CoChat
Sign Up
Cited by 223Neuroscience and Neuropharmacology ResearchCellular transport and secretionGenetics and Neurodevelopmental Disorders

The DOI matches its Crossref record; 66 of the 67 references it cites were found in a registry or an index.

Bassoon Speeds Vesicle Reloading at a Central Excitatory Synapse

Open access
Hallermann, Stefan, Fejtova, Anna, Schmidt, Hartmut, Weyhersmüller, Annika, Silver, R. Angus, Gundelfinger, Eckart D., Eilers, Jens·2010·Neuron
DOI 10.1016/j.neuron.2010.10.026PMC PMC3004039
Open this paper in CoChat — free account

Abstract

Sustained rate-coded signals encode many types of sensory modalities. Some sensory synapses possess specialized ribbon structures, which tether vesicles, to enable high-frequency signaling. However, central synapses lack these structures, yet some can maintain signaling over a wide bandwidth. To analyze the underlying molecular mechanisms, we investigated the function of the active zone core component Bassoon in cerebellar mossy fiber to granule cell synapses. We show that short-term synaptic depression is enhanced in Bassoon knockout mice during sustained high-frequency trains but basal synaptic transmission is unaffected. Fluctuation and quantal analysis as well as quantification with constrained short-term plasticity models revealed that the vesicle reloading rate was halved in the absence of Bassoon. Thus, our data show that the cytomatrix protein Bassoon speeds the reloading of vesicles to release sites at a central excitatory synapse.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.neuron.2010.10.026

