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The Journal of Neuroscience, February 22, 2006, 26(8):2184-2196; doi:10.1523/JNEUROSCI.4437-05.2006

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Behavioral/Systems/Cognitive
Behavioral and Neurochemical Alterations in Mice Lacking the RNA-Binding Protein Translin

Joel M. Stein,¹ Wayland Bergman,² Yanshan Fang,¹ LaKesha Davison,¹ Colleen Brensinger,³ Michael B. Robinson,² Norman B. Hecht,⁴ and Ted Abel¹

¹Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, ²Departments of Pediatrics and Pharmacology, Children’s Hospital of Philadelphia, University of Pennsylvania, Philadelphia, Pennsylvania 19104, and Centers for ³Clinical Epidemiology and Biostatistics and ⁴Research on Reproduction and Women’s Health, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Correspondence should be addressed to Ted Abel, Department of Biology, University of Pennsylvania, 319 Leidy Labs, 38th and Hamilton Walk, Philadelphia, PA 19104. Email: abele{at}sas.upenn.edu

Synapse-specific local protein synthesis is thought to be important for neurodevelopment and plasticity and involves neuronal RNA-binding proteins that regulate the transport and translation of dendritically localized transcripts. The best characterized of these RNA-binding proteins is the fragile X mental retardation protein (FMRP). Mutations affecting the expression or function of FMRP cause fragile X syndrome in humans, and targeted deletion of the gene encoding FMRP results in developmental and behavioral alterations in mice. Translin is an RNA-binding protein that regulates mRNA transport and translation in mouse male germ cells and is proposed to play a similar role in neurons. Like FMRP, translin is present in neuronal dendrites, binds dendritically localized RNA, and associates with microtubules and motor proteins. We reported previously the production of viable homozygous translin knock-out mice, which demonstrate altered expression of multiple mRNA transcripts in the brain and mild motor impairments. Here, we report that translin knock-out mice also exhibit sex-specific differences in tests of learning and memory, locomotor activity, anxiety-related behavior, and sensorimotor gating, as well as handling-induced seizures and alterations in monoamine neurotransmitter levels in several forebrain regions. Similar behavioral and neurochemical alterations have been observed in mice lacking FMRP, suggesting that both proteins may act within the same neuronal systems and signaling pathways. Our results in mice indicate that mutations in translin may contribute to fragile X-like syndromes, mental retardation, attention deficit hyperactivity disorder, epilepsy, and autism spectrum disorders in humans.

Key words: anxiety; attention; RNA trafficking; local translation; fragile X syndrome; norepinephrine

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Received Oct. 18, 2005; revised Dec. 19, 2005; accepted Jan. 12, 2006.

Correspondence should be addressed to Ted Abel, Department of Biology, University of Pennsylvania, 319 Leidy Labs, 38th and Hamilton Walk, Philadelphia, PA 19104. Email: abele{at}sas.upenn.edu

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