na v 1 3 rb  (Alomone Labs)

Journal: bioRxiv

Article Title: Increased expression of developmental Nav1.3 promotes hippocampal CA3 hyperexcitability in early-stage 5xFAD mice

doi: 10.64898/2026.07.28.741298

Figure Lengend Snippet: a) Representative confocal images of dorsal hippocampus CA3 showing c-Fos (green, top), Nav1.3 + (red, middle), and merged channels (yellow, bottom) for WT and 5xFAD at 3 months (left) and 7 months (right). The inset on the top-left panel indicates the CA3 subregion delineated using the Allen Brain Atlas where c-Fos/Nav1.3 were quantified. Scale bar = 400 μm. b) Quantification of neuronal activation in CA3, shown as c-Fos + cells per 1000 μm 2 . c-Fos expression was higher in 3-month 5xFAD mice than in 3-month WT mice or 7-month 5xFAD mice (two-way ANOVA genotype x age interaction: F(1, 8) =12.0, p = 0.009; post-hoc Sidak: 5xFAD 3 months vs WT 3 months, p =0.015; 5xFAD 3 months vs 5xFAD 7 months, p = 0.049). c) Quantification of Nav1.3/c-Fos colocalization, shown as the percentage of c-Fos + neurons that are Nav1.3 +. The genotype x age interaction was not significant for colocalization, but there was a significant main effect of genotype, with higher Nav1.3/c-Fos co-expression at 3 months in 5xFAD mice vs age-matched WT controls (F(1, 8) = 11.8, p = 0.009); post-hoc Sidak’s comparisons indicate increased colocalization in 3-month 5xFAD mice relative to 3-month WT (p = 0.035). No other comparisons reached significance. Data are mean ± SD; n = 3 mice per group, 9 fields analyzed per mouse.

Article Snippet: An anti-Nav1.3 antibody (rabbit polyclonal; Alomone Labs #ASC-004; Jerusalem, Israel) was used, directed against an epitope in the C-terminal region of Nav1.3.

Techniques: Confocal, Activation Assay, Expressing, Immunofluorescence

Journal: bioRxiv

Article Title: Increased expression of developmental Nav1.3 promotes hippocampal CA3 hyperexcitability in early-stage 5xFAD mice

doi: 10.64898/2026.07.28.741298

Figure Lengend Snippet: a) Schematic of mossy fiber terminal (red) contact (red arrowhead, right) on CA3 pyramidal cell dendritic spine (light blue). Inset (left) shows an enlarged representation of mossy terminal-CA3 spine contact b) Representative pre-embedding immuno-electron micrographs showing Nav1.3 in a mossy-fiber terminal (top, presynaptic) and a CA3 dendritic spine (bottom, postsynaptic). Purple arrowheads indicate silver-intensified immunogold (SIG) labeling for Nav1.3. Scale bar = 400 nm. c) Quantification of Nav1.3 SIG particles from 50 MFTs in WT and 5xFAD mice at 3 and 7 months. Data are mean ± SD; n = 3 mice per group. Two-way ANOVA revealed a significant genotype x age interaction (F(1, 8) = 7.68, p = 0.024). Post-hoc Sidak comparisons showed increased Nav1.3 SIG particles in MFTs from 3-month 5xFAD mice compared with 3-month WT mice (p = 0.007); no other pairwise comparisons reached significance. d) Quantification of postsynaptic Nav1.3 SIG particles per 50 CA3 spines per mouse per condition. Two-way ANOVA showed no significant effect of genotype p = 0.42, age p = 0.96, or interaction p = 0.58; n= 3 mice per group.

Article Snippet: An anti-Nav1.3 antibody (rabbit polyclonal; Alomone Labs #ASC-004; Jerusalem, Israel) was used, directed against an epitope in the C-terminal region of Nav1.3.

Techniques: Labeling, Transmission Electron Microscopy

Journal: bioRxiv

Article Title: Increased expression of developmental Nav1.3 promotes hippocampal CA3 hyperexcitability in early-stage 5xFAD mice

doi: 10.64898/2026.07.28.741298

Figure Lengend Snippet: (a-c) Representative confocal images showing GCaMP6s expression (green, a), Nav1.3 immunolabeling (red, b) and merged channel (yellow, c) in dorsal CA3 following viral delivery. Arrowheads indicate examples of GCaMP6s + neurons with reduced Nav1.3 labeling after Nav1.3-shRNA; panel C also shows the implanted fiber tract (dashed outline) used for photometry. Scale bar = 400 μm d) Quantification of CA3 calcium activity (AUC/1000 frames) in 3-month-old WT, 5xFAD, 5xFAD+scrambled-shRNA, and 5xFAD+Nav1.3-shRNA mice. 3-month WT and 5xFAD data from are replotted for comparison. Nav1.3 knockdown significantly reduced CA3 activity relative to both untreated 5xFAD and 5xFAD+scrambled controls. Data are mean ± SD; n = 6-7 mice per group. One-way ANOVA was used to assess treatment effects at 3 months (F (3, 21) = 5.63, p = 0.005), followed by post-hoc tests (Tukey) for pairwise comparisons: 5xFAD vs 5xFAD+Nav1.3-shRNA, p = 0.030; 5xFAD+scrambled vs 5xFAD+Nav1.3-shRNA, p = 0.032; WT vs 5xFAD, p = 0.047. WT vs 5xFAD+Nav1.3-shRNA, p = 0.987. WT and 5xFAD here are the 3-month subset re-analyzed by one-way ANOVA, so the WT and 5xFAD p-value differs from the full two-way model in ).

