The spine coverage rate was higher in immature mice at P10 (Figures 5I–5K). Because the total perimeter of the spines was not different between adult and immature mice (Figure 5L), higher spine coverage rates were most probably caused by the structural differences in the PF terminals. Taken together, our results show that PFs extend axonal protrusions that cover the surface of PC spines in the immature cerebellum in vivo during the peak of PF-PC synapse formation. To examine whether PF protrusions require Cbln1-GluD2 interaction in vivo, we introduced GFP into EGL by

electroporation at P7 in cbln1-null, glud2-null, and wild-type cerebella and analyzed PFs at later postnatal days ( Figure 6A). We found that PF protrusions were reduced in cbln1-null and glud2-null mice both at P18 and P25 ( Figure 6B). Similarly, www.selleckchem.com/products/cobimetinib-gdc-0973-rg7420.html modest but statistically significant reduction in PF boutons was observed selleck chemicals in cbln1-null mice at P18 and P25 and glud2-null mice at P25 ( Figure 6C). We have previously shown by electron

microscopy that the density of PF-PC synapses is reduced by as much as 80% in adult cbln1-null mice ( Hirai et al., 2005). Thus, in the present analysis, we may have overestimated PF boutons by including boutons that belong to PF-interneuron synapses and bouton-like axonal swellings lacking postsynaptic contacts. Nevertheless, these results suggest that morphological changes in PFs require Cbln1 and GluD2 in vivo. We have

previously shown that single injection of recombinant WT-Cbln1 into adult cbln1-null mice in vivo induces significant increase in PF-PC synapses ( Ito-Ishida et al., 2008). Therefore, we next examined whether complementation of cbln1-null mice with recombinant WT-Cbln1 could also restore PF protrusions during development. Indeed, injection of WT-Cbln1 into cbln1-null mice at P14 increased the density of PF protrusions ( Figures 6D and 6E) and PF boutons ( Figures 6D and 6F) at P15. Such changes were not induced by injection of CS-Cbln1 ( Figures 6D–6F). These results indicate that PF protrusions depend on the Cbln1-GluD2 Mirabegron interaction in vivo. Our results from the coculture assay suggested that interaction between Nrx and Cbln1 is required for protrusion formation (Figures 4H and 4I). To clarify the roles of Nrx in vivo, we examined the effect of altering Nrx levels on PF structure in the developing cerebellum. Overexpression of Flag tagged Nrx1β (+S4), a splice variant which binds to Cbln1, specifically increased the density of PF protrusions, while no change was observed in the density of boutons (Figures 7A–7C). The result suggests that endogenous Nrx level is not saturated and protrusive changes can be triggered by increasing Nrx. The bouton density, which should be determined by the number of PF-PC contacts, may be already too high in endogenous condition to induce any additional changes.

24 ± 0.02 to 0.85 ± 0.24 Hz; Student’s t test, p < 0.01; Figures 4D1 and 4D2). Preincubation with the OT-receptor antagonist (OTA), though not affecting basic AP frequencies, significantly and reversibly blocked these increases (>70% remaining response 0.46 ± 0.09 Hz, n = 5; one-way analysis of variance [ANOVA], p < 0.05; Figures 4D1 and 4D2). The GABA(A) blocker picrotoxin (PTX) caused, on average, a significant increase in baseline AP frequencies (from 0.27 ± 0.09 to 0.61 ± 0.26 Hz, n = 5; one-way ANOVA, p < 0.05), possibly as a result of inhibition of local inhibitory circuits in the CeL (Ciocchi et al.,

2010 and Haubensak et al., 2010). In summary, endogenous release of OT from hypothalamic fibers leads to an efficient, OT-R-mediated activation of CeL neurons. Because CeL neurons project to and release GABA in the CeM (Huber selleck products et al., 2005), we also tested for rapid transient increases in IPSC frequencies in the CeM. CeL exposure to BL (20 s) evoked abrupt increases in IPSC frequencies in 36 out of 107 tested

