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. 2025 Sep 25;2025:0897. doi: 10.34133/research.0897

Fig. 2.

Fig. 2.

Chemogenetic inhibition of the TNC neurons improved AR. (A) Flowchart of experimental design and effects of the chemogenetic inhibition of the TNC neurons of AR mice. (B) Illustration of the AAV-hSyn-hM4D(Gi)-EGFP/AAV-hSyn-hM4Di-EGFP construct. (C) Schematic diagram showing chemogenetic virus injection into the TNC of mice. (D) hM4Di-EGFP fluorescence localization in the TNC region. Scale bar, 500 μm. (E and F) Quantification of nasal rubbing and sneezing episodes within 10 min. N = 6 mice per group. (G) Hematoxylin–eosin (H&E) and periodic acid–Schiff (PAS) staining of nose sections. Scale bars, 20 μm. (H and I) Quantification of eosinophil and goblet cell counts in a ×400 high-power field. N = 6 mice per group. (J) Immunofluorescence staining with sympathetic nerve markers (tyrosine hydroxylase [TH] and neuropeptide Y [NPY]) and parasympathetic nerve markers (choline acetyltransferase [ChAT] and vasoactive intestinal peptide [VIP]) in the nasal mucosa. Scale bars, 20 μm. (K to N) Quantification of the immunofluorescence intensity of TH, NPY, ChAT, and VIP in the nasal mucosa. N = 3 mice per group. (O to R) Contents of interferon-γ (IFN-γ), interleukin (IL)-4, IL-5, and IL-13 in the nasal lavage fluid (NLF). N = 6 mice per group. *P < 0.05; **P < 0.01; ***P < 0.001. ip, intraperitoneal; OVA, ovalbumin; CNO, clozapine-N-oxide; in, intranasal; HPF, high-power field.