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{"title"=>"An ancient duplication of exon 5 in the Snap25 gene is required for complex neuronal development/function", "type"=>"journal", "authors"=>[{"first_name"=>"Jenny U.", "last_name"=>"Johansson", "scopus_author_id"=>"57198175975"}, {"first_name"=>"Jesper", "last_name"=>"Ericsson", "scopus_author_id"=>"18433803300"}, {"first_name"=>"Juliette", "last_name"=>"Janson", "scopus_author_id"=>"7006351535"}, {"first_name"=>"Simret", "last_name"=>"Beraki", "scopus_author_id"=>"23481098400"}, {"first_name"=>"Davor", "last_name"=>"Stanić", "scopus_author_id"=>"6602739986"}, {"first_name"=>"Slavena A.", "last_name"=>"Mandic", "scopus_author_id"=>"6603558210"}, {"first_name"=>"Martin A.", "last_name"=>"Wikström", "scopus_author_id"=>"7102367772"}, {"first_name"=>"Tomas", "last_name"=>"Hökfelt", "scopus_author_id"=>"24499918300"}, {"first_name"=>"Sven Ove", "last_name"=>"Ögren", "scopus_author_id"=>"7102994628"}, {"first_name"=>"Björn", "last_name"=>"Rozell", "scopus_author_id"=>"7003700024"}, {"first_name"=>"Per Olof", "last_name"=>"Berggren", "scopus_author_id"=>"7101706643"}, {"first_name"=>"Christina", "last_name"=>"Bark", "scopus_author_id"=>"7004583679"}], "year"=>2008, "source"=>"PLoS Genetics", "identifiers"=>{"scopus"=>"2-s2.0-57149099976", "pmid"=>"19043548", "sgr"=>"57149099976", "doi"=>"10.1371/journal.pgen.1000278", "isbn"=>"1553-7404 (Electronic)\\n1553-7390 (Linking)", "issn"=>"15537390", "pui"=>"352773658"}, "id"=>"a2787584-ede0-3420-a532-f3c573103edb", "abstract"=>"Alternative splicing is an evolutionary innovation to create functionally diverse proteins from a limited number of genes. SNAP-25 plays a central role in neuroexocytosis by bridging synaptic vesicles to the plasma membrane during regulated exocytosis. The SNAP-25 polypeptide is encoded by a single copy gene, but in higher vertebrates a duplication of exon 5 has resulted in two mutually exclusive splice variants, SNAP-25a and SNAP-25b. To address a potential physiological difference between the two SNAP-25 proteins, we generated gene targeted SNAP-25b deficient mouse mutants by replacing the SNAP-25b specific exon with a second SNAP-25a equivalent. Elimination of SNAP-25b expression resulted in developmental defects, spontaneous seizures, and impaired short-term synaptic plasticity. In adult mutants, morphological changes in hippocampus and drastically altered neuropeptide expression were accompanied by severe impairment of spatial learning. We conclude that the ancient exon duplication in the Snap25 gene provides additional SNAP-25-function required for complex neuronal processes in higher eukaryotes.", "link"=>"http://www.mendeley.com/research/ancient-duplication-exon-5-snap25-gene-required-complex-neuronal-developmentfunction", "reader_count"=>51, "reader_count_by_academic_status"=>{"Unspecified"=>3, "Professor > Associate Professor"=>7, "Researcher"=>9, "Student > Doctoral Student"=>3, "Student > Ph. D. Student"=>12, "Student > Postgraduate"=>3, "Student > Master"=>3, "Other"=>1, "Student > Bachelor"=>5, "Professor"=>5}, "reader_count_by_user_role"=>{"Unspecified"=>3, "Professor > Associate Professor"=>7, "Researcher"=>9, "Student > Doctoral Student"=>3, "Student > Ph. D. Student"=>12, "Student > Postgraduate"=>3, "Student > Master"=>3, "Other"=>1, "Student > Bachelor"=>5, "Professor"=>5}, "reader_count_by_subject_area"=>{"Unspecified"=>4, "Biochemistry, Genetics and Molecular Biology"=>9, "Agricultural and Biological Sciences"=>22, "Medicine and Dentistry"=>7, "Neuroscience"=>4, "Pharmacology, Toxicology and Pharmaceutical Science"=>2, "Veterinary Science and