Disease relevance of Syn2

• Increases in mRNA levels for synapsin I but not synapsin II in the hippocampus of the rat kindling model of epilepsy [1].
• Aberrant neurites and synaptic vesicle protein deficiency in synapsin II-depleted neurons [2].
• Using the cDNA encoding rat synapsin IIb, we employed an Escherichia coli expression system to synthesize a variety of fusion proteins containing a truncated protein A linked to different portions of the NH2-terminal region of synapsin II [3].

Psychiatry related information on Syn2

• Synapsin II variants were also present in 56% of samples from individuals with schizophrenia and 41% of samples from individuals with Huntington's disease [4].

High impact information on Syn2

• Synapsin I and synapsin II are neuron-specific phosphoproteins that have a role in the regulation of neurotransmitter release and in the formation of nerve terminals [2].
• These data suggest that synapsin II participates in cytoskeletal organization during the early stages of nerve cell development [2].
• Synapsin II variants were not found in any of 18 rodent models of alcoholism, aging, or vitamin B deficiency, suggesting that synapsin II variants may be a uniquely human trait [4].
• To determine the source of synapsin II immunoreactivity in the glomeruli, the olfactory epithelium was damaged to decrease the primary afferent input to the bulb [5].
• These experiments identified a region between amino acids 43 and 121 of the amino-terminal portion of synapsin II which binds to synaptic vesicles [3].

Biological context of Syn2

• We hypothesize that the beta-adrenergic agonist-stimulated phosphorylation of synapsin I and synapsin II in young rats plays a role in the increase in transmitter release produced by NE in the dentate [6].
• The opiate-induced regulation of the gene expression of synapsin II isoforms could be viewed as one of the cellular adaptations to the persistent opiate effects and may be involved in the molecular mechanism underlying opiate tolerance and/or dependence [7].
• A possible mechanism for the observed haloperidol-induced increase in striatal synapsin II expression, along with the implications of this up-regulation in chronic haloperidol treatment, is presented [8].

Anatomical context of Syn2

• However, we have recently shown that phorbol dibutyrate increased the phosphorylated of synapsin II (formerly protein III, Browning et al., 1987) in chromaffin cells (Haycock et al., 1988) [9].
• Quantitative reverse transcriptase-polymerase chain reaction and in situ hybridization techniques were used to determine the regional distribution of synapsin IIa and IIb mRNAs in rat central nervous system and to assess the effect of chronic morphine administration on the gene expression of these two isoforms of synapsin II [7].

Associations of Syn2 with chemical compounds

• NE (10 microM) and isoproterenol (250 nM) produced an increase in the phosphorylation of synapsin I and synapsin II in dentate slices from young rats [6].
• Synapsin II. Mapping of a domain in the NH2-terminal region which binds to small synaptic vesicles [3].
• This study is the first to show the regulation of synapsin II expression by haloperidol at the transcript and protein level in rat striatum [8].

Other interactions of Syn2

• ATP binding to the different synapsins is directly regulated by Ca2+ in a dramatically different fashion: Ca2+ activates ATP binding to synapsin I, has no effect on synapsin II, and inhibits synapsin III [10].

Analytical, diagnostic and therapeutic context of Syn2

• Western blots of tissue derived from microdissection of the surface and core regions of the olfactory bulb were performed using antibodies to synapsin I and synapsin II [5].
• Following denervation, both OMP and synapsin II immunoreactivities were diminished, and continued to colocalize in regions retaining immunoreactivity [5].
• Immunoblotting revealed that protein levels of both the a and b isoforms of synapsin II were also increased by comparable amounts following haloperidol treatment [8].
• cDNA array reveals differential gene expression following chronic neuroleptic administration: implications of synapsin II in haloperidol treatment [8].

References