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1.
Figure 6

Figure 6. From: General and variable features of varicosity spacing along unmyelinated axons in the hippocampus and cerebellum.

Models of synapse-varicosity relationships. (A) Positions (arrows) along an axon where synapses and subsequently varicosities will form. (B and C) Two models of how varicosities form near synapses. In the varicosity fusion model, varicosities 1.0 μm in length form around every synapse. If two synapses are closer than the varicosity length, their varicosities are fused into one longer varicosity, creating a MSB. In the varicosity fission model, MSBs are converted into two single-synapse boutons by sliding synapses apart. (D and E) SD vs. mean spacing for axons simulated according to the two models. (F and G) Indices of dispersion for simulated axons. ●, Varicosity data; ○, synaptic data; and gray circles, overlapping synaptic and varicosity data.

Gordon M. G. Shepherd, et al. Proc Natl Acad Sci U S A. 2002 April 30;99(9):6340-6345.
2.
Figure 3

Figure 3. From: General and variable features of varicosity spacing along unmyelinated axons in the hippocampus and cerebellum.

Regional variability in mean varicosity spacing.

Gordon M. G. Shepherd, et al. Proc Natl Acad Sci U S A. 2002 April 30;99(9):6340-6345.
3.
Fig.3

Fig.3. From: Cocaine Exposure Results in Formation of Dendritic Varicosity in Rat Primary Hippocampal Neurons.

Gp120 and cocaine caused enhanced dendritic varicosity formation. (a) MAP2 immunofluorescence of primary hippocampal neurons exposed to cocaine, gp120 and cocaine plus gp120 demonstrated increased dendritic varicosity formation in the presence of both cocaine and gp120 as compared with neurons exposed to either agent alone. Arrows indicate the sites of dendritic varicosity formation. (b) Quantification of percentage of cells with dendritic varicosities. All the data are presented as mean±SD of four individual experiments. *p<0.05; **p<0.01 vs control group

Honghong Yao, et al. Am J Infect Dis. ;5(1):26-30.
4.
Figure 2

Figure 2. From: General and variable features of varicosity spacing along unmyelinated axons in the hippocampus and cerebellum.

Examples of linearly transformed axons from each synaptic region, illustrating the variability in varicosity numbers and positions. Vertical lines indicate varicosities. Small vertical gaps at two of the branch points indicate branching that occurred along a bare axon (i.e., not at a varicosity).

Gordon M. G. Shepherd, et al. Proc Natl Acad Sci U S A. 2002 April 30;99(9):6340-6345.
5.
Fig. 5

Fig. 5. From: Innervation of Orexin/Hypocretin Neurons by GABAergic, Glutamatergic or Cholinergic Basal Forebrain Terminals Evidenced by Immunostaining for Presynaptic Vesicular Transporter and Postsynaptic Scaffolding Proteins.