Veterinary Medicine"=>1, "Psychology"=>2}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>7}, "Neuroscience"=>{"Neuroscience"=>4}, "Psychology"=>{"Psychology"=>2}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>22}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>9}, "Unspecified"=>{"Unspecified"=>4}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>2}, "Veterinary Science and Veterinary Medicine"=>{"Veterinary Science and Veterinary Medicine"=>1}}, "reader_count_by_country"=>{"Canada"=>1, "Sweden"=>1, "United States"=>2, "Japan"=>2, "Germany"=>1}, "group_count"=>4}

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• {"month"=>"10", "year"=>"2017", "pdf_views"=>"2", "xml_views"=>"1", "html_views"=>"23"}
• {"month"=>"11", "year"=>"2017", "pdf_views"=>"7", "xml_views"=>"0", "html_views"=>"24"}
• {"month"=>"12", "year"=>"2017", "pdf_views"=>"5", "xml_views"=>"0", "html_views"=>"26"}
• {"month"=>"1", "year"=>"2018", "pdf_views"=>"6", "xml_views"=>"1", "html_views"=>"17"}
• {"month"=>"2", "year"=>"2018", "pdf_views"=>"6", "xml_views"=>"0", "html_views"=>"3"}
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• {"month"=>"5", "year"=>"2018", "pdf_views"=>"5", "xml_views"=>"0", "html_views"=>"6"}
• {"month"=>"6", "year"=>"2018", "pdf_views"=>"4", "xml_views"=>"0", "html_views"=>"12"}
• {"month"=>"7", "year"=>"2018", "pdf_views"=>"1", "xml_views"=>"3", "html_views"=>"8"}
• {"month"=>"8", "year"=>"2018", "pdf_views"=>"3", "xml_views"=>"1", "html_views"=>"6"}
• {"month"=>"9", "year"=>"2018", "pdf_views"=>"5", "xml_views"=>"0", "html_views"=>"18"}
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• {"month"=>"1", "year"=>"2019", "pdf_views"=>"3", "xml_views"=>"0", "html_views"=>"7"}
• {"month"=>"2", "year"=>"2019", "pdf_views"=>"3", "xml_views"=>"0", "html_views"=>"8"}
• {"month"=>"3", "year"=>"2019", "pdf_views"=>"8", "xml_views"=>"1", "html_views"=>"4"}
• {"month"=>"4", "year"=>"2019", "pdf_views"=>"6", "xml_views"=>"0", "html_views"=>"7"}
• {"month"=>"5", "year"=>"2019", "pdf_views"=>"17", "xml_views"=>"0", "html_views"=>"13"}
• {"month"=>"6", "year"=>"2019", "pdf_views"=>"6", "xml_views"=>"0", "html_views"=>"5"}
• {"month"=>"7", "year"=>"2019", "pdf_views"=>"6", "xml_views"=>"0", "html_views"=>"6"}
• {"month"=>"8", "year"=>"2019", "pdf_views"=>"7", "xml_views"=>"0", "html_views"=>"2"}

Figshare

• {"files"=>["https://ndownloader.figshare.com/files/914999"], "description"=>"<p>(A) CCK-ir in HF of WT mice, shown at higher magnification in (E). In SNAP-25b deficient mice (B), CCK-ir disappears in PoDG and SLu, higher magnification in (F). (C) NPY-ir in WT HF, shown at higher magnification in (G). (D) Increased NPY-ir in PoDG, Mol, and SLu of SNAP-25b deficient (KO) mice, the latter at higher magnification in (H). Confocal micrographs of double-staining experiments taken from WT (I-K), and <i>neo</i>-excised SNAP-25b deficient (L) mice. CCK- (I) and SNAP-25-ir (J) in fibers/terminals of SLu in WT mice. Arrowheads in (J) point to strong SNAP-25⁺ fibers. (K) Double-staining of CCK- (green) and SNAP-25-ir (red) in WT SLu. (L) NPY-ir, lacking in fibers/terminals of WT SLu, is highly expressed in <i>neo</i>-excised SNAP-25b deficient mutants. In homozygous <i>neo</i>-excised SNAP-25b deficient mice, SNAP-25-ir fibers in SLu are often thicker (arrowheads in (L) compared to WT mice [(L) cf. (J,K)]. Insets in (K,L) show respective photomicrographs at higher magnification. (M) BDNF-ir in WT HF, the PoDG, and SLu shown at higher magnification in (O). (N) Increased BDNF-ir in PoDG and SLu of mutant mice, the DG shown at higher magnification in (P). (Q) Strong DCx⁺ cell bodies in SGZ of WT