CeM neurons (Figure 4B, bottom trace and Figure 4E1), on average from 0.5 ± 0.1 Hz to 3.7 ± 0.8 Hz (Figure 4E2, first panel; Student’s t test, p < 0.01), Selleckchem Crenolanib without affecting average IPSC amplitudes (Figure S4B). These increases depended on the precise area exposed to BL. Thus, BL applied outside the CeL, e.g., focused on the CeM (Figure 4E2, fifth panel, n = 6), never modified IPSC frequencies in CeM neurons that responded with increases in IPSCs after BL exposure of the CeL. Similar to the AP increases in the CeL (Figure 4D2), these increases in IPSC frequencies in CeM were significantly and reversibly blocked by OTA (>70%, 1.3 ± 0.2 Hz, n = 9; one-way ANOVA, p < 0.05; Figure 4E2, third panel). Subsequent PTX application blocked spontaneous IPSCs

as well as any further BL effects (n = 5, Figure 4E2, fourth panel), confirming the GABAergic nature of the observed responses. Although OTA significantly inhibited BL-induced increases of AP frequencies in the CeL and IPSC frequencies in the CeM, in the both cases small but significant responses remained. In both CeA subdivisions, these responses could be entirely abolished by adding the AMPA-receptor antagonist NBQX to the OTA incubations (Figure 4D2, left panel, 0.25 ± 0.01 Hz for APs, n = 5; and Figure 4E2, third panel, 0.6 ± 0.1Hz for IPSCs, n = 4). This suggests that the BL-evoked release of OT in the CeA is accompanied by the release of another factor, which requires AMPA-receptor activation. Indeed, we found that NBQX alone also decreased BL-induced IPSC responses in the CeM (Figure 4E2, second panel). To determine whether BL-evoked release in vivo of endogenous OT in the CeA affects behavior, we expressed the ChR2-mCherry fusion protein in all hypothalamic OT structures of virgin female rats (see above).

” In LPP, we found that responses to photographs of scenes correlate with responses to line drawings of those same scenes, showing that neurons are tuned to specific layouts invariant to their content and providing additional support for the spatial-layout hypothesis. However, further experiments revealed that the spatial-layout hypothesis is an incomplete account of the information represented in LPP and MPP. The responses of individual LPP and MPP neurons

to systematically varied 3D renderings of a room containing objects show that these regions represent both spatial and nonspatial selleck kinase inhibitor information, suggesting that their role extends beyond analysis of spatial layout. In both LPP and MPP, more cells were modulated by texture than by viewpoint, distance from walls, or objects present (Table 1), and most LPP neurons also represented information about objects present in the scene. While a significant number of neurons in both regions represented information about viewpoint and distance, either alone or in interaction

with texture, no cells encoded only viewpoint or distance. Sensitivity to object ensemble and texture statistics has also been reported in the PPA (Cant and Goodale, 2011 and Cant and Xu, 2012). Because texture is important for defining scene identity but irrelevant for specifying GW3965 mouse spatial layout, we suggest that LPP and MPP may selectively represent both spatial and nonspatial information about scenes in order to facilitate

identification of specific locations. Given that neurons in LPP and MPP respond to some nonscene images and do not represent high-level spatial layout invariant to texture, it is likely that these neurons, like other IT neurons, are tuned to specific sets of complex shapes and visual features. LPP and MPP probably Astemizole differ from other parts of IT not in the way they represent visual information but in their organization and the type of information that they represent: these regions are macroscale clusters of neurons showing selectivity for shapes and features present in scenes. Our scene and nonscene stimuli could be easily distinguished by a linear classifier trained on the output of the HMAX C1 complex cell model, suggesting that these scene and nonscene images (and perhaps most natural scene and nonscene images) are easily distinguishable from low-level features alone. The nature of the features to which LPP and MPP neurons respond, and their specificity to scenes, remains unresolved, although we suggest that specific configurations of long, straight lines may play an important role. We found that units in LPP and MPP respond more strongly to nonscene stimuli with such lines (Figures 6 and S5C–S5E).

5 Tesla MAGNETOM Vision

MRI scanner (Erlangen, Germany) as described in Dosenbach et al. (2010). The third data set (n = 106: a 53 subject cohort, 52 subject cohort, and an additional single subject) was acquired on a Siemens MAGNETOM Tim Trio 3.0T Scanner with a Siemens 12 channel Head Matrix Coil (Erlangen, Germany) as described in Dosenbach et al. INCB024360 clinical trial (2010). See Supplemental Experimental Procedures for acquisition details. Functional images underwent standard fMRI preprocessing to reduce artifacts, register subjects to a target atlas, and resample the data on a 3 mm isotropic grid (Shulman et al., 2010). See Supplemental Experimental Procedures for further details. For rs-fcMRI analyses, several additional preprocessing steps were utilized to reduce spurious variance unlikely to reflect neuronal activity (Fox et al., 2009). These steps included: (1), a temporal band-pass filter (0.009 Hz < f < 0.08 Hz) and spatial smoothing

