Immunohistochemical Examination of S-100 Protein and Substance P in the Inner Ear of the Rat

Igarashi, Syuichi; Sasaki, Hiroyuki; Nakano, Yuichi; Ino, H.

doi:10.3109/00016489109131371

Cited by 8 publications

(4 citation statements)

References 3 publications

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“…To obtain high quality sections that retain antigenicity, decalcification procedures based on the chelator EDTA have been developed (Ryan et al 1991;Igarashi et al 1991). To exclude the possibility that EDTA treatment interferes with PEDF immunohistochemistry, we have analysed PEDF expression in positive control tissue (kidney, eye, brain) processed with EDTA as described below (see Supplementary material, Fig.…”

Section: Methodsmentioning

confidence: 99%

Protein expression of pigment-epithelium-derived factor in rat cochlea

Gleich

Piña

2008

Cell Tissue Res

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Pigment-epithelium-derived factor (PEDF) is a 50-kDa glycoprotein with well-recognised expression in various mammalian organs showing diverse (e.g. anti-angiogenic and neuroprotective) activities. However, at present, no information is available regarding the potential function of this cytokine in the inner ear. As a first approach to investigating whether PEDF is involved in cochlear function, we have explored its protein expression in the rat cochlea by immunocytochemistry. Our results show that PEDF expression in the cochlea is most prominent in the basilar membrane below the organ of Corti, in the lateral wall (especially in the stria vascularis), in ganglion neurons, and in the endothelia of blood vessels. Our findings on its distribution in the cochlea suggest that PEDF in the basilar membrane prevents blood vessel formation that would disturb cochlear micromechanics and would interfere with the mechano-electrical transduction in the organ of Corti. In cochlear ganglion neurons, PEDF might serve a neuroprotective function possibly protecting these neurons from excessive glutamate released by the inner hair cells. Our data constitute the first report on the morphological protein distribution of this multifunctional molecule in the rat cochlea and suggest its role in important functions of the internal ear.

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Section: Methodsmentioning

confidence: 99%

Protein expression of pigment-epithelium-derived factor in rat cochlea

Gleich

Piña

2008

Cell Tissue Res

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“…Substance P‐sensitive neurons have been described in the rat auditory brainstem (Wang & Robertson, 1998). In the cochlea, although the presence of SP was doubted at first (Davies, 1982), its existence has been demonstrated with the advent of more sophisticated immunocytochemical techniques (Ylikoski et al ., 1989; Nowak et al ., 1990; Igarashi et al ., 1991; Rabejac et al ., 1994; Anniko et al ., 1995; Schikinger et al ., 1996). However, the effect of substance P in vivo remains controversial (McLaren et al ., 1993; Nario et al ., 1995; Schikinger et al ., 1996), and no remarkable in vitro effect of SP on auditory peripheral neurons has been shown.…”

Section: Introductionmentioning

confidence: 99%

Substance P mobilizes intracellular calcium and activates a nonselective cation conductance in rat spiral ganglion neurons

Ito

Rome

Bouleau

et al. 2002

Eur J of Neuroscience

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We demonstrate the expression of functional tachykinin receptors in rat spiral ganglion neurons (SGNs) using calcium signal measurement and whole-cell patch clamp recording. Substance P (SP; 10 microm, 1 s application) induced a transient increase in intracellular calcium. The SP dose-response study showed an EC50 of 18.8 microm and a Hill slope of 0.77. Comparison between specific agonists for the three tachykinin receptor (NKR) types showed the potency NKR3 > NKR1 > NKR2 at 10 microm. The Ca2+ response could be evoked in Ca2+-free medium and was blocked by N-ethylmaleimide and U-73122, indicating that Ca2+ was released from intracellular stores via a G-protein and phospholipase C pathway. Under whole-cell voltage clamp recording at a holding potential of -50 mV, SP (10 microm, 1 s) evoked a slowly developing transient inward current. The current reversed near to 0 mV and ionic permeability experiments revealed a cation nonselective conductance also permeable to large organic cations such as N-methyl-D-glucamine and tetraethylammonium. Neither removing extracellular calcium nor chelating intracellular calcium with 10 mm BAPTA could block the SP-evoked current. This conductance appeared coupled to G-protein activation as intracellular GDP-betaS blocked the SP-evoked current. Mutual desensitization and occlusion studies with acetylcholine and ATP showed that the SP-evoked conductance share effector channels and/or intracellular processes with the purinergic/cholinergic conductance. In SGNs, SP could have both a trophic action, via a calcium response, and a neuromodulatory role, by a depolarizing action through the activation of nonselective cation channels.

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“…There are numerous putative roles for the S100 family of proteins, including cell proliferation, differentiation, protein phosphorylation and Ca 2+ homeostasis (Donato, 2001). S100 is localized within subdomains of the spiral ligament in rodents (Igarashi et al, 1991;Foster et al, 1994) and in humans (Shi et al, 1992). S100B is expressed by glia and released following injury (Rothermundt et al, 2003;Steiner et al, 2008).…”

Section: Changes In Protein Expression In the Inner Ear Following Postnatal Zikv Infection In Ifnar1 −/− Micementioning

confidence: 99%

Zika virus infection causes widespread damage to the inner ear

et al. 2020

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Zika virus (ZIKV) has been recently recognized as a causative agent of newborn microcephaly, as well as other neurological consequences. A less well recognized comorbidity of prenatal ZIKV infection is hearing loss, but cases of hearing impairment following adult ZIKV infection have also been recognized. Diminished hearing following prenatal ZIKV infection in a mouse model has been reported, but no cellular consequences were observed. We examined the effects of ZIKV infection on inner ear cellular integrity and expression levels of various proteins important for cochlear function in type I interferon receptor null (Ifnar1 −/− ) mice following infection at 5-6 weeks of age. We show that ZIKV antigens are present in cells within the cochlear epithelium, lateral wall, spiral limbus and spiral ganglion. Here we show that ZIKV infection alters cochlear expression of genes that signal cell damage (S100B), transport fluids (AQP1), are gaseous transmitters (eNOs) and modulate immune response (F4/80). Morphological analyses shows that not only are cochlear structures compromised by ZIKV infection, but damage also occurs in vestibular end organs. ZIKV produces a graded distribution of cellular damage in the cochlea, with greatest damage in the apex similar to that reported for cytomegalovirus (CMV) infection. The graded distribution of damage may indicate a differential susceptibility to ZIKV along the cochlear tonotopic axis. Collectively, these data are the first to show the molecular and morphological damage to the inner ear induced by ZIKV infection in adults and suggests multiple mechanisms contributing to the hearing loss reported in the human population.

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Immunohistochemical Examination of S-100 Protein and Substance P in the Inner Ear of the Rat

Cited by 8 publications

References 3 publications

Protein expression of pigment-epithelium-derived factor in rat cochlea

Protein expression of pigment-epithelium-derived factor in rat cochlea

Substance P mobilizes intracellular calcium and activates a nonselective cation conductance in rat spiral ganglion neurons

Zika virus infection causes widespread damage to the inner ear

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