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Musk Expressed in the Brain Mediates Cholinergic Responses, Synaptic Plasticity, and Memory Formation

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Musk Expressed in the Brain Mediates Cholinergic Responses, Synaptic Plasticity, and Memory Formation The Journal of Neuroscience, July 26, 2006 • 26(30):7919–7932 • 7919 Behavioral/Systems/Cognitive MuSK Expressed in the Brain Mediates Cholinergic Responses, Synaptic Plasticity, and Memory Formation Ana Garcia-Osta,1 Panayiotis Tsokas,3* Gabriella Pollonini,1* Emmanuel M. Landau,2,3,4 Robert Blitzer,3 and Cristina M. Alberini1,2 Departments of 1Neuroscience, 2Psychiatry, and 3Pharmacology, Mount Sinai School of Medicine, New York, New York 10029, and 4Psychiatry Service, Bronx Veterans Affairs Medical Center, Bronx, New York 10468 Muscle-specific tyrosine kinase receptor (MuSK) has been believed to be mainly expressed and functional in muscle, in which it mediates the formation of neuromuscular junctions. Here we show that MuSK is expressed in the brain, particularly in neurons, as well as in non-neuronal tissues. We also provide evidence that MuSK expression in the hippocampus is required for memory consolidation, because temporally restricted knockdown after training impairs memory retention. Hippocampal disruption of MuSK also prevents the learning-dependent induction of both cAMP response element binding protein (CREB) phosphorylation and CCAAT enhancer binding protein ␤ (C/EBP␤) expression, suggesting that the role of MuSK during memory consolidation critically involves the CREB–C/EBP pathway. Furthermore, we found that MuSK also plays an important role in mediating hippocampal oscillatory activity in the theta frequency as well as in the induction and maintenance of long-term potentiation, two synaptic responses that correlate with memory formation. We conclude that MuSK plays an important role in brain functions, including memory formation. Therefore, its expression and role are broader than what was believed previously. Key words: MuSK; brain; long-term plasticity; memory; oscillatory response; C/EBP Introduction This function requires the interaction of MuSK with the heparan- Muscle-specific tyrosine kinase receptor (MuSK) is a receptor sulfate proteoglycan agrin and additional proteins, which include tyrosine kinase first discovered in the Torpedo electric organ (Jen- rapsyn and other unknown components. Together these proteins nings et al., 1993) and subsequently cloned in rat, human (Valen- form the agrin receptor complex (DeChiara et al., 1996; Sanes zuela et al., 1995), mouse (Ganju et al., 1995), Xenopus (Fu et al., and Lichtman, 1999; Hoch, 2003). In muscle, the activation of 1999), and chicken (Ip et al., 2000). Although some studies based MuSK via the ErbB–neuregulin pathway results in an increase of on Northern blot analyses and in situ hybridizations have re- AChR expression and triggers the activation of signaling path- ported that MuSK mRNA is present in both developing and adult ways that lead to postsynaptic differentiation (Sandrock et al., tissues of mouse, chicken, and Xenopus (Ganju et al., 1995; Fu et 1997; Burden, 2002). Both agrin and MuSK are essential for NMJ al., 1999; Ip et al., 2000), it has been generally accepted that this formation and specifically for AChR organization at the NMJs, receptor is mainly expressed and functional only in muscle, in because knock-out mice of agrin or MuSK do not form neuro- which it plays an essential role in neuromuscular junction (NMJ) muscular synapses, lack AChRs clustering, and die soon after formation (DeChiara et al., 1996; Sanes and Lichtman, 1999). birth (DeChiara et al., 1996; Gautam et al., 1996). Agrin is ex- Recently, however, MuSK has been reported to also be expressed pressed in several tissues, including the CNS, in which it partici- in sperm (Kumar et al., 2006). pates in synapse formation (Hoch et al., 1993; Stone and Nikolics, At the NMJ, MuSK is critically involved in redistributing the 1995; Ferreira, 1999; Smith and Hilgenberg, 2002). Despite agrin acetylcholine receptors (AChRs) in the postsynaptic apparatus. isoforms with high AChR aggregating activity being widespread throughout the brain, their receptor complex has not yet been Received April 19, 2006; revised June 15, 2006; accepted June 16, 2006. identified (Smith and Hilgenberg, 2002). This work was supported by National Institute of Mental Health Grant R01 MH65635 (C.M.A.) and by the Hirschl In the brain, synaptogenesis and remodeling of existing syn- TrustFoundation.A.G.