|1.||Benfenati, Fabio: 10 articles (10/2015 - 06/2011)|
|2.||Mishra, Ram K: 8 articles (09/2015 - 09/2002)|
|3.||Etholm, Lars: 6 articles (01/2015 - 04/2009)|
|4.||Heggelund, Paul: 5 articles (09/2013 - 04/2009)|
|5.||Baldelli, Pietro: 4 articles (10/2015 - 06/2011)|
|6.||Valtorta, Flavia: 4 articles (01/2014 - 01/2013)|
|7.||Gomez-Pinilla, Fernando: 4 articles (06/2010 - 07/2002)|
|8.||He, Lin: 4 articles (11/2009 - 08/2004)|
|9.||Medrihan, Lucian: 3 articles (10/2015 - 01/2013)|
|10.||Bahonjic, Elma: 3 articles (01/2015 - 05/2012)|
|1.||Brain Ischemia (Cerebral Ischemia)
11/27/2012 - "We tested this hypothesis by evaluating the motor skill relearning and the immunocontent of Synapsin-I, PSD-95 and GFAP (pre and post-synaptic elements, as well as surrounding astroglia) in sensorimotor cortex of both hemispheres 6 weeks after endothelin-1-induced focal brain ischemia in rats. "
01/01/1992 - "In a gerbil model of bilateral cerebral ischemia, immunoreaction for synapsin I was persistently preserved after seven days to two months recirculation following a brief period of global forebrain ischemia in the CA1 region of the hippocampus, where delayed neuronal death was consistently observed.(ABSTRACT TRUNCATED AT 250 WORDS)"
01/16/2004 - "These results suggested that the neuronal damage and degenerations were observed as a result of GOD/reperfusion and the increase in synapsin I and its phosphorylation might play a role in modulating the release of neurotransmitters via exocytosis and in the formation of new synapses after brain ischemia."
01/01/1992 - "In selective neuronal death, which is typically found in the CA1 neurons of the hippocampus after 5-min bilateral cerebral ischemia, selective damage of postsynaptic components with intact presynaptic sites was demonstrated by immunohistochemical examination for microtubule-associated protein 2 and synapsin I, and albumin extravasation did not become apparent before postsynaptic structures were destroyed. "
01/10/2005 - "These results suggest that enhancement of BDNF and synapsin I expression by nefiracetam treatment may be, at least in part, due to the improvement in the CREB binding activity, contributing to the prevention of learning and memory dysfunction after sustained cerebral ischemia."
|2.||Schizophrenia (Dementia Praecox)
11/20/2009 - "Association and expression study of synapsin III and schizophrenia."
11/01/2004 - "This confirms our previous study and provides further support for the role of synapsin II variants in susceptibility to schizophrenia."
11/01/2004 - "Synapsin II has been proposed as a candidate gene for vulnerability to schizophrenia on the basis of its function and its location in a region of the genome implicated by linkage studies in families with schizophrenia. "
11/01/2004 - "Family-based association study of synapsin II and schizophrenia."
08/01/2004 - "This study suggests a positive association between synapsin II and schizophrenia, implying that synapsin II is involved in the etiology of schizophrenia."
03/01/2008 - "The present study examined the role of phospholipase D2 (PLD2) in the regulation of depolarization-induced neurite outgrowth and the expression of growth-associated protein-43 (GAP-43) and synapsin I in rat pheochromocytoma (PC12) cells. "
04/25/1990 - "Previous studies identified synapsin I as a potential substrate for a newly discovered growth factor-sensitive, proline-directed protein kinase originally isolated from rat pheochromocytoma. "
04/15/1998 - "Using the ELISA, neither synapsin I nor synaptophysin could be determined in serum or cerebrospinal fluid (CSF) from healthy donors or patients suffering various neurological disorders or pheochromocytomas. "
11/02/2015 - "We have been studying the phosphorylation state of the presynaptic protein, synapsin I at ERK1/2-dependent and -independent sites in various types of seizure models and showed that ERK1/2-dependent phosphorylation of synapsin I was indeed under control of ERK1/2 activity in vivo. "
09/01/2013 - "In mice lacking synapsin II (synapsin 2 knock-out mice, Syn2KO mice) all seizures are in the form of generalized tonic-clonic seizures. "
08/25/2011 - "We therefore suggest that while deletion of the synapsins initially increases cortical network activity, this enhanced excitability is insufficient to elicit seizures. "
04/06/2011 - "Electroencephalographic characterization of seizure activity in the synapsin I/II double knockout mouse."
10/15/2010 - "Seizures were studied in Synapsin I/II double knock-out (SynDKO) mice, a genetically engineered mouse line that shows seizures upon daily handling procedures such as tail lifting during cage changes, much in resemblance to the more studied El mouse. "
08/15/2013 - "Nonsense and missense mutations in the SYN1 gene encoding for Synapsin I have been identified in families segregating for idiopathic epilepsy and ASD and genetic mapping analyses have identified variations in the SYN2 gene as significantly contributing to epilepsy predisposition. "
01/01/2013 - "Here, we investigated possible epileptogenic abnormalities in the function of the DG neuronal network in the Synapsin II (Syn II) knockout mouse (Syn II(-/-)), a genetic mouse model of epilepsy. "
01/01/2013 - "We investigated the impact of the c.1067G>A nonsense transition, the first mutation described in a family affected by X-linked syndromic epilepsy, on the expression and functional properties of the synapsin I protein. "
01/01/2013 - "Nonsense-mediated mRNA decay and loss-of-function of the protein underlie the X-linked epilepsy associated with the W356× mutation in synapsin I."
11/02/2012 - "Seven of these potential markers were identified using a top-down approach, in particular a fragment of Synapsin-I. This protein is yet suspected to be involved in epilepsy. "
|1.||Brain-Derived Neurotrophic Factor (BDNF)
|3.||Proteins (Proteins, Gene)
|4.||Calcium-Calmodulin-Dependent Protein Kinase Type 2
|5.||Messenger RNA (mRNA)
|7.||Kainic Acid (Kainate)
|10.||Proline-Directed Protein Kinases
|2.||Transplantation (Transplant Recipients)