SYN2

Last update 08 May 2025

Basic Info

Synonyms

SYN2, synapsin II, Synapsin-2

+ [3]

Introduction

Neuronal phosphoprotein that coats synaptic vesicles, binds to the cytoskeleton, and is believed to function in the regulation of neurotransmitter release. May play a role in noradrenaline secretion by sympathetic neurons (By similarity).

100 Clinical Results associated with SYN2

100 Translational Medicine associated with SYN2

0 Patents (Medical) associated with SYN2

285

Literatures (Medical) associated with SYN2

01 Dec 2025·Neural Regeneration Research

Nerve root magnetic stimulation regulates the synaptic plasticity of injured spinal cord by ascending sensory pathway

Article

Author: Gu, Chunya ; Zheng, Ya ; Yang, Qi ; Zhao, Dan ; Zhu, Yulian ; Cao, Lingyun ; Xu, Dongsheng ; Zhao, Jing ; Mao, Yeran ; Zhu, Guangyue

JOURNAL/nrgr/04.03/01300535-202512000-00026/figure1/v/2025-01-31T122243Z/r/image-tiff Promoting synaptic plasticity and inducing functional reorganization of residual nerve fibers hold clinical significance for restoring motor function following spinal cord injury. Neuromagnetic stimulation targeting the nerve roots has been shown to improve motor function by enhancing nerve conduction in the injured spinal cord and restoring the synaptic ultrastructure of both the sensory and motor cortex. However, our understanding of the neurophysiological mechanisms by which nerve root magnetic stimulation facilitates motor function recovery in the spinal cord is limited, and its role in neuroplasticity remains unclear. In this study, we established a model of spinal cord injury in adult male Sprague–Dawley rats by applying moderate compression at the T10 vertebra. We then performed magnetic stimulation on the L5 nerve root for 3 weeks, beginning on day 3 post-injury. At day 22 post-injury, we observed that nerve root magnetic stimulation downregulated the level of interleukin-6 in the injured spinal cord tissue of rats. Additionally, this treatment reduced neuronal damage and glial scar formation, and increased the number of neurons in the injured spinal cord. Furthermore, nerve root magnetic stimulation decreased the levels of acetylcholine, norepinephrine, and dopamine, and increased the expression of synaptic plasticity-related mRNA and proteins PSD95, GAP43, and Synapsin II. Taken together, these results showed that nerve root magnetic stimulation alleviated neuronal damage in the injured spinal cord, regulated synaptic plasticity, and suppressed inflammatory responses. These findings provide laboratory evidence for the clinical application of nerve root magnetic stimulation in the treatment of spinal cord injury.

02 Dec 2024·Journal of Biomolecular Structure and Dynamics

Gene expression analysis reveals GRIN1, SYT1, and SYN2 as significant therapeutic targets and drug repurposing reveals lorazepam and lorediplon as potent inhibitors to manage Alzheimer’s disease

Article

Author: Sundararajan, Vino ; T., Premkumar ; Lulu S., Sajitha ; Katta, Bhavana

Alzheimer's disease (AD) is a slowly progressive neurodegenerative disease and a leading cause of dementia. We aim to identify key genes for the development of therapeutic targets and biomarkers for potential treatments for AD. Meta-analysis was performed on six microarray datasets and identified the differentially expressed genes between healthy and Alzheimer's disease samples. Thereafter, we filtered out the common genes which were present in at least four microarray datasets for downstream analysis. We have constructed a gene-gene network for the common genes and identified six hub genes. Furthermore, we investigated the regulatory mechanisms of these hub genes by analysing their interaction with miRNAs and transcription factors. The gene ontology analysis results highlighted the enriched terms significantly associated with hub genes. Through an extensive literature survey, we found that three of the hub genes including GRIN1, SYN2, and SYT1 were critically involved in disease development. To leverage existing drugs for potential repurposing, we predicted drug-gene interaction using the drug-gene interaction database, and performed molecular docking studies. The docking results revealed that the drug compounds had strong interactions and favorable binding with selected hub genes. Lorazepam exhibits a binding energy of -7.3 kcal/mol with GRIN1, Lorediplon exhibits binding energies of -7.7 kcal/mol and -6.3 kcal/mol with the SYT1, and SYN2 respectively. In addition, 100 ns molecular dynamics simulations were carried out for the top complexes and apo protein as well. Furthermore, the MM-PBSA free energy calculations also revealed that these complexes are stable and had favorable energies. According to our study, the identified hub gene could serve as a biomarker as well as a therapeutic target for AD, and the proposed repurposed drug molecules appear to have promising efficacy in treating the disease.Communicated by Ramaswamy H. Sarma.

01 Dec 2024·Cellular and Molecular Life Sciences

Early endocannabinoid-mediated depolarization-induced suppression of excitation delays the appearance of the epileptic phenotype in synapsin II knockout mice

Article

Author: Benfenati, Fabio ; D'Angelo, Livia ; Cristino, Luigia ; De Girolamo, Paolo ; Forte, Nicola ; Scandurra, Anna ; Baldelli, Pietro ; Marfella, Brenda ; Piscitelli, Fabiana ; Nicois, Alessandro ; Mavaro, Isabella ; Di Marzo, Vincenzo

The mechanism underlying the transition from the pre-symptomatic to the symptomatic state is a crucial aspect of epileptogenesis. SYN2 is a member of a multigene family of synaptic vesicle phosphoproteins playing a fundamental role in controlling neurotransmitter release. Human SYN2 gene mutations are associated with epilepsy and autism spectrum disorder. Mice knocked out for synapsin II (SynII KO) are prone to epileptic seizures that appear after 2 months of age. However, the involvement of the endocannabinoid system, known to regulate seizure development and propagation, in the modulation of the excitatory/inhibitory balance in the epileptic hippocampal network of SynII KO mice has not been explored. In this study, we investigated the impact of endocannabinoids on glutamatergic and GABAergic synapses at hippocampal dentate gyrus granule cells in young pre-symptomatic (1-2 months old) and adult symptomatic (5-8 months old) SynII KO mice. We observed an increase in endocannabinoid-mediated depolarization-induced suppression of excitation in young SynII KO mice, compared to age-matched wild-type controls. In contrast, the endocannabinoid-mediated depolarization-induced suppression of inhibition remained unchanged in SynII KO mice at both ages. This selective alteration of excitatory synaptic transmission was accompanied by changes in hippocampal endocannabinoid levels and cannabinoid receptor type 1 distribution among glutamatergic and GABAergic synaptic terminals contacting the granule cells of the dentate gyrus. Finally, inhibition of type-1 cannabinoid receptors in young pre-symptomatic SynII KO mice induced seizures during a tail suspension test. Our results suggest that endocannabinoids contribute to maintaining network stability in a genetic mouse model of human epilepsy.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

SYN2

Basic Info

Related

Analysis