(6 mm full width at half maximum); (2), regression of six parameters obtained by rigid body head motion correction; (3), regression of the whole brain signal averaged across the whole brain; (4), regression of ventricular signal averaged from ventricular ROIs; and (5), regression of white matter signal Y-27632 cell line averaged from white matter ROIs. The first derivatives of these regressors were also regressed. The first method of identifying putative functional areas searched a large fMRI data set acquired in a single scanner (data set 1) for brain regions that reliably displayed significant activity when certain tasks were performed (e.g., button-pressing) or certain signal types (e.g., error-related activity) were expected (see Table S1). Meta-analyses identified 322 ROIs (10 mm diameter spheres, see Figure S1), which were reduced to a final collection of 151 nonoverlapping meta-analytic ROIs. Full details of meta-analyses are available in Supplemental Experimental Procedures. fc-Mapping techniques were applied to

eyes-open fixation rs-fcMRI data from 40 healthy young adults (data set 2: 27 M/13 F, average age = 26.4 years old, average RMS movement = Pramipexole 0.42 mm, average number of volumes = 432). See Cohen et al. (2008) and Nelson et al. (2010a) for full conceptual and technical descriptions of fc-Mapping on cortical patches. Here, patches extending over the entire cortical surface (one per hemisphere) were used to define putative functional areas. This technique generated 254 ROIs across the cortex, which were reduced to a final set of 193 nonoverlapping ROIs. See Supplemental Experimental Procedures for further details. Meta-analytic ROIs and fc-Mapping ROIs were merged to form a maximally-spanning collection of ROIs. Meta-analytic ROIs were given preference, and nonoverlapping fc-Mapping ROIs were then added, resulting in 264 independent ROIs. A 90-node parcel-based network was formed by using the 90-parcel automated anatomical labeling (AAL) atlas (Tzourio-Mazoyer et al.

On the basis of the pigment production, the isolate klmp33 was selected and maintained on fresh SCA medium checked for its purity and stored at 4 °C for further work. The isolate klmp33 was identified as S. coelicolor based on 16S rRNA sequencing and the sequences were submitted

to Gene Bank under the accession number JQ27722. The blue pigment produced by S. BMN 673 cell line coelicolor after 3 days of incubation was separated from the biomass by centrifuging the starch casein medium at 10,000 rpm for 10 min. The resultant supernatant was analyzed using Thin Layer Chromatography conducted on silica-gel 60 F254 plates (Merck) with benzene-acetic acid (9:1; v/v) as solvent. The pigment obtained a single spot with an Rf value of 0.28 indicating the presence of actinorhodin (now onwards the pigment is referred

as actinorhodin). 15 For the synthesis of silver nanoparticles, 15 ml of AgNO3 (10−3 M) solution was treated with the 1 ml actinorhodin and exposed to inhibitors direct sun light. A color change from colorless to brown took place within few minutes indicating the formation of silver nanoparticles. A yield about 1.4 g of silver nanoparticles per liter click here was obtained from the above method. Further, the same silver nanoparticles were used for antimicrobial studies. The synthesis of silver nanoparticles was preliminary confirmed by UV–visible spectroscopy, which is an important technique to verify the formation of metal nanoparticles provided that surface plasmon resonance exists for the metal.16 The UV–visible spectroscopy was analyzed for period of 20 min, conducted on Systronics double-beam UV–visible spectrophotometer 2200, operated at 0.1 nm resolution with scanning rate 270 nm/min. The synthesis of silver

nanoparticles was further confirmed using XRD. The X-ray diffraction patterns for the synthesized silver nanoparticles were recorded using a Rigaku Ultima 4 XRD instrument. The radiation used was Cu-Kα (0.154 nm) at 40 kV and 35 nm with scanning rate of 2°/min. The TEM technique why was employed to determine the size and shape of the silver nanoparticles. The TEM image was obtained using a Philips CM200 instrument. Sample for this analysis was prepared by coating carbon-coated copper grid with aqueous silver nanoparticles. After 5 min, the extra solution was removed using blotting paper, and then the film on the grid was dried under IR light. A powder of silver nanoparticles was prepared by centrifuging the solution of synthesized silver nanoparticles at 10,000 rpm for 20 min. The solid residue was then washed with distilled water to remove any unattached biological moieties from the surface of the nanoparticles. The resultant residue was then dried completely, and the powder was used for FTIR measurement, which was performed on a NICOLET iS5 with Diamond ATR. The FTIR peaks were identified and expressed in wave numbers (cm−1).