The presence of presynaptic VGluT2 or VGAT and postsynaptic PSD-95 or Gephyrin (Geph) proteins in contacts between BDA-labeled varicosities and Orx+ neurons. A: Rendered 3D confocal image (16 serial 0.50-μm thick optical sections) of a BDA-labeled axon (in green, Cy2), whose varicosities (in yellow) are positive for VGluT2 (in red, Cy3). One of these varicosities is in apposition (arrowhead) to an Orx+ neuron (in pseudocolor blue, Cy5), as evident in the rendered zoom images on the right (6 serial 0.5-μm thick optical sections) depicting in detail the relation between the BDA+ varicosity (top) or the contained VGluT2 (middle) with the Orx+ neuron surface and showing the three elements together in the merged image (bottom). Note also on the left other VGluT2+ varicosities in contact with the Orx+ neuron. B: Rendered 3D confocal image (9 serial 0.33-μm thick optical sections) of a BDA+ varicosity (arrowhead, in green, Cy2) facing a PSD-95+ profile (opposite pointer, in pseudocolor red, Cy5) located between the varicosity and the surface of the Orx+ neuron (in pseudocolor blue, Cy3). As evident in the zoom rendered images on the right (13 serial 0.33-μm thick optical sections), the BDA+ varicosity is apposed to the Orx+ process (top image), opposite the PSD-95+ punctum, which is on the surface of the Orx+ process (pointer, middle image) and between the BDA+ varicosity and the Orx+ process (pointer in the merged image, bottom). Note the presence of other PSD-95+ puncta over the Orx+ neuron (upper pointer) at the left panel. C: Rendered 3D confocal image (28 serial 0.5-μm thick optical sections) of a BDA-labeled axon (in green, Cy2), from which most varicosities (in yellow) are positive for VGAT (in red, Cy3) and come into contact (large arrowhead) with the dendrites and soma of the Orx+ neuron. As seen in the rendered zoom images on the right (8 serial 0.5-μm thick optical sections), the BDA+ varicosity (top image) containing VGAT (middle image) appears to be in contact with the surface of the Orx+ neuron (merged image, bottom). Note in the left image other VGAT+ varicosities also appear to appose the Orx+ neuron. D: Rendered 3D confocal image (14 serial 0.33-μm thick optical sections) of BDA-labeled axonal varicosities (arrowhead, green, Cy2) facing Geph+ puncta (facing pointer, pseudocolor red, Cy5) over an Orx+ neuron (pseudocolor blue, Cy3). As evident in the zoom rendered images at the right (12 serial 0.33-+m thick optical sections), the apposition of the BDA+ varicosity with the Orx+ neuron (top image) is associated with a Geph+ punctum on the surface of the Orx+ neuron (pointer, middle image) and between the BDA+ varicosity and the Orx+ neuron (merged image, pointer, bottom). Note the presence of other Geph+ puncta over the Orx+ neuron (upper pointers) in the left panel. Deconvolution iterative restoration (see Materials and Methods) was applied to the Cy5 channel (in B and C, left panels, and in A–D, right panels), the Cy3 channel (in C, left panel, and in C,D, right panels) and the Cy2 channel (in B–D). Tonal range adjustments for each individual RGB channel were made for all pictures. Scale bars = 10 μm in left large panel in D (applies to large left panels in A–C); 1 μm in D, zoom bottom image (applies to zoom images in A–C).

PABLO HENNY, et al. J Comp Neurol. ;499(4):645-661.
6.
Fig. 3.

Fig. 3. From: Role of PSD95 in membrane association and catalytic activity of nNOS? in nitrergic varicosities in mice gut.

PSD95 in the varicosity membrane associates with both serine847-phospho-nNOSα dimer and dephospho-nNOSα dimer. Purified varicosity membrane samples were immunoprecipitated with anti-PSD95 antibody. The immunoprecipitate was immunoblotted with anti-nNOS1–20 antibody. 320-kDa band of nNOSα dimer was seen, suggesting that PSD95 is associated with nNOSα dimer in the varicosity membrane. Incubation with IgG served as negative control. Furthermore, varicosity membrane samples immunoprecipitated with anti-PSD95 was again immunoprecipitated with anti-serine847-phospho-nNOS antibody. The resulting immunoprecipitate and supernatant were separately loaded for SDS-PAGE and probed with anti-nNOS1–20 antibody. Both the immunoprecipitate and the supernatant showed 320-kDa bands, suggesting that the PSD95 in varicosity membrane is associated with both serine847-phospho-nNOSα dimer and dephospho-nNOSα dimer. When probed with anti-calmodulin (CaM) antibody, in the presence of Ca2+, only the supernatant showed a 17-kDa band. IgG negative control and purified bovine brain CaM as a positive control for the 17-kDa signal were used for the coimmunoprecipitation experiments.

Arun Chaudhury, et al. Am J Physiol Gastrointest Liver Physiol. 2009 October;297(4):G806-G813.
7.
Fig. 5.

Fig. 5. From: Regulation of C. elegans presynaptic differentiation and neurite branching via a novel signaling pathway initiated by SAM-10.

