| Title | Direction-specific disruption of subcortical visual behavior and receptive fields in mice lacking the beta2 subunit of nicotinic acetylcholine receptor. | | Author(s) | Wang L, Rangarajan KV, Lawhn-Heath CA, Sarnaik R, Wang BS, Liu X, Cang J | | Institution | Department of Neurobiology and Physiology and Interdepartmental Neuroscience Program, Northwestern University, Evanston, Illinois 60208, USA. | | Source | J Neurosci 2009 Oct 14; 29(41):12909-18. | | MeSH | Analysis of Variance
Animals
Brain Mapping
Disease Models, Animal
Evoked Potentials, Visual
Head Movements
Mice
Mice, Inbred C57BL
Mice, Knockout
Nystagmus, Optokinetic
Orientation
Perceptual Disorders
Photic Stimulation
Receptors, Nicotinic
Sensory Receptor Cells
Space Perception
Superior Colliculi
Visual Cortex
Visual Fields
Visual Pathways
| | Abstract | Retinotopic mapping is a basic feature of visual system organization, but its role in processing visual information is unknown. Mutant mice lacking the beta2 subunit of nicotinic acetylcholine receptor have imprecise maps in both visual cortex (V1) and the superior colliculus (SC) due to the disruption of spontaneous retinal activity during development. Here, we use behavioral and physiological approaches to study their visual functions. We find that beta2-/- mice fail to track visual stimuli moving along the nasotemporal axis in a subcortical optomotor behavior, but track normally along the dorsoventral axis. In contrast, these mice display normal acuity along both axes in the visual water task, a behavioral test of cortical functions. Consistent with the behavioral results, we find that V1 neurons in beta2-/- mice have normal response properties, while SC neurons have disrupted receptive fields, including enlarged structure and decreased direction and orientation selectivity along the nasotemporal axis. The subcortical-specific deficits indicate that retinotopic map disruption has different impacts on the development of functional properties in V1 and the SC. | | Language | eng | | Pub Type(s) | Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
| | PubMed ID | 19828805 |
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