Mobility of Synaptic Vesicles in Different Pools in Resting and Stimulated Frog Motor Nerve Terminals

Gaffield, Michael A.; Rizzoli, Silvio O.; Betz, William J.

doi:10.1016/j.neuron.2006.06.031

Cited by 97 publications

(118 citation statements)

References 33 publications

(61 reference statements)

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“…However, there have been reports that challenge synapsin's role in vesicular mobility. Disruption of actin in frog motor nerve terminals showed no significant changes in vesicular mobility (Gaffield et al 2006). In knockout mice lacking synapsins, the neurons display no gross anatomical abnormalities (Rosahl et al 1995) or changes in synaptic vesicle trafficking (Gaffield and Betz 2007).…”

Section: Discussionmentioning

confidence: 97%

Synaptic activity slows vesicular replenishment at excitatory synapses of rat hippocampus

Bui

Glavinović

2012

Cogn Neurodyn

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Short-term synaptic depression mainly reflects the depletion of the readily releasable pool (RRP) of quanta. Its dynamics, and especially the replenishment rate of the RRP, are still not well characterized in spite of decades of investigation. Main reason is that the vesicular storage and release system is treated as time-independent. If it is time-dependent all parameters thus estimated become problematic. Indeed the reports about how prolonged stimulation affects the dynamics are contradictory. To study this, we used patterned stimulation on the Schaeffer collateral fiber pathway and model-fitting of the excitatory post-synaptic currents (EPSC) recorded from CA1 neurons in rat hippocampal slices. The parameters of a vesicular storage and release model with two pools were estimated by minimizing the squared difference between the ESPC amplitudes and simulated model output. This yields the 'basic' parameters (release coupling, replenishment coupling and RRP size) that underlie the 'derived' and commonly used parameters (fractional release and replenishment rate). The fractional release increases when [Ca ?? ] o is raised, whereas the replenishment rate is [Ca ?? ] o independent. Fractional release rises because release coupling increases, and the RRP becomes less able to contain quanta. During prolonged stimulation, the fractional release remains generally unaltered, whereas the replenishment rate decreases down to *10 % of its initial value with a decay time of *15 s, and this decrease in the replenishment rate significantly contributes to synaptic depression. In conclusion, the fractional release is [Ca ?? ] odependent and stimulation-independent, whereas the replenishment rate is [Ca ?? ] o -independent and stimulation-dependent.

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Section: Discussionmentioning

confidence: 97%

Synaptic activity slows vesicular replenishment at excitatory synapses of rat hippocampus

Bui

Glavinović

2012

Cogn Neurodyn

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“…nals as described previously (Gaffield et al, 2006). The bleaching protocol we used was the same as before when we found the bleach did not damage the nerve terminals (Gaffield et al, 2006).…”

Section: Methodsmentioning

confidence: 99%

“…Directed transport via an actin-myosin mechanism has been proposed to facilitate movement, based primarily on evidence of myosin involvement in vesicle recruitment (Prekeris and Terrian, 1997;Ryan, 1999;Verstreken et al, 2005) (but see Tokuoka and Goda, 2006). Direct evidence for an actin role, however, is mostly lacking (Sankaranarayanan et al, 2003;Richards et al, 2004;Gaffield et al, 2006) (but see Nunes et al, 2006). In addition to directed transport of vesicles, evidence for diffusion has been presented.…”

Section: Introductionmentioning

confidence: 99%

“…In addition to directed transport of vesicles, evidence for diffusion has been presented. Models for caged diffusion (Jordan et al, 2005), stick and diffuse (Shtrahman et al, 2005;Yeung et al, 2007), free diffusion (Holt et al, 2004;Rea et al, 2004), and hindered diffusion (Gaffield et al, 2006) have all suggested that diffusion may account entirely for synaptic vesicle movement. Most of these observations can be combined into a simple mechanism involving a protein that reversibly glues synaptic vesicles together.…”

Section: Introductionmentioning

confidence: 99%

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Synaptic Vesicle Mobility in Mouse Motor Nerve Terminals with and without Synapsin

Gaffield¹,

Betz²

2007

J. Neurosci.

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We measured synaptic vesicle mobility using fluorescence recovery after photobleaching of FM 1-43 [N-(3-triethylammoniumpropyl)-4-(4-(dibutylamino)styryl) pyridinium dibromide] stained mouse motor nerve terminals obtained from wild-type (WT) and synapsin triple knock-out (TKO) mice at room temperature and physiological temperature. Vesicles were mobile in resting terminals at physiological temperature but virtually immobile at room temperature. Mobility was increased at both temperatures by blocking phosphatases with okadaic acid, decreased at physiological temperature by blocking kinases with staurosporine, and unaffected by disrupting actin filaments with latrunculin A or reducing intracellular calcium concentration with BAPTA-AM. Synapsin TKO mice showed reduced numbers of synaptic vesicles and reduced FM 1-43 staining intensity. Synaptic transmission, however, was indistinguishable from WT, as was synaptic vesicle mobility under all conditions tested. Thus, in TKO mice, and perhaps WT mice, a phospho-protein different from synapsin but otherwise of unknown identity is the primary regulator of synaptic vesicle mobility.

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“…Actin has little impact on synaptic vesicle clusters and on the rate of refilling of the readily releasable pool (Dillon and Goda, 2005). The mobility of synaptic vesicles displays little dependence on actin and myosin motors but is controlled by synapsin-1, which can tether synaptic vesicles together in a stimulus-dependent manner and by vesicle packing density (Jordan et al, 2005;Gaffield et al, 2006;Schweizer and Ryan, 2006). Vesicle supply to release sites seems to be primarily governed by diffusion, a conclusion that we propose to extend to the case of SGs.…”

Section: Mobility Of Synaptic Vesicles and Role Of Myova In Neuronsmentioning

confidence: 99%

Myosin Va Mediates Docking of Secretory Granules at the Plasma Membrane

Desnos¹,

Huet²,

Fanget³

et al. 2007

J. Neurosci.

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Ϫ4 m 2 ⅐ s Ϫ1 ) were considered as docked at the plasma membrane based on two properties: (1) SGs that undergo exocytosis have a D xy below this threshold value for at least 2 s before fusion; (2) a negative autocorrelation of the vertical motion was found in subtrajectories with a D xy below the threshold. Using this criterion of docking, we found that the main effect of MyoVa inhibition was to reduce the number of docked granules, leading to reduced secretory responses. Surprisingly, this reduction was not attributable to a decreased transport of SGs toward release sites. In contrast, MyoVa silencing reduced the occurrence of long-lasting, but not short-lasting, docking periods. We thus propose that, despite its known motor activity, MyoVa directly mediates stable attachment of SGs at the plasma membrane.

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Mobility of Synaptic Vesicles in Different Pools in Resting and Stimulated Frog Motor Nerve Terminals

Cited by 97 publications

References 33 publications

Synaptic activity slows vesicular replenishment at excitatory synapses of rat hippocampus

Synaptic activity slows vesicular replenishment at excitatory synapses of rat hippocampus

Synaptic Vesicle Mobility in Mouse Motor Nerve Terminals with and without Synapsin

Myosin Va Mediates Docking of Secretory Granules at the Plasma Membrane

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