rotarod test  (Panlab)

Journal: Neural Regeneration Research

Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

doi: 10.4103/NRR.NRR-D-23-01511

Figure Lengend Snippet: Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an AMPK agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.

Article Snippet: The rotarod test was performed using a five-lane rotarod apparatus (Jinan Yiyan Technology Development Co., Ltd, Jinan, China, YLS-4C) as described previously (Kumar et al., 2013), with some modifications.

Techniques: Control, Expressing, Western Blot, Immunofluorescence, Staining, Tandem Mass Spectroscopy

Journal: Neural Regeneration Research

Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

doi: 10.4103/NRR.NRR-D-23-01511

Figure Lengend Snippet: Chitosan may reduce acetate levels, thereby activating the PPARD-AMPK signaling pathway, which promotes repair of the intestinal barrier and reduces neuroinflammation in an MPTP-induced mouse model of PD. (A, B) Western blot analysis of p-AMPK, AMPK, and PPARD levels in mouse colon tissue ( n = 3/group). Treatment with acetate significantly increased p-AMPK and PPARD expression. (C) Treatment with a PPARD antagonist significantly decreased mouse body weight ( n = 6/group). (D) There were no significant differences in fall latency among the groups in the rotarod test, which was used to assess motor dysfunction ( n = 6/group). (E–G) PPARD antagonist treatment significantly decreased PPARD, TH, ZO-1, and occludin expression, as determined by western blot ( n = 3/group). (H) Immunofluorescence staining for ZO-1 (green, Alexa Fluor 488) and occludin (red, Alexa Fluor 594) in mouse colon tissue ( n = 3/group). The PPARD antagonist treatment group exhibited markedly reduced ZO-1 and occludin mRNA expression levels in colon tissue. Scale bars: 10 μm. (I) QPCR was used to measure the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in mouse colon tissue ( n = 3/group). Treatment with the PPARD antagonist increased IL-6 and TNF-α mRNA levels, while IL-8 and iNOS levels were reduced. (J) ELISA was used to detect IL-1β, IL-6, IL-10, and TNF-α expression levels in mouse plasma ( n = 5/group). IL-1β, IL-6, and TNF-α expression levels were significantly increased in the PPARD antagonist treatment group. (K) QPCR was used to measure mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in the SN ( n = 3/group). Treatment with the PPARD antagonist significantly increased the mRNA levels of IL-1β, IL-6, and IL-8. (L) Treatment with the PPARD antagonist reduced p-AMPK, but not AMPK, expression ( n = 3/group). GAPDH was used as the internal reference. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test (A, B) or unpaired t -test (C–L)). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 Beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: not significant; NaA: sodium acetate; p-AMPK: phosphorylation adenosine 5′-monophosphate-activated protein kinase; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; QPCR: quantitative polymerase chain reaction; SN: substantia nigra; TH: tyrosine hydroxylase; TNF-α: tumor necrosis factor alpha; ZO-1: Zonula occludens-1.

Article Snippet: The rotarod test was performed using a five-lane rotarod apparatus (Jinan Yiyan Technology Development Co., Ltd, Jinan, China, YLS-4C) as described previously (Kumar et al., 2013), with some modifications.

Techniques: Western Blot, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Phospho-proteomics, Real-time Polymerase Chain Reaction

Journal: bioRxiv

Article Title: Progressive neuroinflammation and deficits in motor function in a mouse model with an Epg5 pathogenic variant of Vici syndrome

doi: 10.1101/2025.05.16.654529

Figure Lengend Snippet: A,B. Weight comparison of mutant homozygous mutants with sibling control wild-type mice at 4 weeks ( A ) and 8 weeks of age ( B ). C-E. Compared with control mice ( C ), W860X homozygous mutant mice ( D ) display poorly placed hindlimbs when attempting to bear weight at 4 months of age. Hindlimb function in homozygous W860X mice progressively worsened by 7 months of age ( E ). F-I. Assessment of the motor function of W860X ( F, G ) and KO ( H, I ) mutant mice via the rotarod test. Compared with age-matched control siblings, homozygous mutant mice have a poor capacity to navigate the rotarod test of coordination. Mutant mice fail the test at a lower speed of rotation (‘speed at fall’; F, H ) and at a shorter time (‘latency to fall’; G, I ) on the apparatus. At 12 weeks of age, some homozygous mutant animals are unable to initiate the rotarod test, all W860X mice fail at 14 weeks, and all KO mice fail at 16 weeks. wt ; homozygous wild-type, KO ; homozygous mutant for the KO allele; W860X ; homozygous mutant for the W860X allele. Analysis of data from wild-type and mutant mice at a given timepoint was performed via an unpaired t test. ****, p<0.0001; ***, p<0.001; **, p<0.01. *, p<0.05.

Article Snippet: The analysis of motor coordination, endurance, and fatigue resistance was performed via the rotarod test (Panlab, Barcelona, Spain).

Techniques: Comparison, Mutagenesis, Control