title: Neural activity and branching of embryonic retinal ganglion cell dendrites.
abstract: The shape of a neuron's dendritic arbor is critical for its function as it determines the number of inputs the neuron can receive and how those inputs are processed. During development, a neuron initiates primary dendrites that branch to form a simple arbor. Subsequently, growth occurs by a process that combines the extension and retraction of existing dendrites, and the addition of new branches. The loss and addition of the fine terminal branches of retinal ganglion cells (RGCs) is dependent on afferent inputs from its synaptic partners, the amacrine and bipolar cells. It is unknown, however, whether neural activity regulates the initiation of primary dendrites and their initial branching. To investigate this, Xenopus laevis RGCs developing in vivo were made to express either a delayed rectifier type voltage-gated potassium (KV) channel, Xenopus Kv1.1, or a human inward rectifying channel, Kir2.1, shown previously to modulate the electrical activity of Xenopus spinal cord neurons. Misexpression of either potassium channel increased the number of branch points and the total length of all the branches. As a result, the total dendritic arbor was bigger than for control green fluorescent protein-expressing RGCs and those ectopically expressing a highly related mutant non-functional Kv1.1 channel. Our data indicate that membrane excitability regulates the earliest differentiation of RGC dendritic arbors.
authors.affiliation: University of Calgary, Hotchkiss Brain Institute, NW Calgary, AB, Canada T2N 4N1. jhocking@ualberta.ca
authors.forename: J C
authors.initials: JC
authors.lastname: Hocking
authors.forename: N S
authors.initials: NS
authors.lastname: Pollock
authors.forename: J
authors.initials: J
authors.lastname: Johnston
authors.forename: R J A
authors.initials: RJ
authors.lastname: Wilson
authors.forename: A
authors.initials: A
authors.lastname: Shankar
authors.forename: S
authors.initials: S
authors.lastname: McFarlane
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D019521:Body Patterning / Q000187:drug effects; D055396:Bone Morphogenetic Protein 2 / Q000494:pharmacology; D015220:Calcium Channels; D003712:Dendrites / Q000187:drug effects / Q000378:metabolism*; D004625:Embryo, Nonmammalian / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D049452:Green Fluorescent Proteins / Q000378:metabolism; D006801:Humans; D011188:Potassium / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D014982:Xenopus laevis / Q000196:embryology* / Q000235:genetics
chemical_list: D055396:Bone Morphogenetic Protein 2; D015220:Calcium Channels; D015221:Potassium Channels; D016760:Proto-Oncogene Proteins c-fos; D049452:Green Fluorescent Proteins; D011188:Potassium