DG, shown at higher magnification in (S). (R) Increased number of cell bodies randomly distributed in SGZ and granular cell layer of <i>neo</i>-excised SNAP-25b deficient mutants, with higher levels of DCx⁺ fibers in Mol, shown at higher magnification in (T). Arrowheads in (T) point to DCx⁺ cell bodies in the granular cell layer. Cx, cortex; DG, dentate gyrus; LMol, lacunosum Mol; Mol, molecular layer of DG; Or, oriens layer of HF; PoDG, polymorph layer of DG; Py, pyramidal layer of HF; Rad, stratum radiatum of HF; SGrDG, supragranular layer of DG; SGZ, subgranular zone of DG; SLu, stratum lucidum of HF. Scale bars: (D = A–C = 500 µm), (H = E–G = 200 µm), (I = J–L = 50 µm), (K, inset = L inset = 10 µm), (M = N = 500 µm), (O = P = 200 µm), (Q = R = 100 µm), (S = T = 50 µm). WT (n = 2), SNAP-25b mutant mice (n = 2).</p>", "links"=>[], "tags"=>["dcx", "immunoreactivity", "hippocampal", "snap-25b", "deficient", "wt"], "article_id"=>585442, "categories"=>["Neuroscience", "Cell Biology", "Developmental Biology", "Physiology"], "users"=>["Jenny U. Johansson", "Jesper Ericsson", "Juliette Janson", "Simret Beraki", "Davor Stanić", "Slavena A. Mandic", "Martin A. Wikström", "Tomas Hökfelt", "Sven Ove Ögren", "Björn Rozell", "Per-Olof Berggren", "Christina Bark"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1000278.g006", "stats"=>{"downloads"=>1, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_SNAP_25_CCK_NPY_BDNF_and_DCx_Immunoreactivity_in_the_Hippocampal_Formation_of_Adult_Neo_excised_SNAP_25b_Deficient_and_WT_Mice_/585442", "title"=>"SNAP-25, CCK, NPY, BDNF, and DCx Immunoreactivity in the Hippocampal Formation of Adult <i>Neo</i>-excised SNAP-25b Deficient and WT Mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-11-28 01:30:42"}
• {"files"=>["https://ndownloader.figshare.com/files/914414"], "description"=>"<p>(A) A schematic diagram demonstrating the <i>in vivo</i> excision of the <i>Tkneo</i> gene. Heterozygous <i>neo-</i>containing SNAP-25b deficient females were mated with heterozygous Prm1Cre males. Male offspring carrying both the mutation in the <i>Snap25</i> gene and the Cre transgene were mated with B6 females. <i>In vivo</i> excision was demonstrated by PCR, and the Cre transgene was crossed out from the confirmed <i>neo-</i>excised SNAP-25b deficient mice. (B) To investigate total SNAP-25 mRNA levels in mouse brain of <i>neo-</i>excised SNAP-25b deficient mutants at PN14-15, the same radioactive semi-quantitative RT-PCR assay as for <i>neo-</i>containing mouse mutants (see <a href=\"http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000278#pgen-1000278-g001\" target=\"_blank\">Figure 1B</a>) was used. Total SNAP-25 mRNA levels (SNAP-25a + SNAP-25b) in <i>neo-</i>excised SNAP-25b deficient mice brain at PN14-15 were 117.3±6.8% of WT (n = 6 mice for each genotype, repeated three times each, mean±S.E.M., *<i>p = </i>0.0625, Wilcoxon's signed-rank test). (C) SNAP-25a/SNAP-25b mRNA ratio at PN14 were for WT littermates 17.5±1.2% and 82.5±1.2%, respectively (mean±S.E.M., ***<i>p</i><0.0001 Student's t-test), in heterozygous <i>neo-</i>excised SNAP-25b mutants 68.9±2.1% SNAP-25a and 31.1±2.1% SNAP-25b (***<i>p</i><0.0001), and in homozygous <i>neo-</i>excised SNAP-25b deficient mice 100% SNAP-25a (n = 5 mice for each genotype, repeated twice). (D) Protein levels in brain at PN14-15. In <i>neo-</i>excised SNAP-25b deficient mice, there was 110.9±2.3% (*<i>p = </i>0.0312) SNAP-25 protein, 106.4±4.2% (<i>p = </i>0.3125, n.s) SNAP-23, and 99.4±3.5% (<i>p = </i>0.8438, n.s.) syntaxin 1 relative to WT expression levels (n = 6 mice for each genotype, run in three replicates, mean±S.E.M., Wilcoxon's signed-rank test). (E) Immunoblot demonstrating temperature dependence and stability of the ternary SDS resistant SNARE complex in <i>neo</i>-excised SNAP-25b deficient (KO) and WT mouse brain cortex. The samples separated in lanes 1–5 (from left to right) are from adult WT brain cortex, and the preparations in lanes 6–10 are from <i>neo</i>-excised SNAP-25b deficient mutants (KO only expressing SNAP-25a). The high molecular weight ∼97 kD complex was identified as SNAP-25 in ternary SNARE complex, while the band migrating as ∼28 kDa is free SNAP-25 protein. KO brain homogenates heated to 80°C showed 44±8% SNAP-25 still present in ternary complex compared to 4°C samples, significantly lower than for SNAP-25 in WT brain (71.2±7.2, *<i>p = </i>0.01). At 85°C and 90°C, the difference in percentage of SNAP-25 remaining in complex between WT and KO was as following: 59.8±7 and 36.9±3.4 (*<i>p = </i>0.018), and 48.3±12.3 and 4.5±2.2 (**<i>p = </i>0.0081), respectively. All experiments were repeated at least three times. Results were analyzed with unpaired Student's t-test and summarized as mean±S.E.M.</p>", "links"=>[], "tags"=>["excision", "altered"], "article_id"=>584862, "categories"=>["Neuroscience", "Cell Biology", "Developmental Biology", "Physiology"], "users"=>["Jenny U. Johansson", "Jesper Ericsson", "Juliette Janson", "Simret Beraki", "Davor Stanić", "Slavena A. Mandic", "Martin A. Wikström", "Tomas Hökfelt", "Sven Ove Ögren", "Björn Rozell", "Per-Olof Berggren", "Christina Bark"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1000278.g002", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_In_vivo_Excision_of_the_Tkneo_Gene_Results_in_Altered_Gene_Expression_/584862", "title"=>"<i>In vivo</i> Excision of the <i>Tkneo</i> Gene Results in Altered Gene Expression.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-11-28 01:21:02"}
• {"files"=>["https://ndownloader.figshare.com/files/451880", "https://ndownloader.figshare.com/files/451939", "https://ndownloader.figshare.com/files/452003", "https://ndownloader.figshare.com/files/452061"], "description"=>"<div><p>Alternative splicing is an evolutionary innovation to create functionally diverse proteins from a limited number of genes. SNAP-25 plays a central role in neuroexocytosis by bridging synaptic vesicles to the plasma membrane during regulated exocytosis. The SNAP-25 polypeptide is encoded by a single copy gene, but in higher vertebrates a duplication of exon 5 has resulted in two mutually exclusive splice variants, SNAP-25a and SNAP-25b. To address a potential physiological difference between the two SNAP-25 proteins, we generated gene targeted SNAP-25b deficient mouse mutants by replacing the SNAP-25b specific exon with a second SNAP-25a equivalent. Elimination of SNAP-25b expression resulted in developmental defects, spontaneous seizures, and impaired short-term synaptic plasticity. In adult mutants, morphological changes in hippocampus and drastically altered neuropeptide expression were accompanied by severe impairment of spatial learning. We conclude that the ancient exon duplication in the <em>Snap</em>25 gene provides additional SNAP-25-function required for complex neuronal processes in higher eukaryotes.</p></div>", "links"=>[], "tags"=>["duplication", "exon", "neuronal"], "article_id"=>149046, "categories"=>["Neuroscience", "Cell Biology", "Developmental Biology", "Physiology"], "users"=>["Jenny U. Johansson", "Jesper Ericsson", "Juliette Janson", "Simret Beraki", "Davor Stanić", "Slavena A. Mandic", "Martin A. Wikström", "Tomas Hökfelt", "Sven Ove Ögren", "Björn Rozell", "Per-Olof Berggren", "Christina Bark"], "doi"=>["https://dx.doi.org/10.1371/journal.pgen.1000278.s001", "https://dx.doi.org/10.1371/journal.pgen.1000278.s002", "https://dx.doi.org/10.1371/journal.pgen.1000278.s003", "https://dx.doi.org/10.1371/journal.pgen.1000278.s004"], "stats"=>{"downloads"=>6, "page_views"=>11, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/An_Ancient_Duplication_of_Exon_5_in_the_Snap_25_Gene_Is_Required_for_Complex_Neuronal_Development_Function/149046", "title"=>"An Ancient Duplication of Exon 5 in the <em>Snap</em>25 Gene Is Required for Complex Neuronal Development/Function", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2008-11-28 02:30:46"}
• {"files"=>["https://ndownloader.figshare.com/files/914663"], "description"=>"<p>(A-D) Anxiety-like behavior in the elevated plus maze test. Time spent on open arms (A) (***<i>p<</i>0.001), time spent on closed arms (C) (***<i>p<</i>0.001), and number of crossings to the open (B) and closed arms (D). Each value represents the mean (±S.E.M.) from the four groups of animals. The homozygous <i>neo</i>-excised SNAP-25b deficient females (n = 4), the <i>neo</i>-excised SNAP-25b deficient male mice (n = 5), WT females (n = 5), and WT males (n = 5). (E–H) Spatial learning in the Morris water maze. Latency of the four experimental groups to locate a visible platform placed randomly within the water tank (E). The latency to find the hidden platform (F) as well as swim speed (G) and swim length (H) are shown. The results are presented as mean values±S.E.M. (average over four trials per session), from <i>neo</i>-excised SNAP-25b deficient mutant females (n = 4), SNAP-25b deficient males (n = 5), WT females (n = 5), and WT males (n = 5). The mutants differed from the control groups during the five days of training, both regard to escape latency and swim distance (<i>p</i><0.001). Data from the behavioral testing was analyzed by non-parametric statistics using Kruskal-Wallis ANOVA followed by the Mann-Whitney U test as the post-hoc test.</p>", "links"=>[], "tags"=>["maze", "morris"], "article_id"=>585112, "categories"=>["Neuroscience", "Cell Biology", "Developmental Biology", "Physiology"], "users"=>["Jenny U. Johansson", "Jesper Ericsson", "Juliette Janson", "Simret Beraki", "Davor Stanić", "Slavena A. Mandic", "Martin A. Wikström", "Tomas Hökfelt", "Sven Ove Ögren", "Björn Rozell", "Per-Olof Berggren", "Christina Bark"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1000278.g004", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Elevated_Plus_Maze_Test_and_the_Morris_Water_Maze_Task_/585112", "title"=>"Elevated Plus Maze Test and the Morris Water Maze Task.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-11-28 01:25:12"}
• {"files"=>["https://ndownloader.figshare.com/files/914304"], "description"=>"<p>(A) Schematic diagram demonstrating the targeting construct and the development of a modified <i>Snap25</i> allele with eliminated SNAP-25b expression. The mouse genomic sequence was derived from the WT <i>Snap25</i> gene and addition of an additional exon 5a was performed using PCR. A <i>Tkneo</i> selection gene, surrounded by loxP repeats, was inserted at the <i>EcoRI</i> (E) site located downstream of the two tandemly arranged exons 5a and upstream of exon 6. Letters denote restriction sites: E, <i>EcoRI</i>; H, <i>HindIII</i>; P, <i>PstI</i>; S, <i>SacI</i>; X, <i>XbaI</i>. (B) Total SNAP-25 mRNA level in mouse brain at PN14 was investigated by semi-quantitative RT-PCR. Levels of SNAP-25 mRNA, quantified relative to GAPDH mRNA levels, were determined in <i>neo-</i>containing SNAP-25b deficient mutants (KO) and compared to WT littermates. SNAP-25 mRNA in <i>neo-</i>containing SNAP-25b deficient mutant brain was significantly reduced to 55.5±2.7% compared to WT (mean±S.E.M., n = 6 mice for each genotype, each sample repeated three times, *<i>p = </i>0.0312, Wilcoxon's signed-rank test). (C) A semi-quantitative RT-PCR restriction enzyme assay was used to determine relative levels of SNAP-25a and SNAP-25b isoform mRNAs in WT (+/+), <i>neo-</i>containing heterozygous (+/−) and <i>neo-</i>containing homozygous (−/−) mutant brains at PN14. A <i>PvuI</i> restriction site exclusive for exon 5a and a <i>StyI</i> site only present in exon 5b was used to determine relative levels of SNAP-25a and SNAP-25b. WT mice had 16.7±1.9% SNAP-25a mRNA, <i>neo-</i>containing heterozygous mutants 51.6±1.7% SNAP-25a mRNA, and homozygous SNAP-25b deficient mutants only, the SNAP-25a mRNA isoform (n = 5 mice of each genotype, run in two replicates, mean±S.E.M., ***<i>p</i><0.0001, Student's t-test). (D) Western blotting was used to analyze synaptic protein levels in brain at PN14-15, standardized against α-tubulin. The level of SNAP-25 protein in <i>neo</i>-containing SNAP-25b deficient mutants was 80.7±3.6% compared to WT (mean±S.E.M., *<i>p = </i>0.0312, Wilcoxon's signed-rank test), whereas expression of SNAP-23 protein was 98.9±3.5% (<i>p = </i>1, n.s.) and that of syntaxin 1 protein 107.6±4.9% (<i>p = </i>0.4375, n.s.), compared to WT animals. The levels of SNAP-25 protein differed significantly in <i>neo</i>-containing SNAP-25b deficient mutants compared to WT littermates, but not the levels of SNAP-23 and syntaxin 1 proteins (n = 6 mice of each genotype, run in three replicates). (E) Representative images of SNAP-25 immunoreactivity in coronal sections at low magnification (i, iii) and in the hippocampus at higher magnification (ii, iv). No obvious differences in immunoreactivity pattern was observed between <i>neo</i>-containing SNAP-25b deficient (iii, iv) and WT (i, ii) mice at PN14 (n = 2 mice of each genotype, and three levels were analyzed from each animal). Identical microscope settings were used for WT and KO (<i>neo</i>-containing SNAP-25b deficient mutants) images. Scale bar = 1 mm for the low magnification and 200 µm for the high magnification figures. (F) Weight curves of homozygous <i>neo-</i>containing SNAP-25b deficient mutants compared to WT littermates between PN5 to PN15. Body weight gain was significantly reduced in young <i>neo-</i>containing SNAP-25b deficient mutants when compared to WT (***<i>p</i><0.0001, two-way repeated measures ANOVA, n = 7 mice of each genotype). (G) Bone growth is affected in <i>neo-</i>containing SNAP-25b deficient mice. Mean±S.E.M. thickness of the hypertrophic, proliferative, and reserve zones in femur and tibia in WT (black bars) and <i>neo-</i>containing SNAP-25b deficient (white bars) PN14 mice. *<i>p</i><0.05 (n = 4). Data was analyzed with unpaired Student's t-test.</p>", "links"=>[], "tags"=>["snap-25b", "deficient"], "article_id"=>584745, "categories"=>["Neuroscience", "Cell Biology", "Developmental Biology", "Physiology"], "users"=>["Jenny U. Johansson", "Jesper Ericsson", "Juliette Janson", "Simret Beraki", "Davor Stanić", "Slavena A. Mandic", "Martin A. Wikström", "Tomas Hökfelt", "Sven Ove Ögren", "Björn Rozell", "Per-Olof Berggren", "Christina Bark"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1000278.g001", "stats"=>{"downloads"=>1, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Generation_of_SNAP_25b_Deficient_Mouse_Mutants_/584745", "title"=>"Generation of SNAP-25b Deficient Mouse Mutants.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-11-28 01:19:05"}
• {"files"=>["https://ndownloader.figshare.com/files/914832"], "description"=>"<p>(A–B) Cresyl violet stained coronal sections of adult WT (A) and <i>neo</i>-excised SNAP-25b deficient (B) mice at the level of the hippocampus. The box indicates the CA3 area that is shown at higher magnification in (C–H). Scale bars = 1 mm. (C–H) Representative images of synaptophysin (green) and SNAP-25 (red) (E,F) immunoreactivity in the hippocampus of 4-month-old WT (left column) and <i>neo</i>-excised SNAP-25b deficient mutants (right column), and double immunofluorescence images (G,H). Scale bar = 50 µm (n = 3 animals of each genotype, each brain analyzed at least at three different levels).</p>", "links"=>[], "tags"=>["pathology", "develops", "snap-25b", "deficient"], "article_id"=>585274, "categories"=>["Neuroscience", "Cell Biology", "Developmental Biology", "Physiology"], "users"=>["Jenny U. Johansson", "Jesper Ericsson", "Juliette Janson", "Simret Beraki", "Davor Stanić", "Slavena A. Mandic", "Martin A. Wikström", "Tomas Hökfelt", "Sven Ove Ögren", "Björn Rozell", "Per-Olof Berggren", "Christina Bark"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1000278.g005", "stats"=>{"downloads"=>2, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Brain_Pathology_Develops_in_Adult_Neo_excised_SNAP_25b_Deficient_Mice_/585274", "title"=>"Brain Pathology Develops in Adult <i>Neo</i>-excised SNAP-25b Deficient Mice.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-11-28 01:27:54"}
• {"files"=>["https://ndownloader.figshare.com/files/914538"], "description"=>"<p>Paired-pulse facilitation (PPF) is reduced at Schaffer collateral-CA1 pyramidal cell synapses in both <i>neo</i>-containing and <i>neo</i>-excised SNAP-25b deficient slices. PPF (PPF ratio = EPSC₂/EPSC₁) was recorded in the whole-cell voltage clamp mode as a function of the interpulse interval (IPI) at two different frequencies in slices from PN12-16 animals. Error bars indicate S.E.M. (A) Reduced PPF at 0.2 Hz in <i>neo</i>-containing SNAP-25b deficient mutants compared to WT mice (*<i>p</i><0.05). (B) Reduced PPF at 0.2 Hz in <i>neo</i>-excised SNAP-25b deficient mice compared to WT (*<i>p</i><0.05). (C) Reduced PPF at 0.5 Hz in <i>neo</i>-containing SNAP-25b deficient mutants compared to WT (*<i>p</i><0.05). (D) PPF at 0.5 Hz in <i>neo</i>-excised SNAP-25b deficient mice compared to WT (<i>p = </i>0.085 n.s.). (E) An example of a typical PPF trace of Schaffer collateral-CA1 EPSCs from a <i>neo</i>-containing SNAP-25b deficient mutant mouse recorded at 70 ms IPI. Statistical comparisons of PPF ratios between WT and SNAP-25b deficient mice were made with two-way repeated measurements analysis of variance, ANOVA.</p>", "links"=>[], "tags"=>["plasticity", "snap-25b", "deficient"], "article_id"=>584974, "categories"=>["Neuroscience", "Cell Biology", "Developmental Biology", "Physiology"], "users"=>["Jenny U. Johansson", "Jesper Ericsson", "Juliette Janson", "Simret Beraki", "Davor Stanić", "Slavena A. Mandic", "Martin A. Wikström", "Tomas Hökfelt", "Sven Ove Ögren", "Björn Rozell", "Per-Olof Berggren", "Christina Bark"], "doi"=>"https://dx.doi.org/10.1371/journal.pgen.1000278.g003", "stats"=>{"downloads"=>1, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Short_term_Plasticity_Analyzed_in_SNAP_25b_Deficient_Mouse_Mutants_/584974", "title"=>"Short-term Plasticity Analyzed in SNAP-25b Deficient Mouse Mutants.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-11-28 01:22:54"}

PMC Usage Stats | Further Information

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Relative Metric

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F1000Prime