Threshold shifts and enhancement of cortical evoked responses after noise exposure in rats

Syka, Josef; Rybalko, Natalia

doi:10.1016/s0378-5955(99)00175-6

Cited by 91 publications

(71 citation statements)

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“…Their down-regulation following deafening would reduce the potential for this leak and therefore be associated with improving intrinsic neuronal excitability when extrinsic excitation is removed. There is now extensive literature showing increased excitability of IC neurons following deafness (Bledsoe et al, 1995, Bledsoe et al, 1997, Mossop et al, 2000, Salvi et al, 2000, Syka and Rybalko, 2000, Vale and Sanes, 2002and Vale et al, 2004; for reviews Moller, 2005 andSyka, 2002), with these reports often suggesting increased excitability is a consequence of decreases in inhibitory influences (Bledsoe et al, 1995(Bledsoe et al, , 1997Mossop et al 2000, Salvi et al, 2000, Syka, 2002. The results of the current study showing deafness-associated decreases in "leak" channels suggests that changes in intrinsic membrane properties could also contribute to decreased neuronal excitability.…”

Section: Discussionsupporting

confidence: 50%

“…These channels could play a role in activitydependent synaptic plasticity, where intracellular signaling induced by changes in activity level can alter the properties of target neurons. Neurons in the inferior colliculus (IC) have been reported to have increased excitability following deafness (Bledsoe et al, 1995;Bledsoe et al, 1997;Mossop et al, 2000;Salvi et al, 2000;Syka and Rybalko, 2000;Sanes, 2002 andVale et al, 2004; for reviews Moller, 2005 andSyka, 2002). Decreases in inhibitory influences, such as GABA input, have been suggested as a mechanism for the increased neuronal excitability in the IC after deafness (Bledsoe et al, 1995(Bledsoe et al, , 1997Mossop et al 2000;Salvi et al, 2000;Syka, 2002).…”

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confidence: 99%

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Deafness associated changes in two-pore domain potassium channels in the rat inferior colliculus

et al. 2007

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Two-pore potassium channels can influence neuronal excitability by regulating background leakage of potassium ions and resting membrane potential. The present study used quantitative real time PCR and in situ hybridization to determine if the decreased activity from deafness would induce changes in two-pore potassium channel subunit expression in the rat inferior colliculus. Ten subunits were assessed with qRT-PCR at 3 days, 3 weeks and 3 months following bilateral cochlear ablation. TASK-1, TASK-5 and THIK-2 showed significant decreases in expression at all three times assessed. TASK-5, relatively specific to auditory neurons, had the greatest decrease. TWIK-1 was significantly decreased at 3 weeks and 3 months following deafness and TREK-2 was only significantly decreased at 3 days. TASK-3, TWIK-2, THIK-1, TRAAK and TREK-1 did not show any significant changes in gene expression. In situ hybridization was used to examine TASK-1, TASK-5, TWIK-1 and THIK-2 in the central nucleus, dorsal cortex and lateral (external) cortex of the IC in normal hearing animals and at 3 weeks following deafening. All four subunits showed expression in neurons throughout IC subdivisions in normal hearing rats, with TASK-5 having the greatest overall number of labeled neurons. There was no co-localization of subunit expression with GFAP immunostaining, indicating no expression in glia. Three weeks following deafening there was a significant decrease in the number of neurons expressing TASK-1 and THIK-2 in the IC, while TASK-5 had significant decreases in the central nucleus and dorsal cortex and TWIK-1 in the lateral and dorsal cortices. Two-pore potassium channels (K 2p ) are a class of open rectifying potassium selective channels (Ketchum et al., 1995) that, when activated, allow a background leakage of potassium ions that raises the resting membrane potential to hyperpolarizing levels, resulting in decreased neuronal excitability (see Lesage and Lazdunski, 2000;Goldstein et al., 2001;Patel and Honore, 2001; Plant et al., 2005 for reviews). There are, to date, 18 subunits in the K 2p channel family that have been divided into different classes based on what is know about their sensitivities. The TASK-1 (K 2p 3.1, KCNK3), TASK-3 (K 2p 9.1, KCNK9) and TWIK-1 (K 2p 1.1, KCNK1) subunits are widely expressed throughout the brain but have been reported to have only moderate expression in the auditory brain stem Talley et al., 2001). The TASK-5 (K 2p 15.1, KCNK15) subunit has a relatively selective expression, primarily found in Author for correspondence: Dr. Richard A. Altschuler, KHRI, Department of Otolaryngology, The University of Michigan, 1301 East Ann Street, Ann Arbor, MI, Tel: (734) Fax: (734) 764-0014, E-mail: E-mail: shuler@umich.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof befo...