Article Snippet: An anti-Nav1.3 antibody (rabbit polyclonal; Alomone Labs #ASC-004; Jerusalem, Israel) was used, directed against an epitope in the C-terminal region of Nav1.3.

Techniques: Confocal, Expressing, Immunolabeling, Labeling, shRNA, Activity Assay, Comparison, Knockdown, Immunofluorescence

Journal: The Journal of Comparative Neurology

Article Title: Distribution of Voltage‐Gated Sodium Channels and Scaffolding Proteins on Vestibular Calyx Ending Delineates the Axon Initial Segment

doi: 10.1002/cne.70127

Figure Lengend Snippet: Antibody provenances.

Article Snippet: Na V 1.3 (rb) , Alomone , ASC‐004 RRID:AB_2040007 , , X (DRG) , , X , X (w) , Datasheet.

Techniques: Western Blot

Journal: The Journal of Comparative Neurology

Article Title: Distribution of Voltage‐Gated Sodium Channels and Scaffolding Proteins on Vestibular Calyx Ending Delineates the Axon Initial Segment

doi: 10.1002/cne.70127

Figure Lengend Snippet: Na V 1.3 antibody labels Domain 3 in presumed C units. (A, A’) In this maximum intensity projection image of a stack from a crista, the presumption is based on the relatively superficial location of Caspr1‐stained hemi‐paranodes (red, arrows) and the location of the units in the CZ. Na V 1.3 labeling ( green in A’) is absent in the PZ ( not shown ), which contains D , but not C , units. In the three units marked by arrows in A, MBP ( blue ) can be traced from the parent axons below the basement membrane (BM) (dashed line) to the stained hemi‐paranodes. In A’, Caspr1 immunostaining ( red ) has been removed, leaving Na V 1.3 labeling ( green ) of Domain 3, including the outer surface of the calyx endings (COF, Domain 3a) and the unmyelinated parent axons above the heminodes (Domain 3b, locations indicated by arrows ). Inset, upper right , schematic of entire calyx, showing Domain 3 in red. (B, C) Additional examples of calyx afferents labeled with Na V 1.3. Same color conventions as in A. Scale bars = 5 µm.

Article Snippet: Na V 1.3 (rb) , Alomone , ASC‐004 RRID:AB_2040007 , , X (DRG) , , X , X (w) , Datasheet.

Techniques: Staining, Labeling, Membrane, Immunostaining, Immunofluorescence

Journal: Experimental Brain Research

Article Title: Voluntary running wheel exercise induces cognitive improvement post traumatic brain injury in mouse model through redressing aberrant excitation regulated by voltage-gated sodium channels 1.1, 1.3, and 1.6

doi: 10.1007/s00221-023-06734-2

Figure Lengend Snippet: Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of Nav1.1 ( a – e ), Nav1.3 ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)

Article Snippet: Then, they were incubated against Nav1.1 (1:800; cat. no. ASC-001; Alomone), Nav1.3 (1:500; cat. no. ASC-004; Alomone), or Nav1.6 (1:600; cat. no. ASC-009; Alomone) using antibodies.

Techniques: Expressing, Western Blot

Journal: Experimental Brain Research

Article Title: Voluntary running wheel exercise induces cognitive improvement post traumatic brain injury in mouse model through redressing aberrant excitation regulated by voltage-gated sodium channels 1.1, 1.3, and 1.6

doi: 10.1007/s00221-023-06734-2

Figure Lengend Snippet: Either voluntary RW before TBI or prior-injury combined with post-injury exercise training redressed abnormal VGSCs protein expression of TBI mice. a – c The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in preliminary voluntary RW group. d – f The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in pre-training combined with TBI post-injury exercise training group. Data are expressed as Means ± SD ( n = 9)

Article Snippet: Then, they were incubated against Nav1.1 (1:800; cat. no. ASC-001; Alomone), Nav1.3 (1:500; cat. no. ASC-004; Alomone), or Nav1.6 (1:600; cat. no. ASC-009; Alomone) using antibodies.

Techniques: Expressing, Western Blot

Journal: Experimental Brain Research

Article Title: Voluntary running wheel exercise induces cognitive improvement post traumatic brain injury in mouse model through redressing aberrant excitation regulated by voltage-gated sodium channels 1.1, 1.3, and 1.6

doi: 10.1007/s00221-023-06734-2

Figure Lengend Snippet: Exercise-conditioned serum treatment redressed the abnormal expressions of Nav1.1, Nav1.3, Nav1.6 proteins in cortical neurons. The Nav1.1 protein expression showed in ( a – c ), the Nav1.3 protein expression showed in (d-f), while the Nav1.6 protein expression showed in ( g – i ). Data are expressed as Mean ± SD ( n = 7)

Article Snippet: Then, they were incubated against Nav1.1 (1:800; cat. no. ASC-001; Alomone), Nav1.3 (1:500; cat. no. ASC-004; Alomone), or Nav1.6 (1:600; cat. no. ASC-009; Alomone) using antibodies.

Techniques: Expressing, Western Blot