Cites

66 of 66 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Enhanced Synaptic Depression in Cerebellar MF-GC Synapses in Bsn−/− Mice during Sustained Synaptic Signaling (A) Immunohistochemical stainings of Bassoon, Piccolo, and Synapsin in cerebellar slices of Bassoon knockout mice (Bsn−/−, bottom) and their wild-type littermates (control, top). The granular cell (g), purkinje cell (p), and molecular layer (m) are indicated (scale bar: 100 μm). (B) Western blot analysis of Bassoon expression in homogenates from whole brains of Bsn+/+, Bsn+/−, and Bsn−/− mice. With anti-Bassoon antibodies, two major protein bands of 420 and 350 kDa were detected in Bsn+/+ and Bsn+/−, but not in Bsn−/−, mice. (C) Examples of EPSCs recorded during 20 and 100 Hz (100 stimuli) and 300 Hz (20 stimuli) in one control and one Bsn−/− MF-GC connection. For each frequency, three traces (gray) and the corresponding average (control: black; Bsn−/−: dark gray) are superimposed. The phasic and tonic components are indicated by horizontal black lines and were automatically determined for each EPSC and each trace (see Experimental Procedures). (D) Average phasic EPSC amplitude versus time for a 20, 100, and 300 Hz stimulation for control mice (black; n = 13) and Bsn−/− mice (gray; n = 11; mean ± SEM; normalized to the first EPSC within the train; asterisks indicate significant differences, p < 0.05; note the logarithmic scale). (E) Average steady-state EPSC amplitude (see brackets in D) of phasic and tonic EPSC amplitudes in control mice (black; n = 13) and Bsn−/− mice (gray; n = 11; mean ± SEM; for data on BsnΔEx4/5 see Figure S1).
Figure 1 Enhanced Synaptic Depression in Cerebellar MF-GC Synapses in Bsn−/− Mice during Sustained Synaptic Signaling (A) Immunohistochemical stainings of Bassoon, Piccolo, and Synapsin in cerebellar slices of Bassoon knockout mice (Bsn−/−, bottom) and their wild-type littermates (control, top). The granular cell (g), purkinje cell (p), and molecular layer (m) are indicated (scale bar: 100 μm). (B) Western blot analysis of Bassoon expression in homogenates from whole brains of Bsn+/+, Bsn+/−, and Bsn−/− mice. With anti-Bassoon antibodies, two major protein bands of 420 and 350 kDa were detected in Bsn+/+ and Bsn+/−, but not in Bsn−/−, mice. (C) Examples of EPSCs recorded during 20 and 100 Hz (100 stimuli) and 300 Hz (20 stimuli) in one control and one Bsn−/− MF-GC connection. For each frequency, three traces (gray) and the corresponding average (control: black; Bsn−/−: dark gray) are superimposed. The phasic and tonic components are indicated by horizontal black lines and were automatically determined for each EPSC and each trace (see Experimental Procedures). (D) Average phasic EPSC amplitude versus time for a 20, 100, and 300 Hz stimulation for control mice (black; n = 13) and Bsn−/− mice (gray; n = 11; mean ± SEM; normalized to the first EPSC within the train; asterisks indicate significant differences, p < 0.05; note the logarithmic scale). (E) Average steady-state EPSC amplitude (see brackets in D) of phasic and tonic EPSC amplitudes in control mice (black; n = 13) and Bsn−/− mice (gray; n = 11; mean ± SEM; for data on BsnΔEx4/5 see Figure S1).CC BY · PubMed Central
Figure 2 Basal MF-GC Transmission Is Normal in Bsn−/− (A) Fifteen consecutive EPSCs superimposed with the average EPSC (white) for control (top) and Bsn−/− (bottom) mice recorded at 37°C (stimulus artifacts removed). Biexponential fits to the current decay are superimposed (single components: red and blue; sum: green dashed). (B) Average EPSC amplitude, its coefficient of variation (CV), the 20%–80% rise time, the amplitude-weighted decay time constant, the decay time constant of the fast exponential component (τ1), its relative amplitude (A1), and the decay time constant of the slower exponential component (τ2) for control (black, n = 14) and Bsn−/− (gray, n = 12) mice. (C) Three examples of spontaneous EPSCs and the corresponding amplitude histogram of this control experiment. (D) Cumulative histogram of amplitudes of spontaneous EPSCs from all experiments of control mice (black) and Bsn−/− mice (gray, Kolmogorov-Smirnov test: p = 0.26). (E) Average amplitude of spontaneous EPSCs and estimated quantal content for control mice (black, n = 14) and Bsn−/− mice (gray, n = 12; for data on BsnΔEx4/5 see Figure S2).
Figure 2 Basal MF-GC Transmission Is Normal in Bsn−/− (A) Fifteen consecutive EPSCs superimposed with the average EPSC (white) for control (top) and Bsn−/− (bottom) mice recorded at 37°C (stimulus artifacts removed). Biexponential fits to the current decay are superimposed (single components: red and blue; sum: green dashed). (B) Average EPSC amplitude, its coefficient of variation (CV), the 20%–80% rise time, the amplitude-weighted decay time constant, the decay time constant of the fast exponential component (τ1), its relative amplitude (A1), and the decay time constant of the slower exponential component (τ2) for control (black, n = 14) and Bsn−/− (gray, n = 12) mice. (C) Three examples of spontaneous EPSCs and the corresponding amplitude histogram of this control experiment. (D) Cumulative histogram of amplitudes of spontaneous EPSCs from all experiments of control mice (black) and Bsn−/− mice (gray, Kolmogorov-Smirnov test: p = 0.26). (E) Average amplitude of spontaneous EPSCs and estimated quantal content for control mice (black, n = 14) and Bsn−/− mice (gray, n = 12; for data on BsnΔEx4/5 see Figure S2).CC BY · PubMed Central
