Modulation of the SNARE core complex by dopamine

2000 ◽  
Vol 78 (10) ◽  
pp. 856-859 ◽  
Author(s):  
Heather Fisher ◽  
Janice EA Braun
Keyword(s):  
Synaptic Transmission ◽  
Synaptic Vesicle ◽  
Synaptic Function ◽  
Snare Complex ◽  
Synaptic Proteins ◽  
Core Complex ◽  
Cellular Mechanisms ◽  
Vesicle Release ◽  
Striatal Slices ◽  
Synaptic Vesicle Release

Communication between nerve cells in the brain occurs primarily through specialized junctions called synapses. Recently, many details of synaptic transmission have emerged. The identities of specific proteins important for synaptic vesicle release have now been established. We have investigated three synaptic proteins, VAMP (vesicle associated membrane protein; also called synaptobrevin), syntaxin, and SNAP25 (synaptosomal associated protein of 25kDa) as possible targets in the dopamine-mediated modulation of synaptic function in rat striatal slices. These three proteins form a SNARE (soluble N-ethylmalemide-sensitive factor attachment protein receptors) core complex that is known to be essential for synaptic transmission. Although it is envisioned that the SNAREs undergo dynamic and cyclic interactions to elicit synaptic vesicle release, their precise functions in neurotransmission remains unknown. We have examined SNARE complexes in intact rat striatal slices. Cellular proteins were solubilized, separated electrophoretically by SDS-PAGE, and then identified immunologically. Application of dopamine to striatal slices results in SNAREs favoring the SNARE core complex, a complex which forms spontaneously in the absence of crosslinking agents, rather than the monomer form. In addition, rapid crosslinking of dopamine-treated striatal slices demonstrates that the SNARE complex is increased 4 fold in dopamine treated striatal slices compared with control slices. Haloperidol blocked the dopamine-induced change in the core complex. These results suggest that changes in the activities of SNAREs may be involved in the underlying cellular mechanisms(s) of dopamine-regulated synaptic plasticity of the striatum.Key words: dopamine, striatium, VAMP, syntaxin, SNAP25.

scholarly journals Ammonium chloride alters neuronal excitability and synaptic vesicle release

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Roman M. Lazarenko ◽  
Claire E. DelBove ◽  
Claire E. Strothman ◽  
Qi Zhang
Keyword(s):  
Synaptic Vesicle ◽  
Ammonium Chloride ◽  
Neuronal Excitability ◽  
Vesicle Release ◽  
Synaptic Vesicle Release

scholarly journals On the Brink: A New Synaptic Vesicle Release Model at the Calyx of Held

Neuron ◽  
2015 ◽  
Vol 85 (1) ◽  
pp. 6-8 ◽  
Author(s):  
Melissa A. Herman ◽  
Christian Rosenmund
Keyword(s):  
Synaptic Vesicle ◽  
Calyx Of Held ◽  
Vesicle Release ◽  
Synaptic Vesicle Release ◽  
Release Model

scholarly journals The CHD Protein, Kismet, is Important for the Recycling of Synaptic Vesicles during Endocytosis

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Nina K. Latcheva ◽  
Taylor L. Delaney ◽  
Jennifer M. Viveiros ◽  
Rachel A. Smith ◽  
Kelsey M. Bernard ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Chromatin Remodeling ◽  
Neurodevelopmental Disorders ◽  
Synaptic Vesicles ◽  
Synaptic Function ◽  
Synaptic Proteins ◽  
Critical Feature ◽  
Synaptic Localization ◽  
Transcription Start Sites ◽  
Mature Neurons

AbstractChromatin remodeling proteins of the chromodomain DNA-binding protein family, CHD7 and CHD8, mediate early neurodevelopmental events including neural migration and differentiation. As such, mutations in either protein can lead to neurodevelopmental disorders. How chromatin remodeling proteins influence the activity of mature synapses, however, is relatively unexplored. A critical feature of mature neurons is well-regulated endocytosis, which is vital for synaptic function to recycle membrane and synaptic proteins enabling the continued release of synaptic vesicles. Here we show that Kismet, the Drosophila homolog of CHD7 and CHD8, regulates endocytosis. Kismet positively influenced transcript levels and bound to dap160 and endophilin B transcription start sites and promoters in whole nervous systems and influenced the synaptic localization of Dynamin/Shibire. In addition, kismet mutants exhibit reduced VGLUT, a synaptic vesicle marker, at stimulated but not resting synapses and reduced levels of synaptic Rab11. Endocytosis is restored at kismet mutant synapses by pharmacologically inhibiting the function of histone deacetyltransferases (HDACs). These data suggest that HDAC activity may oppose Kismet to promote synaptic vesicle endocytosis. A deeper understanding of how CHD proteins regulate the function of mature neurons will help better understand neurodevelopmental disorders.

scholarly journals Effects of diet on synaptic vesicle release in dynactin complex mutants: a mechanism for improved vitality during motor disease

Aging Cell ◽  
2012 ◽  
Vol 11 (3) ◽  
pp. 418-427 ◽  
Author(s):  
Joel M. Rawson ◽  
Tabita Kreko ◽  
Holly Davison ◽  
Rebekah Mahoney ◽  
Alex Bokov ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Vesicle Release ◽  
Synaptic Vesicle Release ◽  
Dynactin Complex

scholarly journals The Effect of Neural Noise on Spike Time Precision in a Detailed CA3 Neuron Model

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Eduard Kuriscak ◽  
Petr Marsalek ◽  
Julius Stroffek ◽  
Zdenek Wünsch
Keyword(s):  
Synaptic Vesicle ◽  
Neuron Model ◽  
Channel Noise ◽  
Spike Time ◽  
Vesicle Release ◽  
Time Jitter ◽  
Voltage Gated ◽  
Neural Noise ◽  
Quantal Size ◽  
Synaptic Vesicle Release

Experimental and computational studies emphasize the role of the millisecond precision of neuronal spike times as an important coding mechanism for transmitting and representing information in the central nervous system. We investigate the spike time precision of a multicompartmental pyramidal neuron model of the CA3 region of the hippocampus under the influence of various sources of neuronal noise. We describe differences in the contribution to noise originating from voltage-gated ion channels, synaptic vesicle release, and vesicle quantal size. We analyze the effect of interspike intervals and the voltage course preceding the firing of spikes on the spike-timing jitter. The main finding of this study is the ranking of different noise sources according to their contribution to spike time precision. The most influential is synaptic vesicle release noise, causing the spike jitter to vary from 1 ms to 7 ms of a mean value 2.5 ms. Of second importance was the noise incurred by vesicle quantal size variation causing the spike time jitter to vary from 0.03 ms to 0.6 ms. Least influential was the voltage-gated channel noise generating spike jitter from 0.02 ms to 0.15 ms.

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