Lazaroff MA, Taylor AD and Ribera AB (2002) In vivo analysis of Kvb2 function in Xenopus embryonic myocytes. J Physiol 541.3: 673-683. pdf
Kukuljan M, Taylor A, Chouinard H, Olguín P, Rojas, CV and Ribera AB (2003) Selective regulation of xSlo splice variants during Xenopus embryogenesis. J Neurophysiol 90: 3352-3360. pdf
Blaine JT, Taylor AD and Ribera AB (2004) The carboxyl tail region of the Kv2.2 subunit mediates novel developmental regulation of channel density. 92: 3446-3454. pdf (Perspectives and Highlights)
Pineda RH, Ribera AB (2008) Dorsal-Ventral Gradient for Neuronal Plasticity in the Embryonic Spinal Cord. J Neurosci 28: 3824-3834. pdf
Gravagna NG, Knoeckel CS, Taylor AD, Hultgren B, Ribera AB (2008) Localization of Kv2.2 protein in Xenopus laevis embryos and tadpoles. J Comp Neur 510: 508-524. pdf
Pineda RH, Knoeckel CS, Taylor AD, Estrada-Bernal A, Ribera AB (2008) Kv1 potassium channel complexes in vivo require Kvβ2 subunits and drive developmental changes in potassium current in dorsal spinal neurons. J Neurophysiol 100: 2125-2136. pdf
Electrical excitability in wild type and mutant zebrafish (Danio rerio).
Forward genetic strategies uncover genes with irreplaceable functions. Because ion channel activity is developmentally-regulated and essential for generation of organismal behavior, zebrafish motility mutants in which specific behaviors fail to appear may exhibit abnormal developmental expression/function of ion channels. For example, one group of mutants does not respond to touch, although these embryos are motile and can swim (Granato et al., 1996). The specific behavioral phenotype suggests that the defect may originate in mechanosensory Rohon-Beard (RB) neurons. In wildtype embryos, the action potential of RB cells undergoes developmental regulation while the embryo acquires touch sensitivity. The changes in action potential waveform are due to underlying changes in voltage-gated sodium (INa) and potassium currents (Ribera and Nüsslein-Volhard, 1998). The INa of RB cells of the mao touch-insensitive mutant have reduced amplitudes and action potentials are not generated. Further, although the normal developmental changes in potassium current occur, upregulation of INa is absent. These data suggest that developmental regulation of RB INa may underlie stage-specific acquisition of touch sensitivity. We will identify functional, pharmacological and molecular properties of RB INa that are developmentally regulated. In addition, our preliminary data indicate that RB cells of mao mutants exhibit abnormal morphology. Accordingly, we will quantify differences in RB morphology of touch-insensitive and touch-sensitive fish to assess possible contributions of changes in peripheral innervation and central projections to normal developmental acquisition of touch sensitivity. We have recently found that activity of RB cells regulates their programmed cell death. A combination of genetic, molecular, anatomical and physiological methods will be used in these studies.
In related work, we have collaborated with Dr. Winfried Denk (MPI Heidelberg) to examine the appearance of spontaneous calcium transients in the developing zebrafish embryo (/physiology/abr2/movie.htm). Future work will test the possibility that these spontaneous evens influence subsequent development of spinal neurons.
Over the long-term, the studies will provide a framework for analysis of other behavioral mutants and identification of ion channels with essential functions during embryonic development of the nervous system and emergence of stage-specific behaviors.
Ribera, A.B. and Nüsslein-Volhard, C. (1998) Zebrafish touch-insensitive mutants reveal an essential role for developmental regulation of sodium current. J. Neurosci. 18:9181-9191. pdf
Svoboda, K.R., Linares, A.E., and Ribera, A.B. (2001) Activity regulates programmed cell death of zebrafish Rohon-Beard neurons. Development 128(18):3511-3520. pdf
Novak AE and Ribera AB. (2003) Immunocytochemistry as a tool for zebrafish developmental neurobiology. Methods Cell Sci 25: 79-83. pdf
Pineda, RH, Heiser RA and Ribera AB (2005) Molecular determinants of INa in vivo in embryonic zebrafishsensory neurons. J Neurophysiol 93: 3582-3593. pdf
Novak AE, Jost MC, Lu Y, Taylor AD, Zakon HH and Ribera AB (2006) Gene duplications and evolution of vertebrate voltage-gated sodium channels. J Mol Evol 63:208-221. pdf
Novak AE, Taylor AD, Pineda RH, Lasda EL, Wright MA and Ribera AB (2006) Embryonic and larval expression of zebrafish voltage-gated sodium channel a-subunit genes. Dev Dyn 235: 1962-1973. pdf
Pineda RH, Svoboda KR, Wright MA, Wright MA, Taylor AD, Novak AE, Gamse J, Eisen JS and Ribera AB. (2006) Knock-down of Nav1.6a sodium channels affects zebrafish motor neuron development. Development 133: 3827-3836. pdf
Yonkers MA, Ribera AB (2008) Sensory neuron sodium current requires nongenomic actions of thyroid hormone during development. J Neurophysiol 100: 2719-2725 pdf
Fein AJ, Wright MA, Slat EA, Ribera AB, Isom LL (2008) scn1bb, a zebrafish ortholog of SCN1B expressed in excitable and nonexcitable cells, affects motor neuron axon morphology and touch sensitivity. J Neurosci 28: 12510-12522. pdf
PubMed search (Ribera AB)