Alterations of AQP2 expression in trigeminal ganglia in a murine inflammation model

Borsani, Elisa; Bernardi, Simona; Albertini, Roberta; Rezzani, Rita; Rodella, Luigi Fabrizio

doi:10.1016/j.neulet.2008.11.014

Cited by 27 publications

(30 citation statements)

References 33 publications

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“…Otherwise, the AQP1 expression remained unaltered. On the whole, these data do support the hypothesis that AQP2 is involved in pain transmission in the peripheral nervous system [19]. Although the functional significance of AQP2 in vestibular and cochlear sensory cells as well as in spiral and vestibular ganglion cells remains uncertain, it has been suggested that AQP2 may be involved in neurotransmission in the inner ear.…”

Section: Discussionsupporting

confidence: 74%

Localization of aquaporins 1, 2, and 3 and vasopressin type 2 receptor in the mouse inner ear

et al. 2012

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Section: Discussionsupporting

confidence: 74%

Localization of aquaporins 1, 2, and 3 and vasopressin type 2 receptor in the mouse inner ear

et al. 2012

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“…AQP2 is expressed in trigeminal ganglia in a murine inflammation model and might be involved in pain transmission in the peripheral nervous system [Borsani et al, 2009]. Studies in TRPV4 knockout mice identified TRPV4 in the dorsal root ganglia as essential for the normal detection of pressure and as a receptor of the high-threshold mechanosensory complex .…”

Section: Discussionmentioning

confidence: 99%

Functional Expression of an Osmosensitive Cation Channel, Transient Receptor Potential Vanilloid 4, in Rat Vestibular Ganglia

Kamakura

Kondo²,

Koyama³

et al. 2016

Audiol Neurotol

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Transient receptor potential vanilloid (TRPV) 4 is a nonselective cation channel expressed in sensory neurons such as those in the dorsal root and trigeminal ganglia, kidney, and inner ear. TRPV4 is activated by mechanical stress, heat, low osmotic pressure, low pH, and phorbol derivatives such as 4α-phorbol 12,13-didecanoate (4α-PDD). We investigated the expression of TRPV4 in rat vestibular ganglion (VG) neurons. The TRPV4 gene was successfully amplified from VG neuron mRNA using reverse-transcription polymerase chain reaction. Furthermore, immunoblotting showed positive expression of TRPV4 protein in VG neurons. Immunohistochemistry indicated that TRPV4 was localized predominantly on the plasma membrane of VG neurons. Calcium (Ca²⁺) imaging of VG neurons showed that 4α-PDD and/or hypotonic stimuli caused an increase in intracellular Ca²⁺ concentration ([Ca²⁺]_i) that was almost completely inhibited by ruthenium red, a selective antagonist of TRPV channels. Interestingly, a [Ca²⁺]_i increase was evoked by both hypotonic stimuli and 4α-PDD in approximately 38% of VG neurons. These data indicate that TRPV4 is functionally expressed in VG neurons as an ion channel and that TRPV4 likely participates in VG neurons for vestibular neurotransmission as an osmoreceptor and/or mechanoreceptor.

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“…A total number of 30 alternate serial transverse sections of L3-L5 DRG for each group were analyzed in the CBRA. Digitally fixed images of slices were analyzed using an image analyzer (Image ProPlus, Milan, Italy) which recognizes all detectable signals and were calculated as integrated optical density (IOD) for arbitrary areas, measuring five fields of the same area for each section [Borsani et al, 2009].…”

Section: Immunofluorescence Staining and Quantitative Analysismentioning

confidence: 99%

Endothelial Nitric Oxide Synthase in Dorsal Root Ganglia during Chronic Inflammatory Nociception

Borsani

Giovannozzi²,

Cocchi³

et al. 2012

Cells Tissues Organs

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Nitric oxide (NO) is a gaseous molecule implicated both in vascular tone and nociceptive transmission. The capillary blood supply to the dorsal root ganglia (DRG) is unique because it is highly permeable to several low and high molecular-weight compounds. This anatomical situation leads to a potential role of endothelial nitric oxide synthase (eNOS) in inflammatory nociception, which is not well established. Therefore, we examined the role of eNOS in DRG in a murine chronic inflammatory pain model induced by complete Freund’s adjuvant using L-N⁵-(1-iminoethyl)ornithine (L-NIO), a potent inhibitor of eNOS activity. Pain state was examined using a behavioral test. The expression of eNOS, platelet endothelial cell adhesion molecule-1 (CD31) and vascular endothelial growth factor (VEGF) was examined by immunofluorescence. In control animals, CD31 was detected in vessels; VEGF was localized both in vessels and neurons while a weak eNOS immunopositivity was detected in both vessels and in neurons. Under inflammatory pain conditions, eNOS, CD31 and VEGF immunopositivity increased. Administration of L-NIO significantly attenuated thermal hyperalgesia by 24 h and decreased eNOS activity and CD31 immunopositivity by 7 days. VEGF was unaffected. Our results show that eNOS plays a nociceptive role in the early phases of inflammation while in the later phases it may be involved in neurotrophic support.

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Alterations of AQP2 expression in trigeminal ganglia in a murine inflammation model

Cited by 27 publications

References 33 publications

Localization of aquaporins 1, 2, and 3 and vasopressin type 2 receptor in the mouse inner ear

Localization of aquaporins 1, 2, and 3 and vasopressin type 2 receptor in the mouse inner ear

Functional Expression of an Osmosensitive Cation Channel, Transient Receptor Potential Vanilloid 4, in Rat Vestibular Ganglia

Endothelial Nitric Oxide Synthase in Dorsal Root Ganglia during Chronic Inflammatory Nociception

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