Figure 3 Evoked EPSC Amplitudes Recover More Slowly from Synaptic Depression in Bsn−/− Mice Than in Control Mice (A) Twenty consecutive current traces elicited by a 300 Hz train followed by test stimuli of increasing intervals (the first two and the last EPSC out of six are shown) recorded in a control mouse. The average is superimposed in black. Note the spontaneous EPSCs after the train. (B) Average phasic amplitudes of the twentieth EPSC at the end of 300 Hz trains followed by the first and second EPSC (left) and all (first–sixth) EPSCs (right) of the recovery for control mice (black; n = 13) and Bsn−/− mice (gray; n = 11; asterisks indicates significant differences) superimposed with biexponential fits (for recovery from 20 and 100 Hz trains and for data on BsnΔEx4/5, see Figure S3).
Figure 3 Evoked EPSC Amplitudes Recover More Slowly from Synaptic Depression in Bsn−/− Mice Than in Control Mice (A) Twenty consecutive current traces elicited by a 300 Hz train followed by test stimuli of increasing intervals (the first two and the last EPSC out of six are shown) recorded in a control mouse. The average is superimposed in black. Note the spontaneous EPSCs after the train. (B) Average phasic amplitudes of the twentieth EPSC at the end of 300 Hz trains followed by the first and second EPSC (left) and all (first–sixth) EPSCs (right) of the recovery for control mice (black; n = 13) and Bsn−/− mice (gray; n = 11; asterisks indicates significant differences) superimposed with biexponential fits (for recovery from 20 and 100 Hz trains and for data on BsnΔEx4/5, see Figure S3).CC BY · PubMed Central
Figure 4 Spontaneous EPSC Amplitudes Recover Rapidly from Depression in Both Bsn−/− and Control Mice (A and B) Normalized amplitudes of spontaneous EPSCs (black) measured after the 300 Hz trains pooled across all control (A) and Bsn−/− recordings (B). A corresponding average current trace is shown in gray (note gray scale on the right). A sliding average of 11 consecutive spontaneous EPSCs amplitudes is superimposed in dark magenta. An exponential fit to the spontaneous EPSC amplitudes is superimposed in magenta (y[t] = 100 – (100 – q0) exp[−t/τ]). The initial amplitude of the spontaneous EPSC after the trains (q0) and the time constant of recovery (τ) are indicated. The 624 and 261 spontaneous EPSCs were detected in 132 and 101 300-Hz traces. Note that the average frequency of spontaneous EPSCs per MF-GC connection was not significantly different (0.4 ± 0.1 and 0.6 ± 0.2 s−1 for control and Bsn−/−, n = 13 and 11, respectively, p = 0.4). (C) Average current trace of a control 300 Hz experiment (gray). Below, the time course of the average depression of the phasic EPSC amplitude during and after the 300 Hz stimulations in control mice is plotted in black (monoexponential fit to the average depression and biexponential fit to the recovery). In addition, the corresponding postsynaptic (“post,” magenta) and presynaptic components of depression (“pre,” green) are shown.
Figure 4 Spontaneous EPSC Amplitudes Recover Rapidly from Depression in Both Bsn−/− and Control Mice (A and B) Normalized amplitudes of spontaneous EPSCs (black) measured after the 300 Hz trains pooled across all control (A) and Bsn−/− recordings (B). A corresponding average current trace is shown in gray (note gray scale on the right). A sliding average of 11 consecutive spontaneous EPSCs amplitudes is superimposed in dark magenta. An exponential fit to the spontaneous EPSC amplitudes is superimposed in magenta (y[t] = 100 – (100 – q0) exp[−t/τ]). The initial amplitude of the spontaneous EPSC after the trains (q0) and the time constant of recovery (τ) are indicated. The 624 and 261 spontaneous EPSCs were detected in 132 and 101 300-Hz traces. Note that the average frequency of spontaneous EPSCs per MF-GC connection was not significantly different (0.4 ± 0.1 and 0.6 ± 0.2 s−1 for control and Bsn−/−, n = 13 and 11, respectively, p = 0.4). (C) Average current trace of a control 300 Hz experiment (gray). Below, the time course of the average depression of the phasic EPSC amplitude during and after the 300 Hz stimulations in control mice is plotted in black (monoexponential fit to the average depression and biexponential fit to the recovery). In addition, the corresponding postsynaptic (“post,” magenta) and presynaptic components of depression (“pre,” green) are shown.CC BY · PubMed Central
Figure 5 Estimating Quantal Parameters during Short-Term Plasticity with Fluctuation Analysis in Bsn−/− and Control Mice (A) Example of 54 consecutive current traces (30 s intervals) elicited by 300 Hz trains of 20 stimuli followed by test stimuli of increasing intervals (the first three out of six are shown) recorded in a control mouse. On the right, the first five traces are shown in higher resolution (cf. gray boxed area on the left; stimulus artifacts were removed for clarity). (B) Amplitude of the first (blue), second (green), and twentieth (red) EPSC during, and the first (gray) and sixth (dark gray) EPSC after, the train plotted versus the trace number for the control experiment shown in (A). The corresponding mean EPSC amplitude is indicated as a horizontal line in the corresponding color. (C) Variance of the EPSC amplitudes during the train (black) and during the recovery (gray) plotted versus the corresponding mean for the control experiment shown above, superimposed with a parabolic fit, constrained through the origin, the first EPSC during the train, and by the quantal size (qfix) determined independently from the spontaneous EPSCs measured at this connection (the blue straight line indicates the constrained initial slope qfix). The resulting number of release sites (N) and resting release probability (pr) are indicated. A linear fit (red) to the last 15 EPSCs during the train constrained through the origin reveals the quantal size during the train (q). (D) Average data for control and Bsn−/− experiments (n = 5 and 4, respectively).