Caenorhabditis elegans LimHD genes tested are not involved in PLM specifications regulated by sam-10/ldb-1. (A) Distinctive phenotypes of mec-3, sam-10 and ldb-1 mutants. (B) Effects of Lim-HD gene mutations on PLM synaptic branch positioning and synaptic varicosity extension. All varicosity extensions of lim mutants fall in the `medium extension' class (see Materials and methods). lin-11(n389) causes a dramatic increase of varicosity extension. However, a close look revealed that this diffusion appears different from extended varicosities in sam-10(js94): they are more regular and even in shape and shorter than sam-10(js94) varicosities. Plus, we failed to detect LIN-11 expression in PLM neurons, using lyIs32 (whole lin-11::gfp integrant 2013, a gift from Piali Sengupta). We believe that varicosity extension is probably due to VNC defects in lin-11(n389) (Hutter, 2003). Varicosity extensions in other mutants are similar to these in lin-11(n389), albeit at lower frequency as shown in the figure. mec-3 mutants are not scored for PLM synaptic varicosity morphology owing to defective PLM neuronal differentiation. ND, not determined.

Qun Zheng, et al. Development. 2011 January 1;138(1):87-96.
8.
Figure 3

Figure 3. From: Structure activity relationship of synaptic and junctional neurotransmission.

Ultrastructure of nerve varicosities containing different types of vesicles and their relationship to synaptic specialization in the CNS neurons. (A) Shows a varicosity loaded with SCV many of which are in close association with the varicosity membrane at presynaptic membrane specialization (large arrow). The apposing postsynaptic membrane possesses postsynaptic density. This synapse is on a dendrite in superior olive, X 60.000 (From (Heuser JE, 1977), with permission). The specialized active zone is for active synaptic exocytosis. (B) Shows a varicosity with DCV of various sizes. Specialized presynaptic zone with docked vesicles are not found in such varicosities. This illustration represents an adrenergic varicosity in rat vas deferens, X 110,000; (From (Basbaum, 1974), with permission). (C) shows a varicosity containing SCV and LDCV. Note that the synaptic junction is characterized by some widening of cleft and pre- and post-synaptic plaques. Also note an interesting distribution of the vesicles in the varicosity: whereas SCV are clustered around the presynaptic specialization, the LDCV are seen away from the synapse, X77000; From dentate nucleus of cerebellum of Macaca mullata (From (Palay S.L., 1977), with permission).

Raj K Goyal, et al. Auton Neurosci. ;176(0):11-31.
9.
Fig. 1

Fig. 1. From: Cocaine Exposure Results in Formation of Dendritic Varicosity in Rat Primary Hippocampal Neurons.

Cocaine exposure resulted in formation of dendritic varicosity in primary hippocampus neurons. Rat hippocampal neurons exposed to 10 μM but not 1μM cocaine developed dendritic varicosities. The image shown is a representative picture of three independent experiments. Images were captured on a time-lapse confocal microscope. Arrows indicate the sites of dendritic varicosity formation

Honghong Yao, et al. Am J Infect Dis. ;5(1):26-30.
10.
Figure 3

Figure 3. Identification of different nNOS forms in varicosity extracts. From: Active and inactive pools of nNOS in the nerve terminals in mice gut: Implications for nitrergic neurotransmission.

Left Panel; Varicosity extracts under non-denaturing conditions (on ice) immunoblotted with anti-nNOS1422–1433 antibody showed dimers and monomer at 320, 250 and 155kD. Heat treated (37° C) extract probed with the same antibody detected monomers at 155 and 135kD. Right Panel; The nNOSα splice variant was identified in the varicosity extract by anti-nNOS1–20 antibody in the cold condition that detected a 320kD dimer and a 155kD monomer band. Heat treated extract probed with anti-nNOS1–20 antibody detected only the monomer at 155kD. Note that both splice variants of nNOS, nNOSα and nNOSβ, are present in the gut nerve terminals.

Y. Manjula Rao, et al. Am J Physiol Gastrointest Liver Physiol. ;294(3):G627-G634.
11.
Fig. 1.

Fig. 1. From: Role of PSD95 in membrane association and catalytic activity of nNOS? in nitrergic varicosities in mice gut.

