| Reference code: | PT/FB/BL-2012-192.07 |
| Location: | Arquivo PCA - Pasta 15/2012
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Title:
| Foxp2 function in the adult brain
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| Publication year: | 2015
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URL:
| http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=2c9efb03-eec2-435f-a2a2-8a7986b29cee&cKey=bafafdf0-1140-4af2-a429-ac6e288933ce&mKey=d0ff4555-8574-4fbb-b9d4-04eec8ba0c84
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| Abstract/Results: | ABSTRACT:
Disruptions of the FOXP2 gene cause a rare speech and language disorder. In the KE family a heterozygous FOXP2 mutation is dominantly inherited and affected individuals have difficulty producing the sequences of orofacial motor movements necessary for fluent speech. This is considered a core deficit of the disorder, although other expressive and receptive language problems also exist. The FOXP2 transcription factor is expressed in cortico-striatal/ -cerebellar circuits required for sensorimotor integration and motor-skill learning, and imaging studies have identified structural abnormalities in several of these regions in affected KE-family members. FOXP2 is also highly conserved in a number of other vertebrate species, where expression is seen during development and in adulthood. Mice carrying the KE-family mutation have motor-skill learning deficits and lack striatal long-term depression. They also have abnormally high striatal activity in vivo which is aberrantly modulated during the learning of a motor task. Juvenile zebra finches show increased FoxP2 expression during the song learning period in striatal nucleus Area X, and FoxP2 knockdown in this region results in inaccurate and incomplete song imitation. More recently, FoxP2 knockdown in Area X of mature birds was shown to render song more variable and abolished the mediation of song by social context, implicating FoxP2 in adult as well as developmental neural function. We used a conditional Foxp2 line and a tamoxifen-inducible Cre (CAGGS-CreER) to disrupt Foxp2 globally in adult mice. Tamoxifen was administered at 10 weeks of age and substantial Foxp2 deletion was seen 60 days thereafter. Around one third of Foxp2-flox/flox; CAGGS-Cre animals died, with the first deaths occurring 6 weeks after tamoxifen administration. Surviving animals appeared healthy and their performance was indistinguishable from that of littermate controls on the accelerating rotarod. An operant lever-pressing task was used to examine motor-sequence learning in detail in the surviving group. In this task mice must complete 8 lever presses to trigger the release of a sucrose reinforcer. Initially the task is self-paced, but after 12 days of training a time constraint is added and the 8 presses must be completed at increasingly high speeds. Foxp2-flox/flox; CAGGS-Cre mice were able to learn the lever-pressing skill but rates of reinforcer delivery and lever pressing were reduced during both phases of training. Results are compared and contrasted with those from mice carrying aetiological and region-specific Foxp2 disruptions.
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| Accessibility: | Document does not exist in file
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Language:
| eng
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Author:
| French, C.
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Secondary author(s):
| Correia, M., Fisher, S. E., Costa, R. M.
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Document type:
| Online abstract
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Number of reproductions:
| 1
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Reference:
| French, C., Correia, M., Fisher, S. E., & Costa, R. M. (2015, October). Foxp2 function in the adult brain. Paper presented at the Society for Neuroscience Annual Meeting, Chicago, USA. Abstract retrieved from http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=2c9efb03-eec2-435f-a2a2-8a7986b29cee&cKey=bafafdf0-1140-4af2-a429-ac6e288933ce&mKey=d0ff4555-8574-4fbb-b9d4-04eec8ba0c84
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| Indexed document: | No
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| Keywords: | Adult Foxp2 inactivation / Speech and language / Motor-skill learning
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