The topics of the categories

were: reasons to be physically active, reasons to be sedentary, history of physical activity, subjective experience on physical activity, barriers to become physically active and the influence of social support and stress on physical activity. The reasons to be physically active could be categorised into four categories. The most frequently reported reason to be physically active was for the Modulators health PD332991 benefits (reported by 65% of the participants), followed by enjoyment (44%), continuation of an active lifestyle in the past (28%), and functional reasons (26%). An example of a reported functional reason is that physical activity is necessary for certain daily life activities, like transportation or gardening. Topic  Response % Reasons to be physically activea

 health benefits 65  enjoyment 44  continuation of former active lifestyle 28  function 26 History of physical activity  gymnastics at school 88  sports after age 30 yr 49  physically active in lifestyle activities 48 Subjective experience of physical activity  pleasant 85  unpleasant 30  none 10  high self-efficacy for physical activity 85 Social support  positive 47  negative 3  positive and negative 4  none, not applicable 47 Effect of social support on physical see more activity  positive 19  negative 1  none 80 Topic  Response % Reasons to be sedentaryb  poor weather 48  health problems 43  lack of intrinsic motivation 11  miscellaneous answers 16  none 20 Barriers to becoming physically active  weather 75  health 68  weather, health-specific 53  financial constraints 32  not able to pay money 20  not willing to pay money 12  sleep 10  exercise facilities in neighbourhood 7  fear of movement 6  shame 4  time 3 Stress  positive influence on physical activity 18 and  negative influence on physical activity 13  none, not applicable 68 aNumber of reasons reported: one = 47, two = 57, three = 5, four = 6. The reasons to be sedentary could be grouped into three categories and there were 18 responses that did not fit into a category. (See Appendix 1 on the

eAddenda for details of these isolated responses.) The most frequently reported reason to be sedentary was poor weather (48%), followed by health problems (43%) and lack of intrinsic motivation (11%). In addition 20% of the participants reported having no reason to be sedentary. On average, participants reported 1.7 (range 1 to 4) reasons to be physically active and 1.2 (range 0 to 3) reasons to be sedentary. Self-efficacy for physical activity was explored during a conversation with the participant about whether he/she felt confident in the ability to perform the physical activities he/she executes. If a participant reported confidence this was categorised as ‘high self-efficacy’. Positive social support for physical activity was reported by almost 50% of the study population.

Blister packs/tubing were placed on the shelf and a 4 h thermal treatment step was carried out at −28 °C. This temperature was maintained for a further 2 h while the chamber pressure was reduced to 100 mTorr. Primary drying commenced with a 4 h check details hold under these conditions followed by a 1 h ramp to and 2 h hold at −20 °C. The temperature was further ramped to 0 °C over 2 h then held for 2 h at 500 mTorr followed by a 2 h ramp to 20 °C.

Secondary drying was then performed at 27 °C for 4 h at a reduced pressure of 50 mTorr. Following lyophilization samples were transferred into individual sterile universal tubes. Each lyophilized solid dosage tablet formulation tested (n = 5) was weighed and transferred into the test drum of a Copley

Scientific friability tester (25 rpm, 4 min), during which they are subjected to the rolling movement around the drum which has a curved aperture allowing the formulations to rise and then fall over a distance of ∼16 cm. The dosage forms were then expelled, reweighed and any decrease in weight recorded. SVF was prepared as Libraries previously described [17]. NaCl (3.51 g), KOH (1.40 g), Ca(OH)2 (0.222 g), bovine serum albumin (BSA) (0.018 g), lactic acid (2 g), acetic acid (1 g), glycerol (0.16 g), urea (0.4 g) and glucose (5 g) were dissolved in 1 L of deionised water, followed by adjustment to pH 4.2 with HCl. Solid dosage tablet formulations were diluted and thoroughly mixed with a defined volume of SVF (1 ml) and the dynamic rheological properties AZD6244 analyzed. Oscillatory rheometry was conducted within the linear viscoelastic region over a frequency range from 0.1 to 10 Hz as described elsewhere [12]. The dilution ratio of was chosen on the basis of that normally encountered in the vagina following insertion of the delivery vehicle [17]. A heterogeneous indirect

