Synaptic vesicle pools

Max-Planck-Institut für biophysikalische Chemie, Göttingen, Germany.
Nature reviews Neuroscience (Impact Factor: 31.43). 02/2005; 6(1):57-69. DOI: 10.1038/nrn1583
Source: PubMed


Communication between cells reaches its highest degree of specialization at chemical synapses. Some synapses talk in a 'whisper'; others 'shout'. The 'louder' the synapse, the more synaptic vesicles are needed to maintain effective transmission, ranging from a few hundred (whisperers) to nearly a million (shouters). These vesicles reside in different 'pools', which have been given a bewildering array of names. In this review, we focus on five tissue preparations in which synaptic vesicle pools have been identified and thoroughly characterized. We argue that, in each preparation, each vesicle can be assigned to one of three distinct pools.

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    • "Hirano bodies were formed in presynaptic CA3 neurons [28]. Paired-pulse stimulation is a measurement that reflects the active transport recovery of calcium and trafficking of neurotransmitter-containing vesicles to replenish the ready releasable pool of vesicles [74]. The trafficking of these neurotransmitter-containing vesicles is modulated by the actin cytoskeleton. "
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    ABSTRACT: IntroductionHirano bodies are actin-rich intracellular inclusions found in the brains of patients with neurodegenerative conditions such as Alzheimer¿s disease or frontotemporal lobar degeneration-tau. While Hirano body ultrastructure and protein composition have been well studied, little is known about the physiological function of Hirano bodies in an animal model system.ResultsUtilizing a Cre/Lox system, we have generated a new mouse model which develops an age-dependent increase in the number of model Hirano bodies present in both the CA1 region of the hippocampus and frontal cortex. These mice develop normally and experience no overt neuron loss. Mice presenting model Hirano bodies have no abnormal anxiety or locomotor activity as measured by the open field test. However, mice with model Hirano bodies develop age-dependent impairments in spatial working memory performance assessed using a delayed win-shift task in an 8-arm radial maze. Synaptic transmission, short-term plasticity, and long-term plasticity was measured in the CA1 region from slices obtained from both the ventral and dorsal hippocampus in the same mice whose spatial working memory was assessed. Baseline synaptic responses, paired pulse stimulation and long-term potentiation measurements in the ventral hippocampus were indistinguishable from control mice. In contrast, in the dorsal hippocampus, synaptic transmission at higher stimulus intensities were suppressed in 3 month old mice with Hirano bodies as compared with control mice. In addition, long-term potentiation was enhanced in the dorsal hippocampus of 8 month old mice with Hirano bodies, concurrent with observed impairment of spatial working memory. Finally, an inflammatory response was observed at 8 months of age in mice with Hirano bodies as assessed by the presence of reactive astrocytes.Conclusion This study shows that the presence of model Hirano bodies initiates an inflammatory response, alters hippocampal synaptic responses, and impairs spatial working memory in an age-dependent manner. This suggests that Hirano bodies may promote disease progression. This new model mouse provides a tool to investigate how Hirano bodies interact with other pathologies associated with Alzheimer¿s disease. Hirano bodies likely play a complex and region specific role in the brain during neurodegenerative disease progression.
    Full-text · Article · Sep 2014
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    • "However, the RRP was defined as the synaptic vesicles that are in direct contact with the presynaptic membrane, and it is not likely that the morphological estimates of the RRP size and those obtained by kinetic analysis would agree. At the frog neuromuscular junction there is no spatial segregation between the pools, as RRP vesicles appear to be randomly distributed throughout the cluster (Rizzoli and Betz 2005). Moreover the vesicles that are docked but not primed are kinetically not in the RRP. "
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    ABSTRACT: How vesicular dynamics parameters depend on temperature and how temperature affects the parameter change during prolonged high frequency stimulation was determined by fitting a model of vesicular storage and release to the amplitudes of the excitatory post-synaptic currents (EPSC) recorded from CA1 neurons in rat hippocampal slices. The temperature ranged from low (13 oC) to higher and more physiological temperature (34 oC). Fitting the model of vesicular storage and release to the EPSC amplitudes during a single pair of brief high–low frequency stimulation trains yields the estimates of all parameters of the vesicular dynamics, and with good precision. Both fractional release and replenishment rate decrease as the temperature rises. Change of the underlying ‘basic’ parameters (release coupling, replenishment coupling and readily releasable pool size), which the model-fitting also yields is complex. The replenishment coupling between the readily releasable pool (RRP) and resting pool increases with temperature (which renders the replenishment rate higher), but this is more than counterbalanced by greater RRP size (which renders the replenishment rate lower). Finally, during long, high frequency patterned stimulation that leads to significant synaptic depression, the replenishment rate decreases markedly and rapidly at low temperatures (~22 oC), but at high temperatures (>28 oC) the replenishment rate rises with stimulation, making synapses better able to maintain synaptic efficacy.
    Full-text · Article · Jul 2014 · Cognitive Neurodynamics
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    • "Vesicles belonging to the RRP also fuse upon application of hypertonic solution (Rosenmund and Stevens, 1996). Hypertonic shock is the most frequently used and most established technique to quantify the RRP in cultured hippocampal neurons (Rizzoli and Betz, 2005). Moreover, recent work demonstrated that estimation of the RRP size either by tetanic stimulation or by hypertonic challenge provides similar results (Stevens and Williams, 2007). "
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    ABSTRACT: ClC-3 is a member of the CLC family of anion channels and transporters that localizes to early and late endosomes as well as to synaptic vesicles (SV). Its genetic disruption in mouse models results in pronounced hippocampal and retinal neurodegeneration, suggesting that ClC-3 might be important for normal excitatory and/or inhibitory neurotransmission in central neurons. To characterize the role of ClC-3 in glutamate accumulation in SV we compared glutamatergic synaptic transmission in cultured hippocampal neurons from WT and Clcn3-/- mice. In Clcn3-/- neurons the amplitude and frequency of miniature as well as the amplitudes of action-potential evoked EPSCs were significantly increased as compared to WT neurons. The low-affinity competitive AMPA receptor antagonist γ-DGG reduced the quantal size of synaptic events more effectively in WT than in Clcn3-/- neurons, whereas no difference was observed for the high-affinity competitive non-NMDA antagonist NBQX. Paired pulse ratios of evoked EPSCs were significantly reduced, whereas the size of the readily releasable pool was not affected by the genetic ablation of ClC-3. Electron microscopy revealed increased volumes of SV in hippocampi of Clcn3-/- mice. Our findings demonstrate that ClC-3 controls fast excitatory synaptic transmission by regulating the amount of neurotransmitter as well as the release probability of SV. These results provide novel insights into the role of ClC-3 in synaptic transmission and identify excessive glutamate release as a likely basis of neurodegeneration in Clcn3-/-.
    Full-text · Article · May 2014 · Frontiers in Cellular Neuroscience
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