Immunoblots showing distribution of postsynaptic density (PSD) proteins in different fractions of purified varicosity. Note that PSD95 was present in both the membrane and the cytosolic factions and synapse-associated protein 97 (SAP97) was present only in the cytosolic fraction. PSD93 was not detected in varicosity but identified in the whole gut extract using a monoclonal antibody (clone N18/30), and signal was not seen when the crude gut extract was incubated with a 33-kDa control glutathione-S-transferase (GST)-fusion protein of the PSD93 antigen. Also note that SAP102 was not detected in the varicosity. Also note the lack of 117-kDa c-kit signal in varicosity extract but its presence in the whole gut extract and Jurkat cell extract (positive control).

Arun Chaudhury, et al. Am J Physiol Gastrointest Liver Physiol. 2009 October;297(4):G806-G813.
12.
Fig. 9.

Fig. 9. From: PIN/LC8 is associated with cytosolic but not membrane-bound nNOS in the nitrergic varicosities of mice gut: implications for nitrergic neurotransmission.

Cartoon of gut nerve varicosity summarizing key findings of the present study. The cytosol of the nerve varicosity has 3 different nNOS isoforms: nNOSα monomer, nNOSα dimer, and nNOSβ dimer. All these isoforms are phosphorylated at serine847 and do not bind CaM. All these fractions of nNOS in the cytosol are catalytically inactive. The membrane of the nerve varicosity has two types of nNOS: 1) catalytically active, CaM-bound nNOSα dimer and 2) catalytically inactive, CaM-lacking, serine847-phospho-nNOSα dimer. LC8 is associated with only cytosolic nNOS isoforms. These findings indicate that LC8 plays a role in storage or transport of different nNOS isoforms in the nerve varicosity. NO, nitric oxide; PIN, protein inhibitor of nNOS.

Arun Chaudhury, et al. Am J Physiol Gastrointest Liver Physiol. 2008 September;295(3):G442-G451.
13.
Figure 7.

Figure 7. From: Altered gene regulation and synaptic morphology in Drosophila learning and memory mutants.

Lapsyn overexpression regulates synaptic growth. (A) Immunocytochemistry with anti-Complexin antiserum at muscles 6/7 NMJs in segment A3 of Lapsyn overexpression lines of the indicated genotypes. (B) Quantification of varicosity number for the indicated genotypes at muscles 6/7 NMJs in segment A3. Overexpression of UAS-Lapsyn with the elavc155-GAL4 driver increased varicosity number (106.9 ± 3.8, n = 12) compared with white (80.4 ± 4.3, n = 10), UAS-Lapsyn-GFP/+ (67 ± 4.7, n = 11), and elavc155-GAL4/+ (94.3 ± 4.3, n = 12) controls. Overexpression of UAS-Lapsyn with the How24B-GAL4 postsynaptic muscle driver resulted in a decrease in varicosity number (44.9 ± 4.2, n = 12) compared with white, UAS-Lapsyn-GFP/+ , and How24B-GAL4/+ (78.1 ± 4.8, n = 12) controls. Varicosity number was quantified for five to six larvae of each genotype. P-value of Student's t-test: (*) P < 0.05; (**) P < 0.01). Error bars represent SEM.

Zhuo Guan, et al. Learn Mem. 2011 April;18(4):191-206.
14.
Fig. 5.

Fig. 5. From: Role of PSD95 in membrane association and catalytic activity of nNOS? in nitrergic varicosities in mice gut.

Depalmitoylation by 2-bromopalmitate (2-BP) dislocates palmitoyl-PSD95, PSD95, and nNOSα from varicosity membrane. A: 100 μM 2-BP causes depletion of palmitoyl-PSD95 from the varicosity membrane. B: depalmitoylation by 2-BP (100 μM) completely dissociates PSD95 from the membrane. C: 2-BP (100 μM) causes dislocation of 320-kDa nNOSα dimer from the membrane. The nNOS immunoblots were developed by cold SDS-PAGE. 2-BP treatment did not have any effect on nNOSα monomer and dimer in the varicosity cytosolic fractions. Untreated lysates or palmitate treatment served as controls.

Arun Chaudhury, et al. Am J Physiol Gastrointest Liver Physiol. 2009 October;297(4):G806-G813.
15.
Figure 5

Figure 5. From: Dynamic monitoring of NET activity in mature murine sympathetic terminals using a fluorescent substrate.