sandwich ELISA was optimised for quantification of CN54gp140 in PBST (linear concentration range 0.003–0.05 μg/ml, R2 > 0.999). Wells were incubated with 50 μl/well of GNA at 10 μg/ml in deionised water (5 h at 37 °C). The wells were washed (5× 300 μl PBS-T) and blocked for 1 h at 37 °C with PBST containing 5% porcine serum (PBS-T-serum). Standards, samples and controls were prepared in PBS-T (n = 4), and incubated overnight at ambient temperature. The wells were washed and incubated with 50 μl/well HuMab 5F3 (1 μg/ml in PBS-T-serum) for 2 h at 37 °C. Following washing, bound antibody was detected using 50 μl/well goat anti-human IgG peroxidase conjugate diluted 1:5 K in PBS-T-serum and incubated for 1 h at 37 °C. After washing, the wells were incubated with 100 μl TMB/E for 5 min. The reaction was terminated by the addition of 50 μl of 2.5 M H2SO4. Plates were read immediately at A450.

and Coudeville is that ours assumes that people can only undergo natural infection by up to two dengue serotypes while they assume that up to four infections are possible. Our assumption is supported by the low frequency of tertiary and quaternary infections among hospital cohorts [8] and [19] and by the broadly cross-reactive neutralizing antibody response that is maintained after secondary infection. However, whether tertiary and quaternary play some role in the transmission dynamics

of dengue is still under debate. Relaxing this assumption would remove the Libraries competition between serotypes imposed by IOX1 research buy our model, and in general lead to greater reductions in cumulative incidence with the use of partially effective vaccines. Our model makes the assumption that the probability

of developing clinically apparent disease is higher in the presence of pre-existing immunity, regardless of whether this immunity is the result of natural infection or vaccination. A similar assumption is made in the model check details by Coudeville [22]. While in the context of natural infections it is well established that pre-existing immunity against a heterologous serotype is the main risk-factor for the development of severe disease [7], immunopathogenic effects of vaccine-induced immunity are yet to be elucidated. If heterologous vaccine induced immunity protects against infection or clinically apparent disease, the impact of partially effective vaccines will be greater than that estimated by our model. While we calibrated our transmission else parameters to fit the age distribution of seroprevalence and reported cases in Rayong, Thailand, current knowledge of dengue epidemiology can distinguish between

many of the scenarios that we simulated. Multiple studies have found evidence of heterogeneity [14], [31] and [32] but the extent to which heterogeneity in clinical expression, transmissibility or enhancement exists is not known. One of the main objectives of this research was to identify scenarios that could potentially result in adverse population effects after mass vaccination with partially effective vaccines, and therefore we deliberately chose to explore a wide parameter space, even if this resulted in unrealistic dynamics in some cases. There are important gaps in our understanding of serotype dynamics, cross-protection [33], enhancement and pathogenicity [34], [35] and [36]. Our results aim to represent hyperendemic areas generally, but predicting the potential impact of vaccination in any specific setting would require extensive serotype-specific longitudinal data that is only available from cohort studies. While our sensitivity analyses suggest that partially effective vaccines have the potential to be even more useful in settings with stable low transmission, better understanding of the changing epidemiology of dengue in settings of more recent re-emergence (e.g.

This uncertainty has been elegantly clarified in the study published in this issue of Neuron ( Kole, 2011). Using a judicious combination of in vitro methodological approaches including targeted axotomy with two-photon illumination and local pharmacological inactivation of voltage-gated ion channels, Maarten Kole demonstrates that Na+ channels in the first node of Ranvier (FNoR) are essential for intrinsic bursting in L5 pyramidal neurons ( Figure 1B).