Figure 5 Estimating Quantal Parameters during Short-Term Plasticity with Fluctuation Analysis in Bsn−/− and Control Mice (A) Example of 54 consecutive current traces (30 s intervals) elicited by 300 Hz trains of 20 stimuli followed by test stimuli of increasing intervals (the first three out of six are shown) recorded in a control mouse. On the right, the first five traces are shown in higher resolution (cf. gray boxed area on the left; stimulus artifacts were removed for clarity). (B) Amplitude of the first (blue), second (green), and twentieth (red) EPSC during, and the first (gray) and sixth (dark gray) EPSC after, the train plotted versus the trace number for the control experiment shown in (A). The corresponding mean EPSC amplitude is indicated as a horizontal line in the corresponding color. (C) Variance of the EPSC amplitudes during the train (black) and during the recovery (gray) plotted versus the corresponding mean for the control experiment shown above, superimposed with a parabolic fit, constrained through the origin, the first EPSC during the train, and by the quantal size (qfix) determined independently from the spontaneous EPSCs measured at this connection (the blue straight line indicates the constrained initial slope qfix). The resulting number of release sites (N) and resting release probability (pr) are indicated. A linear fit (red) to the last 15 EPSCs during the train constrained through the origin reveals the quantal size during the train (q). (D) Average data for control and Bsn−/− experiments (n = 5 and 4, respectively).CC BY · PubMed Central
Figure 6 Estimating Quantal Parameters and the Kinetics of Vesicle Reloading at MF-GC Synapses with Three Short-Term Plasticity Models (A) In model 1, a MF-GC connection is characterized by N release sites with a release probability, pr, and a rate of vesicle reloading, k. In model 2, the rate of vesicle reloading, k0, is nonlinearly accelerated by the residual Ca2+ concentration with the maximal rate, kCa. In model 3, a MF-GC connection is characterized by N1 and N2 release sites with low and high release probability, pr1 and pr2, respectively. Vesicles in N1 are in equilibrium with a pool of N0 releasable vesicles. (B) Average phasic EPSC amplitudes of 300 Hz control experiments at 37°C superimposed with predictions of model 1, 2, and 3 in green, blue, and red, respectively. Model 1 underestimates the first EPCS amplitude and therefore does not recover to 100%. Note three different partially overlapping timescales (left: during the train, middle: end of train and beginning of recovery, right: complete 5 s lasting recovery). (C and D) Corresponding graphs for 100 and 20 Hz control trains (see Figure S4 for more details). (E) Examples of EPSCs recorded during 300 Hz stimulation (20 stimuli) in control and Bsn−/− MF-GC connections with 1.25 mM [Ca2+]e (average of ∼20 traces each; control: black; Bsn−/−: dark gray). (F) Average phasic EPSC amplitudes of 300 Hz trains at 1.25 mM [Ca2+]e normalized to the basal EPSC amplitude recorded at 2 mM [Ca2+]e in each connection for control mice (black; n = 6) and Bsn−/− mice (gray; n = 5; note the logarithmic scale). (G) Average phasic and tonic steady-state EPSC amplitudes in 300 Hz trains at 1.25 mM [Ca2+]e for control mice (black; n = 6) and Bsn−/− mice (gray; n = 5). (H) Average phasic EPSC amplitudes of 300 Hz control experiments recorded with 1.25 mM [Ca2+]e superimposed with the predictions of model 1, 2, and 3 in green, blue, and red, respectively, in which the release probabilities were scaled down by a factor of 2.
Figure 6 Estimating Quantal Parameters and the Kinetics of Vesicle Reloading at MF-GC Synapses with Three Short-Term Plasticity Models (A) In model 1, a MF-GC connection is characterized by N release sites with a release probability, pr, and a rate of vesicle reloading, k. In model 2, the rate of vesicle reloading, k0, is nonlinearly accelerated by the residual Ca2+ concentration with the maximal rate, kCa. In model 3, a MF-GC connection is characterized by N1 and N2 release sites with low and high release probability, pr1 and pr2, respectively. Vesicles in N1 are in equilibrium with a pool of N0 releasable vesicles. (B) Average phasic EPSC amplitudes of 300 Hz control experiments at 37°C superimposed with predictions of model 1, 2, and 3 in green, blue, and red, respectively. Model 1 underestimates the first EPCS amplitude and therefore does not recover to 100%. Note three different partially overlapping timescales (left: during the train, middle: end of train and beginning of recovery, right: complete 5 s lasting recovery). (C and D) Corresponding graphs for 100 and 20 Hz control trains (see Figure S4 for more details). (E) Examples of EPSCs recorded during 300 Hz stimulation (20 stimuli) in control and Bsn−/− MF-GC connections with 1.25 mM [Ca2+]e (average of ∼20 traces each; control: black; Bsn−/−: dark gray). (F) Average phasic EPSC amplitudes of 300 Hz trains at 1.25 mM [Ca2+]e normalized to the basal EPSC amplitude recorded at 2 mM [Ca2+]e in each connection for control mice (black; n = 6) and Bsn−/− mice (gray; n = 5; note the logarithmic scale). (G) Average phasic and tonic steady-state EPSC amplitudes in 300 Hz trains at 1.25 mM [Ca2+]e for control mice (black; n = 6) and Bsn−/− mice (gray; n = 5). (H) Average phasic EPSC amplitudes of 300 Hz control experiments recorded with 1.25 mM [Ca2+]e superimposed with the predictions of model 1, 2, and 3 in green, blue, and red, respectively, in which the release probabilities were scaled down by a factor of 2.CC BY · PubMed Central