Fluorescence recovery after photobleaching (FRAP) the neurotransmitter transporter uptake assay (NTUA)-labelled terminal at the arrow caused a persistent loss of fluorescence (A) which only slowly recovered with respect to control varicosities on the same terminals (B). In C, three frames from another such experiment are shown, with photobleaching at t= 0 min. Between the recordings at t= 10 and 12 min punctate, fluorescence returned in a diffraction-limited spot within the target varicosity (arrow); this fluorescence persisted throughout the rest of the experiment. Such FRAP experiments were also carried out in nerve terminals filled with Alexa 594 dextran (D). In such cases, the varicosity in the photobleached region (boxed) lost its NTUA labelling, but the Alexa 594 labelling was lost throughout the entire terminal that crossed this target region. For example, note that the varicosity indicated with a # has a significant fall in Alexa 594 (red) labelling but not NTUA labelling; this varicosity is on the nerve terminal that crosses the target region. However, the varicosity at * does not lose labelling on either channel. These findings suggest that the FRAP protocol does not disrupt the nerve terminal (as Alexa 594 can diffuse to the target region through the nerve terminals to be bleached) and confirms that even a 10 kDa cytoplasmically located molecule can readily move between varicosities.

Lauren K Parker, et al. Br J Pharmacol. 2010 February;159(4):797-807.
16.
Figure 3

Figure 3. Evaluation of ChAT+ varicosity density on fiber segments within microproximity of activated or nonactivated pyramidal cells.. From: Axonal Varicosity Density as an Index of Local Neuronal Interactions.

Representative examples of projection images of triple immunostaining for c-Fos (blue), GluT(EAAC1) (red) and ChAT (green) in layer V of the mPFC (A–P) of ChAT+ varicosity in microproximity of activated pyramidal cells in visual/HDB stimulation group, visual stimulation only group, and HDB stimulation only group (the three top panels), and for ChAT+ varicosity in microproximity of nonactivated pyramidal cells in the visual/HDB stimulation group and the control group (the bottom two panels) D',H',L',P', T': Drawing of ChAT+ fibers (green lines) within 3 µm microproximity (dashed line) of c-Fos+ pyramidal cells (red perimeter with a blue nucleus) or non-activated pyramidal cells (red perimeter without blue nucleus) in layer V of the mPFC. Representative images were taken from IL and PrL. ChAT+ varicosities (illustrated by dots on the green ChAT+ fibers) were quantified on fiber segments within 3 µm microproximity of pyramidal cells. Note that an increased density of varicosities was seen in segments in microproximity of activated cells compared to non-activated cells. Abbreviations: ChAT: choline acetyltransferase; GluT(EAAC1): glutamate transporter; Cg1: cingulate cortex; IL: infralimbic cortex; mPFC: medial prefrontal cortex; PrL: prelimbic cortex. Scale bar: 10 µm.

Zi-Wei Zhang, et al. PLoS One. 2011;6(7):e22543.
17.
Figure 5

Figure 5. Onset of PC12 process outgrowth.. From: Varicones and Growth Cones: Two Neurite Terminals in PC12 Cells.

(A–C) Double immunolabeling of calpain-2 (white or red) and actin (phalloidin, green) in PC12 cells at different stages of differentiation. (A) Calpain-2 labeling in the initial stages of process outgrowth of PC12 cells concentrates around and along the initial buds (arrowheads). (B) Some neurites don't have visible accumulations of calpain-2 (empty arrowheads), and they invariably lack a varicosity (as determined by morphology). (C) Some neurites develop a clear varicone (arrowhead) and calpain-2 labeling concentrates at the varicosity. (D) An example of PC12 cell showing multiple processes with a variety of morphologies. Calpain staining uncovers the varicosity contained in the PC12 terminals, including those in which the presence of a varicosity was not easy to determine by morphology, such as those of triangular shape (asterisk). An incipient process is also highlighted by the presence of calpain-2 puncta (arrowhead in D). Scale bar = 10 µm.

