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Cited by 92

Early Postnatal Plasticity in Neocortex of Fmr1 Knockout Mice

Desai, Niraj S., Casimiro, Tanya M., Gruber, Stephen M., Vanderklish, Peter W.·2006·Journal of Neurophysiology
DOI 10.1152/jn.00221.2006
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Abstract

Fragile X syndrome is produced by a defect in a single X-linked gene, called Fmr1, and is characterized by abnormal dendritic spine morphologies with spines that are longer and thinner in neocortex than those from age-matched controls. Studies using Fmr1 knockout mice indicate that spine abnormalities are especially pronounced in the first month of life, suggesting that altered developmental plasticity underlies some of the behavioral phenotypes associated with the syndrome. To address this issue, we used intracellular recordings in neocortical slices from early postnatal mice to examine the effects of Fmr1 disruption on two forms of plasticity active during development. One of these, long-term potentiation of intrinsic excitability, is intrinsic in expression and requires mGluR5 activation. The other, spike timing-dependent plasticity, is synaptic in expression and requires N-methyl-d-aspartate receptor activation. While intrinsic plasticity was normal in the knockout mice, synaptic plasticity was altered in an unusual and striking way: long-term depression was robust but long-term potentiation was entirely absent. These findings underscore the ideas that Fmr1 has highly selective effects on plasticity and that abnormal postnatal development is an important component of the disorder.

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Crossref · 10.1152/jn.00221.2006

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  • Several forms of NMDA-receptor-dependent plasticity are impaired by loss of FMRP, including LTP in cortex and amygdala, increased threshold for spike-timing dependent plasticity, and altered ocular dominance plasticity.

    “Moreover, several forms of NMDA-receptor-dependent plasticity are impaired by loss of FMRP. LTP is abolished in cortex and amygdala (but not hippocampus), the threshold for spike-timing dependent plasticity is increased, and ocular dominance plasticity is altered (Desai et al., 2006; Dolen et al., 2007; Li et al., 2002; Meredith et al., 2007; Zhao et al., 2005).”

    From Regulation of Synaptic Structure and Function by FMRP-Associated MicroRNAs miR-125b and miR-132 (2010) · cites this paper as Desai et al., 2006

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Authors
Desai, N. S., Casimiro, T. M., Gruber, S. M., & Vanderklish, P. W.
Venue
Journal of Neurophysiology
Publisher
American Physiological Society
Published
2006-10
Volume
96
Issue
4
Pages
1734-1745
ISSN
  • 0022-3077
  • 1522-1598
DOI
10.1152/jn.00221.2006
Cited by
92
References
9
Language
en

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