Functional significance of dendritic swelling after loud sounds in the guinea pig cochlea
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2021, Hearing ResearchCitation Excerpt :The release and reuptake of glutamate from IHCs and the number of GluRs expressed on the afferent nerve terminal is tightly regulated to optimize fast synaptic transmission and maintain homeostatic conditions (Chen et al., 2009; Furness and Lehre, 1997; Peppi et al., 2012; Puel et al., 2002b). Excitotoxicity has long been known to occur at the IHC/type I afferent synapse following noise exposure, anoxia and ototoxic drug treatment (Pujol and Puel, 1999; Pujol et al., 1990; Robertson, 1983; Wang et al., 2003; Yamasoba et al., 2005). In many cases, excitotoxic damage to type I afferent terminals induced by glutamate agonists such as AMPA and KA recovers (Eybalin, 1993; Jiang et al., 2013; Puel, 1995; Puel et al., 1998; Pujol et al., 1992, 1993; Sun et al., 2001, 2000; Tabuchi et al., 2012; Zheng et al., 1999).
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2020, NeuroscienceCitation Excerpt :Fast synaptic neurotransmission at the IHC-afferent fiber synapse is via AMPA-preferring glutamate receptors (Ruel et al., 1999). Excess agonist at the synapse, whether through exogenous application (Puel et al., 1991) or sound-evoked endogenous release (Liberman and Mulroy, 1982; Robertson, 1983), produces an acute swelling of synaptic terminals on IHCs. Moreover, exogenous AMPA proportionately reduced ABR wave 1 amplitudes and IHC synapse survivals without permanent effects on DPOAEs in a gerbil model (Diuba et al., 2019).
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