Ana Mingorance-Le Meur, et al. PLoS ONE. 2009;4(2):e4334.
18.
Figure 3

Figure 3. Line scanning confocal microscopy simultaneously monitors nerve terminal [Ca2+]v and NCTs. From: Intermittent ATP release from nerve terminals elicits focal smooth muscle Ca2+ transients in mouse vas deferens.

A, xy-scan showing the position (dashed line) of the line scan images through a smooth muscle cell (sm) and an overlying varicosity. B, three consecutive line scan images through the smooth muscle cell and an adjacent nerve terminal varicosity shown in A. The arrow marks the time of the stimulus. The central panel is shown again in C, but with greater temporal resolution around the time of the stimulus. D, quantification of the changes in fluorescence from a region at the right edge of the smooth muscle cell and from the overlying varicosity. E, magnified view, demonstrating that the [Ca2+] in the varicosity rises before that in the smooth muscle cell.

Keith L Brain, et al. J Physiol. 2002 June 15;541(Pt 3):849-862.
19.
FIGURE 2

FIGURE 2. OXT-immunoreactive innervation of functionally-identified DMV neurons. From: OXYTOCIN-IMMUNOREACTIVE INNERVATION OF IDENTIFIED NEURONS IN THE RAT DORSAL VAGAL COMPLEX.

A–C: Two-color immunoperoxidase staining for OXT plus CTB. D–G: Two-color immunoperoxidase staining for OXT plus Fos plus ChAT. A: An ileum-projecting DMV neuron receives close appositions from OXT-immunoreactive varicosities, one of which is arrowed. Bar, 10 μm. B: A small OXT-immunoreactive varicosity (black) closely apposes the cell body of a corpus-projecting DMV neuron (brown). Bar, 10 μm. C: OXT-immunoreactive varicosities (black) from two separate axons closely appose the proximal dendrite of a corpus-projecting DMV neuron (brown). Bar, 10 μm. D: DVC at mid-AP level. Square E, DMV neurons in Figure 2E. ChAT-immunoreactive neurons (brown) with Fos-immunoreactive nuclei (black) are concentrated in the medial DMV. Bar, 100 μm. E: DMV neurons outlined by box E in panel 2D. The nuclei of 3 ChAT-positive DMV neurons (brown) show 2-DG-induced Fos. The neuron on the left is closely apposed by a large OXT-immunoreactive varicosity (black, arrow). Bar, 20 μm. F: A small varicosity on a fine OXT-immunoreactive axon (black) closely apposes (arrow) a ChAT-positive DMV neuron (brown) with 2-DG-evoked Fos (black). Bar, 10 μm. G: A large varicosity on a thick OXT-immunoreactive axon (black) close apposes (arrow) a ChAT-positive DMV cell body (brown) showing 2-DG-induced Fos (black). This neuron was located near the obex. Bar, 10 μm.

Ida J. Llewellyn-Smith, et al. Neurogastroenterol Motil. ;24(3):e136-e146.
20.
Figure 2

Figure 2. A Late Phase of Sustained Local Protein Synthesis Is Required for The Persistence of 5-HT-Induced Synaptic Growth. From: Several Days of CPEB-Dependent Local Protein Synthesis Are Required to Stabilize Synaptic Growth for Persistence of Long-Term Facilitation in Aplysia.

(A) Local application of emetine 24 hr after 5-HT treatment produced a significant reduction in the total number of sensory neuron varicosities at the treated branch (*, p <0.05, change in varicosity number at 72 hr in the branch treated with 5-HT at time 0 + emetine at 24 hr versus 5-HT alone treated branch). In the control experiment, perfusion of emetine alone at 24 hr had no effect on varicosity number at 72 hr. (B) Selective perfusion of emetine to one branch 72 hr after 5-HT treatment had no significant effect on varicosity number at 120 hr (p = n.s. change in varicosity number at 120 hr in the branch treated with 5-HT at time 0 + emetine at 72 hr versus 5-HT alone treated branch). In both graphs the percent change in the total number of varicosities at 24 hr, 72 hr and 120 hr was obtained by comparing the total number of varicosities measured at each of these different time points to the total number of varicosities measured at time 0.

Maria Concetta Miniaci, et al. Neuron. 2008 September 25;59(6):1024-1036.

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