Figure 7 Testing the Robustness of Presynaptic Parameters Estimated with a Short-Term Plasticity Model at Individual MF-GC Connections (A) Examples of EPSC amplitudes recorded at an individual MF-GC connection in a control mouse at 37°C (20 Hz: red; 100 Hz: green; 300 Hz: blue) superimposed with the corresponding predictions of model 3 (dark colors, best-fit parameters are indicated). The recovery is shown on two different, nonoverlapping timescales and shifted horizontally. Note the color-coded timescales in (C). (B) Quantal content and coefficient of variation (CV) of EPSC amplitudes at 1 Hz stimulation (cf. Figure 1) correlated to the predictions of model 3 for each individual control connection at 37°C (open symbols) and 23°C (closed symbols), respectively (examples in A are highlighted in magenta). For calculation of CV, see Equation 6 in Supplemental Experimental Procedures. Linear fits (constrained through the origins) had slopes (s) as indicated in the graphs (nonparametric Spearman correlation coefficient, r = 0.9 and 0.3 with p < 0.0001 and p = 0.07, for quantal content and CV, respectively). (C) Corresponding example as shown in (A) for Bsn−/−. (D) Corresponding data as shown in (B) for Bsn−/− (nonparametric Spearman correlation coefficient, r = 0.9 and 0.5 with p < 0.0001 and p = 0.008, for quantal content and CV, respectively). See Figure S5 for corresponding test of model 1 and 2.
Figure 7 Testing the Robustness of Presynaptic Parameters Estimated with a Short-Term Plasticity Model at Individual MF-GC Connections (A) Examples of EPSC amplitudes recorded at an individual MF-GC connection in a control mouse at 37°C (20 Hz: red; 100 Hz: green; 300 Hz: blue) superimposed with the corresponding predictions of model 3 (dark colors, best-fit parameters are indicated). The recovery is shown on two different, nonoverlapping timescales and shifted horizontally. Note the color-coded timescales in (C). (B) Quantal content and coefficient of variation (CV) of EPSC amplitudes at 1 Hz stimulation (cf. Figure 1) correlated to the predictions of model 3 for each individual control connection at 37°C (open symbols) and 23°C (closed symbols), respectively (examples in A are highlighted in magenta). For calculation of CV, see Equation 6 in Supplemental Experimental Procedures. Linear fits (constrained through the origins) had slopes (s) as indicated in the graphs (nonparametric Spearman correlation coefficient, r = 0.9 and 0.3 with p < 0.0001 and p = 0.07, for quantal content and CV, respectively). (C) Corresponding example as shown in (A) for Bsn−/−. (D) Corresponding data as shown in (B) for Bsn−/− (nonparametric Spearman correlation coefficient, r = 0.9 and 0.5 with p < 0.0001 and p = 0.008, for quantal content and CV, respectively). See Figure S5 for corresponding test of model 1 and 2.CC BY · PubMed Central
Figure 8 Slower Vesicle Reloading in Bsn−/− and BsnΔEx4/5 Mice as Compared with Control Mice (A) The rates k, kCa, and k+1, which are highlighted in magenta in model 1, 2, and 3, respectively, determine the speed of vesicle reloading during activity. The average reloading rates of the individual MF-GC connections are shown for the indicated temperatures and genotypes. While the remaining free parameters of the models for each MF-GC connection were on average unaltered (see Figure S6), the vesicle reloading rates were significantly reduced in Bsn−/− (37°C, red) and BsnΔEx4/5 (23°C, blue) compared with those of corresponding control mice. (B) Illustration of the hypothesized function of Bassoon at conventional AZs. Our data show that Bassoon speeds the rapid vesicle reloading at AZs during high-frequency transmission (magenta arrows). The basal synaptic transmission and the slower component of recovery from depression, which might be limited by the maturation of vesicles closer to the Ca2+ channels (white arrows), appeared normal in the absence of Bassoon. Based on the comparison with electron-dense structures at ribbon-type synapses and recent high-resolution anatomical studies at conventional synapses (see Discussion), we hypothesize that the large protein Bassoon builds, anchors, or organizes the proper assembly of “miniribbons,” which speed vesicle reloading at conventional synapses.
Figure 8 Slower Vesicle Reloading in Bsn−/− and BsnΔEx4/5 Mice as Compared with Control Mice (A) The rates k, kCa, and k+1, which are highlighted in magenta in model 1, 2, and 3, respectively, determine the speed of vesicle reloading during activity. The average reloading rates of the individual MF-GC connections are shown for the indicated temperatures and genotypes. While the remaining free parameters of the models for each MF-GC connection were on average unaltered (see Figure S6), the vesicle reloading rates were significantly reduced in Bsn−/− (37°C, red) and BsnΔEx4/5 (23°C, blue) compared with those of corresponding control mice. (B) Illustration of the hypothesized function of Bassoon at conventional AZs. Our data show that Bassoon speeds the rapid vesicle reloading at AZs during high-frequency transmission (magenta arrows). The basal synaptic transmission and the slower component of recovery from depression, which might be limited by the maturation of vesicles closer to the Ca2+ channels (white arrows), appeared normal in the absence of Bassoon. Based on the comparison with electron-dense structures at ribbon-type synapses and recent high-resolution anatomical studies at conventional synapses (see Discussion), we hypothesize that the large protein Bassoon builds, anchors, or organizes the proper assembly of “miniribbons,” which speed vesicle reloading at conventional synapses.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 67 references

