title: CaV3.2 KO mice have altered retinal waves but normal direction selectivity.
abstract: Early in development, before the onset of vision, the retina establishes direction-selective responses. During this time period, the retina spontaneously generates bursts of action potentials that propagate across its extent. The precise spatial and temporal properties of these "retinal waves" have been implicated in the formation of retinal projections to the brain. However, their role in the development of direction selective circuits within the retina has not yet been determined. We addressed this issue by combining multielectrode array and cell-attached recordings to examine mice that lack the CaV3.2 subunit of T-type Ca2+ channels (CaV3.2 KO) because these mice exhibit disrupted waves during the period that direction selective circuits are established. We found that the spontaneous activity of these mice displays wave-associated bursts of action potentials that are altered from that of control mice: the frequency of these bursts is significantly decreased and the firing rate within each burst is reduced. Moreover, the projection patterns of the retina demonstrate decreased eye-specific segregation in the dorsal lateral geniculate nucleus (dLGN). However, after eye-opening, the direction selective responses of CaV3.2 KO direction selective ganglion cells (DSGCs) are indistinguishable from those of wild-type DSGCs. Our data indicate that although the temporal properties of the action potential bursts associated with retinal waves are important for activity-dependent refining of retinal projections to central targets, they are not critical for establishing direction selectivity in the retina.
authors: Department of Molecular and Cell Biology,University of California,Berkeley,Berkeley,California.
authors: Aaron M
authors: AM
authors: Hamby
authors: Department of Molecular and Cell Biology,University of California,Berkeley,Berkeley,California.
authors: Juliana M
authors: JM
authors: Rosa
authors: Department of Molecular and Cell Biology,University of California,Berkeley,Berkeley,California.
authors: Ching-Hsiu
authors: CH
authors: Hsu
authors: Department of Molecular and Cell Biology,University of California,Berkeley,Berkeley,California.
authors: Marla B
authors: MB
authors: Feller
mesh_terms: D000200:Action Potentials / Q000235:genetics*; D000818:Animals; D000831:Animals, Newborn; D020747:Calcium Channels, T-Type / Q000172:deficiency* / Q000235:genetics; D005829:Geniculate Bodies / Q000473:pathology; D066298:In Vitro Techniques; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009949:Orientation; D012160:Retina / Q000473:pathology* / Q000503:physiopathology*; D012165:Retinal Ganglion Cells / Q000473:pathology; D014786:Vision Disorders / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D014795:Visual Pathways / Q000502:physiology
chemical_list: C504883:Cacna1h protein, mouse; D020747:Calcium Channels, T-Type
keywords: Neurodevelopment