-O.receivedaFulbrightpostdoctoralfellowship.WethankStevenBurden(SkirballInstituteof apses are abundant throughout development but also occur in BiomolecularMedicine,NewYorkUniversity,NewYork,NY)forgenerouslyprovidingtheratMuSK-myctransfected adulthood after injury and during long-term synaptic plasticity- HEK293 cell line and helpful discussions; Ambion Inc. (Austin, Texas), Nitin Puri, and Chris Echeverri for generously associated functions, including memory formation (Scheff et al., providing the siRNAs; Deanna Benson for teaching us the HNC technique; Khatuna Gagnidze, Maria Milekic, Sophie Tronel, Bridget Vicinski, Anne Rocher, and Jose Moron-Concepcion for technical help; Kelsey Martin (University of 2005; Waites et al., 2005). California,LosAngeles,CA)andStephenTaubenfeldfortheircommentsonthismanuscript;andReginaldMillerand New memories become stable through a process known as the Center for Comparative Medicine and Surgery facility of Mount Sinai for technical support. consolidation, which requires the activation of a cascade of gene *P.T. and G.P. contributed equally to this work. expression that critically involves the cAMP response element CorrespondenceshouldbeaddressedtoCristinaM.Alberini,DepartmentofNeuroscience,Box1065,MountSinai School of Medicine, New York, NY 10029. E-mail: [email protected]. binding protein (CREB) and CCAAT enhancer binding protein DOI:10.1523/JNEUROSCI.1674-06.2006 (C/EBP) transcription factors (Alberini, 1999) and is accompa- Copyright © 2006 Society for Neuroscience 0270-6474/06/267919-14$15.00/0 nied by modifications of synaptic structure and/or number 7920 • J. Neurosci., July 26, 2006 • 26(30):7919–7932 Garcia-Osta et al. • MuSK Expression and Function in the Brain (Bailey et al., 1996; O’Connell et al., 2000; Geinisman et al., 2001). were washed with PBS-diethyl pyrocarbonate (DEPC), permeabilized These synaptic changes are regulated by modulatory neurotrans- with 0.5% Triton X-100, and incubated twice for 10 min in PBS contain- mitter, hormonal, or neurohumoral systems (Power et al., 2000; ing 0.1% active DEPC. The cells were then equilibrated twice for 10 min ϫ Izquierdo and McGaugh, 2000), which include, among others, in 2 SSC. Prehybridization was performed at 56°C for 1 h with the ϫ the nicotinic cholinergic system (Gold, 2003; Hogg et al., 2003). hybridization buffer containing 50% formamide, 5 SSC, 2% blocking reagent (Roche Diagnostics), and 40 ␮g/ml salmon sperm DNA. Following up on the findings that MuSK had been detected in Twenty-micrometer rat brain tissue sections were obtained with a cryo- developing and adult tissues other than muscle (Ganju et al., stat after perfusion with 4% PFA in PBS. Sections were mounted on slides 1995; Fu et al., 1999; Ip et al., 2000) and that agrin is present in the and postfixed with 4% PFA-DEPC for 15 min at RT. After rinsing with CNS (Smith and Hilgenberg, 2002), we investigated the expres- PBS-DEPC, sections were treated with 0.2 M HCl for 10 min and perme- sion and the functional role of MuSK in the brain. abilized with 0.5% Triton X-100 for 10 min at RT. Sections were finally equilibrated in 0.1 M triethanolamine (TEA) for 5 min and acetylated in Materials and Methods freshly prepared 0.25% acetic anhydrite in 0.1 M TEA for 10 min. Sense Animals. Adult male Long–Evans rats weighing between 200 and 250 g or and antisense riboprobes (200 ng/ml for cell cultures and 400 ng/ml for 21- to 28-d-old male Long–Evans rats were used, as specified in Results. tissue sections) were diluted in hybridization buffer, denatured at 75°C Animals were individually housed and maintained on a 12 h light/dark for 10 min, and incubated with either HNCs or brain sections overnight cycle. The behavioral experiments were performed during the light cycle. at 56°C. The next day, the samples were rinsed with 2ϫ SSC twice for 10 All rats were allowed ad libitum access to food and water. All protocols min at RT, treated with RNase A (20 ␮g/ml) for 30 min at 37°C, and complied with the National Institutes of Health Guide for the Care and washed sequentially with 2ϫ SSC for 30 min at RT, 2ϫ SSCfor1hat Use of Laboratory Animals and were approved by the Mt. Sinai School of 65°C, and 0.1ϫ SSCfor1hat65°C. After rinsing with Tris-NaCl buffer Medicine Animal Care Committees. (100 mM Tris, 150 mM NaCl), the samples were incubated with blocking DNA amplifications. Total RNA was isolated with TRIzol (Invitrogen, buffer [1% blocking reagent (Roche Diagnostics) and 0.05% Tween 20 in Carlsbad, CA), and reverse transcription was performed using oligo-dT. Tris-NaCl buffer] for 30 min at 37°C. The hybridization was detected Five sets of primers were designed based on the sequence of rat muscle using AP-conjugated anti-DIG antibody (Roche Diagnostics) diluted in MuSK (GenBank accession number U34985) and used for PCR amplifi- blocking buffer at a final concentration of 1:200 and added to cells for 3 h cations. Primers were as follows: starting from the 5Ј end of MuSK se- at RT. The reaction was revealed by nitroblue tetrazolium/5-bromo-4- quence, forward (F) 1, 5Ј-TTACAGATGCTCACCCTGGT-3Ј; reverse chloro-indolyl-phosphate solution (Roche Diagnostics) diluted in 0.1 M (R) 1, 5Ј-CTTAATCCAGGACACGGATGG-3Ј; F2, 5Ј-CAAGCCATC- Tris pH 9.5/0.1 M NaCl containing
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