The architecture of an excitatory synapse

Chua, John Jia En; Kindler, Stefan; Boyken, Janina; Jahn, Reinhard

doi:10.1242/jcs.052696

Cited by 97 publications

(70 citation statements)

References 59 publications

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“…Similarly, significant changes in the protein composition of synaptic junctions following processes of high (pathological) synaptic activity have been reported more than a decade ago (Hu et al, 1998; Wyneken et al, 2001) using micro-sequencing and immunoblots. Since then, mass spectrometry and proteomic methods have been used to characterize the contents of synaptic protein preparations [for review see: (Sheng and Hoogenraad, 2007), in exquisite detail (Chua et al, 2010; Pielot et al, 2012), http://www.synprot.de/], and to follow changes in the proteome in various brain regions in response to memory-relevant plasticity processes. However, most of these studies analyzed changes in whole cell/tissue extracts and, therefore, could only indirectly infer alterations of the synaptic proteome (e.g., McNair et al, 2006, 2007; Monopoli et al, 2011; Hong et al, 2013).…”

Section: Changes In the Synaptic Proteome Associated With Plasticity mentioning

confidence: 99%

The roles of protein expression in synaptic plasticity and memory consolidation

Rosenberg¹,

Gal-Ben-Ari²,

Dieterich³

et al. 2014

Front. Mol. Neurosci.

140

103

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The amount and availability of proteins are regulated by their synthesis, degradation, and transport. These processes can specifically, locally, and temporally regulate a protein or a population of proteins, thus affecting numerous biological processes in health and disease states. Accordingly, malfunction in the processes of protein turnover and localization underlies different neuronal diseases. However, as early as a century ago, it was recognized that there is a specific need for normal macromolecular synthesis in a specific fragment of the learning process, memory consolidation, which takes place minutes to hours following acquisition. Memory consolidation is the process by which fragile short-term memory is converted into stable long-term memory. It is accepted today that synaptic plasticity is a cellular mechanism of learning and memory processes. Interestingly, similar molecular mechanisms subserve both memory and synaptic plasticity consolidation. In this review, we survey the current view on the connection between memory consolidation processes and proteostasis, i.e., maintaining the protein contents at the neuron and the synapse. In addition, we describe the technical obstacles and possible new methods to determine neuronal proteostasis of synaptic function and better explain the process of memory and synaptic plasticity consolidation.

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Section: Changes In the Synaptic Proteome Associated With Plasticity mentioning

confidence: 99%

The roles of protein expression in synaptic plasticity and memory consolidation

Rosenberg¹,

Gal-Ben-Ari²,

Dieterich³

et al. 2014

Front. Mol. Neurosci.

140

103

View full text Add to dashboard Cite

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“…They produce more than 90% of all neuronal ATP (Harris et al, 2012), which is needed in many steps of the synaptic vesicle cycle (Südhof, 1995; Chua et al, 2010; Sudhof and Rizo, 2011). Mitochondria synthesize the excitatory neurotransmitter glutamate from glutamine (Waagepetersoen et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial support of persistent presynaptic vesicle mobilization with age-dependent synaptic growth after LTP

Smith

Bourne

Cao

et al. 2016

eLife

116

120

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Mitochondria support synaptic transmission through production of ATP, sequestration of calcium, synthesis of glutamate, and other vital functions. Surprisingly, less than 50% of hippocampal CA1 presynaptic boutons contain mitochondria, raising the question of whether synapses without mitochondria can sustain changes in efficacy. To address this question, we analyzed synapses from postnatal day 15 (P15) and adult rat hippocampus that had undergone theta-burst stimulation to produce long-term potentiation (TBS-LTP) and compared them to control or no stimulation. At 30 and 120 min after TBS-LTP, vesicles were decreased only in presynaptic boutons that contained mitochondria at P15, and vesicle decrement was greatest in adult boutons containing mitochondria. Presynaptic mitochondrial cristae were widened, suggesting a sustained energy demand. Thus, mitochondrial proximity reflected enhanced vesicle mobilization well after potentiation reached asymptote, in parallel with the apparently silent addition of new dendritic spines at P15 or the silent enlargement of synapses in adults.DOI: http://dx.doi.org/10.7554/eLife.15275.001

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“…In nerve terminals, synaptic vesicles, also termed small clear vesicles, are used for neurotransmission (Sudhof, 2004;Rizzoli and Betz, 2005;Chua et al, 2010). In contrast, neuroendocrine cells mainly use large dense-core vesicles to release neuropeptides and hormones (Burgoyne and Morgan, 2003;García et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Calcium Triggers Exocytosis from Two Types of Organelles in a Single Astrocyte

Liu¹,

Sun²,

Xiong³

et al. 2011

Journal of Neuroscience

130

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Astrocytes release a variety of signaling molecules including glutamate, D-serine, and ATP in a regulated manner. Although the functions of these molecules, from regulating synaptic transmission to controlling specific behavior, are well documented, the identity of their cellular compartment(s) is still unclear. Here we set out to study vesicular exocytosis and glutamate release in mouse hippocampal astrocytes. We found that small vesicles and lysosomes coexisted in the same freshly isolated or cultured astrocytes. Both small vesicles and lysosome fused with the plasma membrane in the same astrocytes in a Ca 2ϩ -regulated manner, although small vesicles were exocytosed more efficiently than lysosomes. Blockade of the vesicle glutamate transporter or cleavage of synaptobrevin 2 and cellubrevin (both are vesicle-associated membrane proteins) with a clostridial toxin greatly inhibited glutamate release from astrocytes, while lysosome exocytosis remained intact. Thus, both small vesicles and lysosomes contribute to Ca 2ϩ -dependent vesicular exocytosis, and small vesicles support glutamate release from astrocytes.

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The architecture of an excitatory synapse

Cited by 97 publications

References 59 publications

The roles of protein expression in synaptic plasticity and memory consolidation

The roles of protein expression in synaptic plasticity and memory consolidation

Mitochondrial support of persistent presynaptic vesicle mobilization with age-dependent synaptic growth after LTP

Calcium Triggers Exocytosis from Two Types of Organelles in a Single Astrocyte

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