Extended plasticity of visual cortex in dark-reared animals may result from prolonged expression of cpg15-like genes.
cpg15 is an activity-regulated gene that encodes a membrane-bound ligand that coordinately regulates growth of apposing dendritic and axonal arbors and the maturation of their synapses. These properties make it an attractive candidate for participating in plasticity of the mammalian visual system. Here we compare cpg15 expression during normal development of the rat visual system with that seen in response to dark rearing, monocular blockade of retinal action potentials, or monocular deprivation. Our results show that the onset of cpg15 expression in the visual cortex is coincident with eye opening, and it increases until the peak of the critical period at postnatal day 28 (P28). This early expression is independent of both retinal activity and visual experience. After P28, a component of cpg15 expression in the visual cortex, lateral geniculate nucleus (LGN), and superior colliculus (SC) develops a progressively stronger dependence on retinally driven action potentials. Dark rearing does not affect cpg15 mRNA expression in the LGN and SC at any age, but it does significantly affect its expression in the visual cortex from the peak of the critical period and into adulthood. In dark-reared rats, the peak level of cpg15 expression in the visual cortex at P28 is lower than in controls. Rather than showing the normal decline with maturation, these levels are maintained in dark-reared animals. We suggest that the prolonged plasticity in the visual cortex that is seen in dark-reared animals may result from failure to downregulate genes such as cpg15 that could promote structural remodeling and synaptic maturation.
Lee
Wei-Chung Allen
WC
Center for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Nedivi
Elly
E
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003423:Critical Period, Psychological; D003624:Darkness; D015536:Down-Regulation; D004343:Drug Implants; D005123:Eye / Q000187:drug effects; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D017403:In Situ Hybridization; D008024:Ligands; D008027:Light; D008565:Membrane Proteins / Q000096:biosynthesis* / Q000235:genetics; D009419:Nerve Tissue Proteins; D009473:Neuronal Plasticity / Q000502:physiology* / Q000528:radiation effects; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D051381:Rats; D011921:Rats, Inbred WKY; D012160:Retina / Q000187:drug effects / Q000502:physiology; D012683:Sensory Deprivation / Q000502:physiology; D013779:Tetrodotoxin / Q000008:administration & dosage; D014785:Vision, Ocular / Q000187:drug effects / Q000502:physiology; D014793:Visual Cortex / Q000166:cytology / Q000254:growth & development / Q000502:physiology*
C114622:Cpg15 protein, rat; D004343:Drug Implants; D008024:Ligands; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D013779:Tetrodotoxin