Synapsins (Synapsin I)

A family of synaptic vesicle-associated proteins involved in the short-term regulation of NEUROTRANSMITTER release. Synapsin I, the predominant member of this family, links SYNAPTIC VESICLES to ACTIN FILAMENTS in the presynaptic nerve terminal. These interactions are modulated by the reversible PHOSPHORYLATION of synapsin I through various signal transduction pathways. The protein is also a substrate for cAMP- and CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASES. It is believed that these functional properties are also shared by synapsin II.
Also Known As:
Synapsin I; Synapsin II; Synapsin III
Networked: 173 relevant articles (1 outcomes, 24 trials/studies)

Relationship Network

Bio-Agent Context: Research Results


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)

Related Diseases

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)
3. Pheochromocytoma
4. Seizures (Seizure)
5. Epilepsy (Aura)

Related Drugs and Biologics

1. Brain-Derived Neurotrophic Factor (BDNF)
2. nefiracetam
3. Proteins (Proteins, Gene)
4. Calcium-Calmodulin-Dependent Protein Kinase Type 2
5. Messenger RNA (mRNA)
6. Calcium
7. Kainic Acid (Kainate)
8. Antibodies
9. Haloperidol (Haldol)
10. Proline-Directed Protein Kinases

Related Therapies and Procedures

1. Microspheres (Microsphere)
2. Transplantation (Transplant Recipients)
3. Analgesia