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Fig. 2 | Fluids and Barriers of the CNS

Fig. 2

From: Lysophosphatidic acid as a CSF lipid in posthemorrhagic hydrocephalus that drives CSF accumulation via TRPV4-induced hyperactivation of NKCC1

Fig. 2

LPA is a novel endogenous agonist of luminal membraneous TRPV4. A Representative current traces obtained from uninjected or TRPV4-expressing oocytes during a 200 ms step protocol (upper panel, control solution; lower panel, LPA-containing solution). B Averaged I/V curves from TRPV4–expressing oocytes in control solution, n = 9 (black), during application of LPA without, n = 8 (orange) or with TRPV-4 inhibition, n = 8 (+RN, purple). Uninjected oocytes treated with LPA are shown in grey, n = 12. C TRPV4-mediated current activity (at Vm = − 85 mV) summarized in control solution (black) and after exposure to LPA without (orange) or with TRPV4 inhibition (purple). D Transcript abundance (in TPM) of members of the transient receptor potential vanilloid family obtained from RNA sequencing of rat choroid plexus; TRPV1, 0.4; TRPV2, 0.5; TRPV4, 58.5; TRPV6, 0.06. E Transcript abundance of all filtered ion channels. F Representative immunolabeling of TRPV4 in rat choroid plexus. Nuclei staining by DAPI. Scale bar = 5 μm. Statistical evaluation with one-way ANOVA with Dunnett’s post hoc test **P < 0.01; ***P < 0.001

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