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Age at developmental cortical injury differentially alters corpus callosum volume in the rat.

Age at developmental cortical injury differentially alters corpus callosum volume in the rat. Research Abstract Details 

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  • Age at developmental cortical injury differentially alters corpus callosum volume in the rat. Abstract Text:

    steven w threlkeldSteven W Threlkeld,glenn d rosenGlenn D Rosen,r holly fitchR Holly Fitch,

    BACKGROUND: Freezing lesions to developing rat cortex induced between postnatal day (P) one and three (P1 - 3) lead to malformations similar to human microgyria, and further correspond to reductions in brain weight and cortical volume. In contrast, comparable lesions on P5 do not produce microgyric malformations, nor the changes in brain weight seen with microgyria. However, injury occurring at all three ages does lead to rapid auditory processing deficits as measured in the juvenile period. Interestingly, these deficits persist into adulthood only in the P1 lesion case 1. Given prior evidence that early focal cortical lesions induce abnormalities in cortical morphology and connectivity 1234, we hypothesized that the differential behavioral effects of focal cortical lesions on P1, P3 or P5 may be associated with underlying neuroanatomical changes that are sensitive to timing of injury. Clinical studies indicate that humans with perinatal brain injury often show regional reductions in corpus callosum size and abnormal symmetry, which frequently correspond to learning impairments 567. Therefore, in the current study the brains of P1, 3 or 5 lesion rats, previously evaluated for brain weight, and cortical volume changes and auditory processing impairments (P21-90), were further analyzed for changes in corpus callosum volume. RESULTS: Results showed a significant main effect of Treatment on corpus callosum volume [F (1,57) = 10.2, P < .01], with lesion subjects showing significantly smaller callosal volumes as compared to shams. An Age at Treatment x Treatment interaction [F(2,57) = 3.2, P < .05], indicated that corpus callosum size decreased as the age of injury decreased from P5 to P1. Simple effects analysis showed significant differences between P1 and P3 [F(1,28) = 8.7, P < .01], and P1 and P5 [F(1,28) = 15.1, P < .001], subjects. Rats with P1 injury resulting in microgyria had the greatest reduction in corpus callosum volume (22% reduction), followed by the P3 group (11% reduction), which showed a significant reduction in corpus callosum volume compared to shams [F(1,31) = 5.9, P < .05]. Finally, the P5 lesion group did not significantly differ from the sham subjects in callosal volume. CONCLUSION: Decrements in corpus callosum volume in the P1 and 3 lesion groups are consistent with the reductions in brain weight and cortical volume previously reported for microgyric rats 18. Current results suggest that disruption to the cortical plate during early postnatal development may lead to more widely dispersed neurovolumetric anomalies and subsequent behavioral impairments 1, compared with injury that occurs later in development. Further, these results suggest that in a human clinical setting decreased corpus callosum volume may represent an additional marker for long-term behavioral outcome.

    Age at developmental cortical injury differentially alters corpus callosum volume in the rat. Publishing Authors By Initials

    sw threlkeldSW Threlkeld,gd rosenGD Rosen,rh fitchRH Fitch,

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    Age at developmental cortical injury differentially alters corpus callosum volume in the rat. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: BMC neuroscience

    VOLUME: 8

    Page Numbers: 94

    Journal Abbreviation:

    ISSN: 1471-2202

    DAY: 12

    MONTH: 11

    YEAR: 2007

    Age at developmental cortical injury differentially alters corpus callosum volume in the rat. Information

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    LANGUAGE: eng

    NlmUniqueID: 100966986

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    AFFILIATION: Department of Psychology, Behavioral Neuroscience Division, University of Connecticut, 806 Babbidge Road, Storrs, CT 06269-4154, USA. Steven.Threlkeld@uconn.edu

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NICHD

    GRANT: HD20806

    ACRONYM: HD

    MEDLINETA: BMC Neurosci

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