title: Developmental homeostasis of mouse retinocollicular synapses.
abstract: Spontaneous retinal waves during development are thought to provide an instructive signal for precise retinotopic mapping by correlating the activity of neighboring retinal ganglion cells. In mutant mice (beta2-/-) that lack correlated waves, retinocollicular map refinement is impaired. In vivo recordings reveal that neurons in the superior colliculus of beta2-/- mice have large receptive fields and low peak visual responses, resulting in a conservation of total integrated response. We find that this "response homeostasis" is maintained on a cell-by-cell basis, and argue that it does not depend on regulation from the visual cortex during adulthood. Instead, in vitro recordings show that homeostasis arises from the conservation of total synaptic input from the retina, and that it is maintained via different mechanisms over development. In the absence of correlated retinal waves, beta2-/- neurons sample a larger number of weaker retinal inputs relative to controls after the first postnatal week. Once retinal waves are restored, developmental learning rules and homeostasis drive refinement so that fewer, stronger synapses are retained, as in wild-type mice, but from a larger retinal area. Homeostasis in neurons has been shown previously to regulate the gain of synaptic transmission in response to perturbations of activity. Our results suggest that during the development of sensory maps, a unique consequence of homeostatic mechanisms is the precise shaping of neuronal receptive fields in conjunction with activity-dependent competition.
authors.affiliation: Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: Anand R
authors.initials: AR
authors.lastname: Chandrasekaran
authors.forename: Ruchir D
authors.initials: RD
authors.lastname: Shah
authors.forename: Michael C
authors.initials: MC
authors.lastname: Crair
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001931:Brain Mapping; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D006706:Homeostasis / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008954:Models, Biological; D016202:N-Methylaspartate / Q000494:pharmacology; D009474:Neurons / Q000166:cytology / Q000187:drug effects; D011978:Receptors, Nicotinic / Q000172:deficiency; D012160:Retina / Q000502:physiology*; D013477:Superior Colliculi / Q000166:cytology* / Q000254:growth & development*; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D014793:Visual Cortex / Q000502:physiology; D014795:Visual Pathways / Q000502:physiology*; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology
chemical_list: D018690:Excitatory Amino Acid Agonists; D016202:N-Methylaspartate; D011978:Receptors, Nicotinic; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid