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Title: Differential subcellular localization of SNAP-25a and SNAP-25b RNA transcripts in spinal motoneurons and plasticity in expression after nerve injury. Author: Jacobsson G, Piehl F, Bark IC, Zhang X, Meister B. Journal: Brain Res Mol Brain Res; 1996 Apr; 37(1-2):49-62. PubMed ID: 8738135. Abstract: Synaptosomal-associated protein of 25 kDa (SNAP-25) is involved in the molecular regulation of neurotransmitter release. SNAP-25 exists in two isoforms, which arise from alternative splicing of exon 5. In situ hybridization was used to examine whether SNAP-25 isoform mRNA expression may be altered by experimental manipulations. The effect of unilateral nerve injury on SNAP-25 mRNA levels was studied in motoneurons of the rat lumbar spinal cord. In all animals, SNAP-25a RNA transcripts were demonstrated in the nucleus of motoneurons, whereas SNAP-25b mRNA was present mainly in the cytoplasm. Cloning of the rat Snap gene intron spacing the alternative exon 5a and 5b sequences and generation of an intron-specific oligonucleotide probe used for in situ hybridization did not point to the presence of unspliced variants of SNAP-25b mRNA. After unilateral sciatic nerve transection (axotomy), SNAP-25a and SNAP-25b expression decreased in axotomized motoneurons compared with corresponding motoneurons on the unlesioned side. A significant decrease was demonstrated 2 days after axotomy, which reached a maximum after 7 days (62% for SNAP-25a and 67% for SNAP-25b), while levels had slightly recovered by 14 and 28 days. Ventral root avulsion also induced a decrease in levels of SNAP-25 RNA transcripts, suggesting that the axonal injury in itself was responsible for the down-regulation of Snap gene expression. This study shows that, in spinal motoneurons, SNAP-25a and SNAP-25b RNA transcripts have different subcellular localization and that levels of SNAP-25 RNA transcripts are down-regulated after axonal injury.[Abstract] [Full Text] [Related] [New Search]