NoRs are periodic interruptions of the myelin sheath exposing the axonal membrane to the extracellular space. They express a high density of the Nav1.6 isoform of Na+ channels. By limiting the ionic current flow to the nodes, minimal charge Selumetinib solubility dmso is lost in the myelinated internodes, making action potential conduction fast, energy efficient, and saltatory. In L5 pyramidal

neurons, the FNoR is located at ∼100–120 μm from the axon hillock, which corresponds to the location of the first axonal branch point. The function of the FNoR was still controversial until very recently. Like other nodes, it could be simply mediate the propagation of the action potential from the site of initiation to the terminals. Alternatively, being located close to the cell Ibrutinib in vivo body, the FNoR was thought to be involved in spike initiation However, detailed analysis of spike initiation with voltage-imaging of the entire proximal segment of the axon clearly indicates that action potentials are not initiated at the FNoR but at the AIS (Popovic et al., 2011). Kole further clarifies this point by showing that the FNoR is the site of signal amplification through persistent Na+ current that facilitates both post-spike depolarization and burst firing. The experiments reported in the study of Kole (2011) were conducted in an Vasopressin Receptor acute slice preparation of the rat neocortex, and the author

observed that the firing behavior of L5 pyramidal neurons is highly correlated with the integrity of their axon after slicing. Thus, the action potential recorded in neurons with an intact axon exhibits a large after-depolarizing potential (ADP) that may eventually lead to burst firing. In contrast, spikes recorded from neurons with the axon cut proximal to the FNoR have no ADP. And neurons with a severed axon never fire in burst mode. It should be noted that the complexity of the dendritic tree does not enter into consideration here. In fact, Kole demonstrates that a given bursting neuron becomes regular if the FNoR is removed from the axon but not if the cut is made distally. The key point of this study is that the FNoR contains a very high density of Na+ channels that promote bursting. What is the specificity of the Na+ channels in this region? Compared to the soma, the voltage dependence of activation and inactivation of axonal Na+ current is shifted by 10 mV to more hyperpolarized potentials (Kole et al., 2008 and Hu et al., 2009).

Initial studies in Drosophila advanced the knowledge on CSP-α function ( Zinsmaier et al.,

1994). Later, knock-out mice lacking CSP-α opened new possibilities EPZ-6438 in vitro to study different synapses with high resolution physiological methods ( Fernández-Chacón et al., 2004). We know that 1), CSP-α is not an essential molecular component to execute neurotransmitter release early postnatally in fast synapses like the calyx of Held, but it is required to maintain synaptic function after 3 weeks of age ( Fernández-Chacón et al., 2004); 2), CSP-α cooperates with α-synuclein to maintain the stability of the SNARE-complex that fails to assemble efficiently when CSP-α is absent ( Chandra et al., 2005, Sharma et al., 2011a and Sharma et al., 2011b); and 3), CSP-α is likely most required at the synaptic terminals with high activity ( Fernández-Chacón et al., 2004, García-Junco-Clemente et al., 2010 and Schmitz et al., 2006). Those observations indicate that CSP-α acts as a chaperone to rescue proteins that might become unfolded by the effect of

maintained synaptic activity ( Sharma et al., 2011b). SNAP-25 is the most remarkably reduced synaptic protein in CSP-α knockout mice ( Chandra et al., 2005, Sharma et al., 2011a and Sharma et al., 2011b). Perhaps, other synaptic proteins become functionally altered. A systematic functional study of the complete synaptic vesicle cycle in CSP-α KO mice would be useful to investigate further molecular alterations. Now, using quantal analysis at the neuromuscular CHIR-99021 supplier junction (NMJ) we describe a significant decrease in the number of vesicles available for release, likely explained

by a priming defect as a consequence of reduced SNAP-25 levels. In addition, using synaptopHluorin (spH) imaging of the synaptic vesicle cycle at the NMJ, we have found specific alterations in synaptic vesicle recycling that might contribute to nerve terminal progressive degeneration when CSP-α is absent. Specifically, we demonstrate that motorneurons require CSP-α for the maintenance of synaptic release sites and synaptic vesicle recycling. CSP-α KO mice expressing spH developed the strong neurological phenotype that causes Methisazone early lethality within 1–2 months of age as previously described (Fernández-Chacón et al., 2004). We used the levator auris longus (LAL) nerve–muscle preparation ( Angaut-Petit et al., 1987) to study synaptic transmission with electrophysiology ( Rozas et al., 2011) and with spH imaging ( Tabares et al., 2007). We first studied spontaneous release and detected fibers with “bursts” of miniature end-plate potentials (MEPP), as previously described in CSP-α KO mice ( Ruiz et al., 2008). However, when we excluded those fibers from our analysis, MEPP amplitude was similar in control and mutant synapses (1.03 ± 0.08 mV for wild-type (WT) and 1.