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The Journal of Neuroscience, December 15, 2001, 21(24):9724-9732

Experience-Dependent Plasticity of Mouse Visual Cortex in the Absence of the Neuronal Activity-Dependent Marker egr1/zif268

Nobuko Mataga¹, Sayaka Fujishima¹, Brian G. Condie², and Takao K. Hensch¹

¹ Laboratory for Neuronal Circuit Development, Brain Science Institute, RIKEN, 351-0198 Japan, and ² Departments of Medicine and Cellular Biology and Anatomy, Institute for Molecular Medicine and Genetics, Medical College of Georgia, Augusta, Georgia 30912

Neuronal activity elicits a rapid increase in the expression of several immediate early genes (IEGs). To clarify a role for IEG response in activity-dependent development, we examined the contribution of the egr1/zif268 gene during visual cortical processing and plasticity in mice. We first analyzed the expression of egr1 mRNA in wild-type (WT) mice using Northern blot hybridization. In the visual cortex, expression of egr1 mRNA increased dramatically after eye opening, systemic injection of kainate, or 30 min of photostimulation after a brief (5 d) period of dark adaptation. Thus, the expression of egr1 is regulated by synaptic activity in the mouse visual cortex, as it is in other species (e.g., monkeys, cats, and rats).

To evaluate whether this transcription factor is directly involved in activity-dependent plasticity, mice lacking Egr1 were deprived of the use of one eye during the developmental critical period [postnatal day 24 (P24)-P34]. Extracellular in vivo single-unit recordings from the binocular zone of the visual cortex revealed that visual responses developed normally in egr1 knock-out (KO) mice. Moreover, a similarly significant shift of responsiveness in favor of the open eye was produced in both KO and WT mice by either brief (4 d) or long-term (>2 weeks) occlusion of one eye. There was no apparent compensation among egr2, egr3, or c-fos mRNA and protein expression in the visual cortex of egr1 KO mice.

Taken together, these results indicate that egr1 is a useful marker of sensory input in mice but is not intrinsically necessary for the experience-dependent plasticity of the visual cortex. Our findings underscore a mechanistic distinction between sensory plasticity and long-lasting forms of synaptic potentiation in the hippocampus, for which egr1/zif268 was recently found to be essential.

Key words: immediate early gene; transcription factor; monocular deprivation; ocular dominance; development; activity-dependent plasticity

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21249724-09$05.00/0

This article has been cited by other articles:

				C. M. Alberini Transcription Factors in Long-Term Memory and Synaptic Plasticity Physiol Rev, January 1, 2009; 89(1): 121 - 145. [Abstract] [Full Text] [PDF]

				M. Sato and M. P. Stryker Distinctive Features of Adult Ocular Dominance Plasticity J. Neurosci., October 8, 2008; 28(41): 10278 - 10286. [Abstract] [Full Text] [PDF]

				H. Miyamoto and T. K. Hensch Reciprocal Interaction of Sleep and Synaptic Plasticity Mol. Interv., October 1, 2003; 3(7): 404 - 417. [Abstract] [Full Text] [PDF]

				M. Fagiolini, H. Katagiri, H. Miyamoto, H. Mori, S. G. N. Grant, M. Mishina, and T. K. Hensch Separable features of visual cortical plasticity revealed by N-methyl-D-aspartate receptor 2A signaling PNAS, March 4, 2003; 100(5): 2854 - 2859. [Abstract] [Full Text] [PDF]

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				N. Mataga, N. Nagai, and T. K. Hensch Permissive proteolytic activity for visual cortical plasticity PNAS, May 28, 2002; 99(11): 7717 - 7721. [Abstract] [Full Text] [PDF]

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