Differential effects of sodium salicylate on current-evoked firing of pyramidal neurons and fast-spiking interneurons in slices of rat auditory cortex

Su, Yanyan; Luo, Bin; Ht, Wang; Chen, Lin

doi:10.1016/j.heares.2009.03.007

Cited by 39 publications

(40 citation statements)

References 34 publications

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“…The migration of low and high CF units towards the 10-20 kHz regions presumably results from an interaction between certain features of the peripheral losses (Figures 3-4) and central factors: (1) AC neurons receive excitatory inputs from a broad range of frequencies, but inhibition in the AC normally narrows the excitatory response area. When SS is applied to brain slices from AC, it reduces inhibitory post-synaptic currents (Wang et al, 2006) and selectively reduces current-evoked firing in fast-spiking GABAergic AC neurons (Su et al, 2009). Therefore, we speculate that when SS reaches the AC in vivo , it reduces GABAergic inhibition thereby permitting some AC neurons to respond to a broader range of frequencies.…”

Section: Resultsmentioning

confidence: 99%

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Salicylate-induced cochlear impairments, cortical hyperactivity and re-tuning, and tinnitus

et al. 2013

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High doses of sodium salicylate (SS) have long been known to induce temporary hearing loss and tinnitus, effects attributed to cochlear dysfunction. However, our recent publications reviewed here show that SS can induce profound, permanent, and unexpected changes in the cochlea and central nervous system. Prolonged treatment with SS permanently decreased the cochlear compound action potential (CAP) amplitude in vivo. In vitro, high dose SS resulted in a permanent loss of spiral ganglion neurons and nerve fibers, but did not damage hair cells. Acute treatment with high-dose SS produced a frequency-dependent decrease in the amplitude of distortion product otoacoustic emissions and CAP. Losses were greatest at low and high frequencies, but least at the mid-frequencies (10-20 kHz), the mid-frequency band that corresponds to the tinnitus pitch measured behaviorally. In the auditory cortex, medial geniculate body and amygdala, high-dose SS enhanced sound-evoked neural responses at high stimulus levels, but it suppressed activity at low intensities and elevated response threshold. When SS was applied directly to the auditory cortex or amygdala, it only enhanced sound evoked activity, but did not elevate response threshold. Current source density analysis revealed enhanced current flow into the supragranular layer of auditory cortex following systemic SS treatment. Systemic SS treatment also altered tuning in auditory cortex and amygdala; low frequency and high frequency multiunit clusters up-shifted or down-shifted their characteristic frequency into the 10-20 kHz range thereby altering auditory cortex tonotopy and enhancing neural activity at mid-frequencies corresponding to the tinnitus pitch. These results suggest that SS-induced hyperactivity in auditory cortex originates in the central nervous system, that the amygdala potentiates these effects and that the SS-induced tonotopic shifts in auditory cortex, the putative neural correlate of tinnitus, arises from the interaction between the frequency-dependent losses in the cochlea and hyperactivity in the central nervous system.

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Section: Resultsmentioning

confidence: 99%

“…Recent in vitro studies indicate that SS produces dissimilar effects on the current-evoked firing of neurons located in different layers of AC (Su et al, 2009). These results suggest that high doses of SS may induce layer specific electrophysiological changes within the microcircuitry of primary AC (A1).…”

Section: Resultsmentioning

confidence: 99%

Salicylate-induced cochlear impairments, cortical hyperactivity and re-tuning, and tinnitus

et al. 2013

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“…Salicylate suppresses the overall neural output of the cochlea, but the suppression is less at mid-frequencies (blue) than low (green) or high (red) frequencies creating a bandpass-like output as we previously reported (Stolzberg et al, 2011). Salicylate reduces GABA-mediated inhibition in the AC (Lu et al, 2011; Su et al, 2009). The salicylate actions may result in two major changes.…”