Cited by

Sorted by citations

See all 223

Related

Metadata

Authors
Hallermann, S., Fejtova, A., Schmidt, H., Weyhersmüller, A., Silver, R. A., Gundelfinger, E. D., & Eilers, J.
Affiliations
  • Leipzig University (DE)
  • University College London (GB)
  • Leibniz Institute for Neurobiology (DE)
Corresponding author
Hallermann, Stefan
ORCID
Venue
Neuron
Publisher
Elsevier BV
Published
2010-11
Volume
68
Issue
4
Pages
710-723
ISSN
0896-6273 (ISSN-L)
DOI
10.1016/j.neuron.2010.10.026
PMC
PMC3004039
OpenAlex
W2050878615
Cited by
223
References
67
Citations by year
2026: 7 · 2025: 13 · 2024: 7 · 2023: 12 · 2022: 15 · 2021: 11 · 2020: 16 · 2019: 17 · 2018: 13 · 2017: 16 · 2016: 17 · 2015: 13 · 2014: 17 · 2013: 15 · 2012: 16
FWCI
6.34
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuron (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Funders
Wellcome Trust
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
bassoon, short-term synaptic depression, cerebellum, active zone, quantal analysis, rate coding
MeSH terms
Animals, Cells, Cultured, Cerebellum, Hippocampus, Mice, Inbred C57BL, Mice, Transgenic, Nerve Tissue Proteins, Neural Inhibition, Reaction Time, Synapses, Synaptic Vesicles, Time Factors, Mice, Knockout, Excitatory Postsynaptic Potentials, Mice, Mice, 129 Strain

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review