 14, 3413–3425.
  • McQuilton, P., St. Pierre, S. E., Thurmond, J., & the FlyBase Consortium. (2011). FlyBase 101—The basics of navigating FlyBase. Nucleic Acids Res, 40, D706–D714.
  • Noebels, J. (2003). The biology of epilepsy genes. Ann Rev Neurosci, 26, 599–625.
  • Ojemann, G. A. (1987). Surgical therapy for medically intractable epilepsy. J Neurosurg, 66, 489–499.
  • Palladino, M. J., Bower, J. E., Kreber, R., & Ganetzky, B. (2003). Neural dysfunction and neurodegeneration in Drosophila Na + /K + ATPase alpha subunit mutants. J Neurosci, 23, 1276–1286.
  • Parker, L., Padilla, M., Du, Y., Dong, K., & Tanouye, M. A. (2011). Drosophila as a model for epilepsy: bss is a gain-of-function mutation in the para sodium channel gene that leads to seizures. Genetics, 187, 523–534.
  • Pavlidis, P., & Tanouye, M. A. (1995). Seizures and failures in the giant fiber pathway of Drosophila bang-sensitive paralytic mutants. J Neurosci, 15, 5810–5819.
  • Pavlidis, P., Ramaswami, M., & Tanouye, M. A. (1994). The Drosophila easily shocked gene: A mutation in a phospholipid synthetic pathway causes seizure, neuronal failure, and paralysis. Cell, 79, 23–33.
  • Roydon, C. S., Pirrotta, V., & Jan, L. Y. (1987). The tko locus, site of a behavioral mutation in Drosophila melanogaster, codes for a protein homologous to prokaryotic ribosomal protein S12. Cell, 51, 165–173.
  • Shoffner, J. M., Lott, M. T., Lezza, A. M. S., Seibel, P., Ballinger, S. W., & Wallace, D. C. (1990). Myoclonic epilepsy and ragged-red fiber disease (MERRF) is associated with a mitochondrial DNA tRNALys mutation. Cell, 61, 931–937.
  • Ueda, A., Grabbe, C., Lee, J., Lee, J., Palmer, R. H., & Wu, C. F. (2008). Mutation of Drosophila focal adhesion kinase induces bang-sensitive behavior and disrupts glial function, axonal conduction and synaptic transmission. Eur J Neurosci, 27, 2860–2870.
  • Vandervorst, P., & Ghysen, A. (1980). Genetic control of sensory connections in Drosophila. Nature, 286, 65–67.
  • Wu, C.-F., & Ganetzky, B. (1992). Neurogenetic studies of ion channels in Drosophila. In T. Narahashi (Ed.), Ion channels (Vol. 3, pp. 261–314). New York: Plenum Publishing.
  • Wu, C.-F., Ganetzky, B., Jan, L. Y., Jan, Y. N., & Benzer, S. (1978). A Drosophila mutant with a temperature-sensitive block in nerve conduction. Proc Natl Acad Sci USA, 75, 4047–4051.
  • Zhang, H., & Tanouye, M. (2002). The Drosophila slamdance gene: A mutation in an aminopeptidase can cause seizure, paralysis and neuronal failure. Genetics, 162, 1283–1299.

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