Section: Discussionmentioning

confidence: 99%

Amygdala hyperactivity and tonotopic shift after salicylate exposure

2012

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The amygdala, important in forming and storing memories of aversive events, is believed to play a major role in debilitating tinnitus and hyperacusis. To explore this hypothesis, we recorded from the lateral amygdala (LA) and auditory cortex (AC) before and after treating rats with a dose of salicylate that induces tinnitus and hyperacusis-like behavior. Salicylate unexpectedly increased the amplitude of the local field potential (LFP) in the LA making it hyperactive to sounds ≥60 dB SPL. Frequency receptive fields (FRF) of multiunit (MU) clusters in the LA were also dramatically altered by salicylate. Neuronal activity at frequencies below 10 kHz and above 20 kHz was depressed at low intensities, but was greatly enhanced for stimuli between 10 and 20 kHz (frequencies near the pitch of the salicylate-induced tinnitus in the rat). These frequency-dependent changes caused the FRF of many LA neurons to migrate towards 10-20 kHz thereby amplifying activity from this region. To determine if salicylate-induced changes restricted to the LA would remotely affect neural activity in the AC, we used a micropipette to infuse salicylate (20 µl, 2.8 mM) into the amygdala. Local delivery of salicylate to the amygdala significantly increased the amplitude of the LFP recorded in the AC and selectively enhanced the neuronal activity of AC neurons at the mid-frequencies (10-20 kHz), frequencies associated with the tinnitus pitch. Taken together, these results indicate that systemic salicylate treatment can induce hyperactivity and tonotopic shift in the amygdala and infusion of salicylate into the amygdala can profoundly enhance sound-evoked activity in AC, changes likely to increase the perception and emotional salience of tinnitus and loud sounds.

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“…When suprathreshold stimulation levels are considered, whereas maximum response amplitude enhancement has been documented (Willott and Lu, 1982; Salvi et al, 1990; McFadden et al, 1998), more often the loss of IHC integrity appears to engender a reduction in neuronal suprathreshold responsivity (McFadden et al, 1998; Qiu et al, 2000; El-Badry and McFadden, 2007) (Figure 3). This is akin to the effects of cochlear administration of salicylate (Sun et al, 2009a), which is thought to be active against inhibitory pharmacology (Su et al, 2009). In addition, there is a reduction in the proportion of non-monotonic-type rate level functions (Alkhatib et al, 2006), a response pattern that is characteristically reliant upon normal inhibitory activity.…”

Section: Neuronal Spontaneous and Evoked Response Properties Undergo mentioning

confidence: 99%

Insult-induced adaptive plasticity of the auditory system

Gold

Bajo

2014

Front. Neurosci.

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The brain displays a remarkable capacity for both widespread and region-specific modifications in response to environmental challenges, with adaptive processes bringing about the reweighing of connections in neural networks putatively required for optimizing performance and behavior. As an avenue for investigation, studies centered around changes in the mammalian auditory system, extending from the brainstem to the cortex, have revealed a plethora of mechanisms that operate in the context of sensory disruption after insult, be it lesion-, noise trauma, drug-, or age-related. Of particular interest in recent work are those aspects of auditory processing which, after sensory disruption, change at multiple—if not all—levels of the auditory hierarchy. These include changes in excitatory, inhibitory and neuromodulatory networks, consistent with theories of homeostatic plasticity; functional alterations in gene expression and in protein levels; as well as broader network processing effects with cognitive and behavioral implications. Nevertheless, there abounds substantial debate regarding which of these processes may only be sequelae of the original insult, and which may, in fact, be maladaptively compelling further degradation of the organism's competence to cope with its disrupted sensory context. In this review, we aim to examine how the mammalian auditory system responds in the wake of particular insults, and to disambiguate how the changes that develop might underlie a correlated class of phantom disorders, including tinnitus and hyperacusis, which putatively are brought about through maladaptive neuroplastic disruptions to auditory networks governing the spatial and temporal processing of acoustic sensory information.

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Differential effects of sodium salicylate on current-evoked firing of pyramidal neurons and fast-spiking interneurons in slices of rat auditory cortex

Cited by 39 publications

References 34 publications

Salicylate-induced cochlear impairments, cortical hyperactivity and re-tuning, and tinnitus

Salicylate-induced cochlear impairments, cortical hyperactivity and re-tuning, and tinnitus

Amygdala hyperactivity and tonotopic shift after salicylate exposure

Insult-induced adaptive plasticity of the auditory system

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