Effect of Gentamicin on Vestibular Ganglion

Changes in transient receptor potential cation channel superfamily V (TRPV) mRNA expression in the mouse inner ear ganglia after kanamycin challenge

“…Degeneration in the SG was noted initially after KM intoxication (Kellerhals et al, 1967). Morphologic changes were reported in later in guinea pig VG cells after transtympanic gentamicin instillation (Sera et al, 1987;Harada et al, 1991). However, damage to cochlear hair cells is also associated with a secondary degeneration of SG cells (e.g., Kellerhals et al, 1967;Spoendlin, 1975;Webster and Webster, 1981;Zimmermann et al, 1995), which is attenuated markedly in chonically deafened animals by growth factor treatment (Miller et al, 1997;Kanzaki et al, 2002).…”

“…However, damage to cochlear hair cells is also associated with a secondary degeneration of SG cells (e.g., Kellerhals et al, 1967;Spoendlin, 1975;Webster and Webster, 1981;Zimmermann et al, 1995), which is attenuated markedly in chonically deafened animals by growth factor treatment (Miller et al, 1997;Kanzaki et al, 2002). The evidence supporting a direct component to aminoglycoside toxicity in ganglion cells includes human temporal bone cases with SG cell loss and sparing of hair cells (Hinojosa and Lerner, 1987;Zimmermann et al, 1995;Sone et al, 1998) and the time course of histological changes after intoxication in animal studies (Bichler et al, 1983;Sera et al, 1987;Harada et al, 1991;Dodson, 1997), particularly after systemic Km treatment (Webster and Webster, 1981). Hence, it seems prudent to regard biochemical responses of inner ear ganglion cells to KM treatment as a reflection of both rapid direct and prolonged indirect mechanisms of action (e.g., deafferentation).…”

“…Treatment with this KM protocol is known to produce degeneration of cochlear outer hair cells and some vestibular hair cells; these effects are blocked by co-administration of DHB (Wu et al, 2001). Since the combined direct effects of aminoglycosides and secondary effects of hair cell degeneration appear to be factors in eliciting degeneration of spiral and vestibular ganglion cells (Kellerhals et al, 1967;Spoendlin, 1975;Webster and Webster, 1981;Bichler et al, 1983;Hinojosa and Lerner, 1987;Sera et al, 1987;Harada et al, 1991;Zimmermann et al, 1995;Dodson, 1997;Sone et al, 1998), this protocol concurrently provides multiple challenges to survival of inner ear ganglion cells. By contrast, the nephrotoxic effects provide an example of responses to the direct cellular effects of KM alone.…”

Identification of a Lactate-Quinone Oxidoreductase in Staphylococcus aureus that is Essential for Virulence

“…For instance, human sweat can have as high as ∼50 mM l -lactate, possibly resulting in a role for Lqo in skin colonization (Sakharov et al, 2010). Moreover, nasal secretions have also been shown to contain high concentrations of l -lactate making the most common site of S. aureus colonization (the nasal cavity) a prime environment for Lqo activity (Stierna et al, 1991; Westrin et al, 1992). Thus, while Lqo may contribute to S. aureus disease, particularly in various forms of myocarditis and myositis, this newly characterized enzyme may also have more overarching roles in promoting S. aureus colonization.…”

Gentamicin uptake in the chinchilla inner ear

“…These effects were believed to be a secondary consequence of deafferentation due to hair cell damage, because destruction of neuroepithelial cells was known to lead to the degeneration of spiral ganglion cells (Spoendlin, 1975;Webster and Webster, 1981). A later study showed evidence of vestibular hair cell damage 24 h after transtympanic (TT) gentamicin injection and ganglion cell damage at 72 h following injection while the intervening nerve fibers remained intact (Harada et al, 1991), which they attributed to gentamicin uptake by ganglion cells that was noted earlier by Hayashida et al (1985).…”