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Section: Discussionsupporting

confidence: 50%

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confidence: 99%

Deafness associated changes in two-pore domain potassium channels in the rat inferior colliculus

et al. 2007

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“…Earlier studies demonstrated that cochlear injury can be generated by high intensity sound exposure (100-120 dB SPL). This damage is usually accompanied by elevated sound intensity thresholds (18)(19)(20)(21). It was recently shown that such noise-induced peripheral hearing loss also affects cortical tMTFs to amplitudemodulated noises in cats (22).…”

Section: Discussionmentioning

confidence: 99%

Enduring effects of early structured noise exposure on temporal modulation in the primary auditory cortex

Zhou

Merzenich

2008

Proc. Natl. Acad. Sci. U.S.A.

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Studies have shown that acoustic experiences significantly contribute to the functional shaping of the structural organization and signal processing capacities of the mammalian auditory system during postnatal development. Here, we show how an early epoch of exposure to structured noise influences temporal processing in the rat primary auditory cortex documented immediately after exposure and again in adulthood. Pups were continuously exposed to broadband-pulsed noise across the critical period for auditory system development. Immediately after cessation of exposure at postnatal day Ϸ35 (P35) or Ϸ55 days later (i.e., P90) in other rats, the temporal modulation-transfer functions of cortical neurons were documented. We found that pulsed noise exposure at a low modulation rate significantly decreased cortical responses to repetitive stimuli presented across a range of higher modulation rates. The highest temporal rate at which temporal modulationtransfer function was at half of its maximum was reduced when compared with naïve rats. Low-rate pulsed noise exposure also decreased cortical response synchronization at higher stimulus rates, as shown by vector strength and Rayleigh statistic measures. These postexposure changes endured into adulthood. These findings bear significant implications for the role of early sound experiences as contributors to the ontogeny of human auditory and language-related abilities and impairments.cortical plasticity ͉ critical period ͉ temporal modulation-transfer function ͉ temporal processing S ounds in natural environments, such as animal vocalizations and human speech, have complex temporal structures. The importance of temporal structure in acoustic communication and orientation has been demonstrated in many behavioral, psychological, and neurophysiological studies. The auditory cortex plays a critical role in the perception of time-varying features of aural speech and of other complex acoustic stimuli. In humans, speech comprehension is correlated with responses of cortical neurons to temporal envelopes of speech (1), and individuals with impaired language abilities have impaired successive signal evoked cortical responses (2, 3).Earlier studies in different subprimate animal species have shown that cortical neurons display different temporal filtering properties (e.g., low-pass, responding to sound trains below certain rates, or band-pass, responding best to a specific rate, etc.) (4-7). In general, cortical neurons respond to repetitive sounds at far lower rates and with poorer temporal precision when compared with auditory nerve fibers or neurons in subcortical auditory nuclei and, in most mammalian species, are not able to follow individual sound presented at rates faster than Ϸ20 pulses per second (pps). It has been argued that for those more rapidly occurring stimuli (e.g., stimuli with repetition rate Ͼ100 pps), cortical neurons might apply a rate code instead of a temporal code (stimulus-synchronized responses) to represent the temporal structure (7). Most natural sounds, ...

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“…As is the case for age-related changes described below, it is not known whether age-related inhibitory changes in IC are the result of de novo aging changes within the central nervous system or are the direct result of a gradual loss of peripheral input or both. In response to superthreshold acoustic stimulation, noise-exposed animals (modest damage to the auditory periphery) show altered evoked responses in the IC and auditory cortex, providing a functional picture suggestive of hyperexcitability (Willott and Lu, 1982;Popelár et al, 1987;Salvi et al, 1990;Gerken et al, 1991;Syka et al, 1994;Szczepaniak and Møller, 1995;Wang et al, 1996;Syka and Rybalko, 2000;Aizawa and Eggermont, 2007). Neurochemical findings in support of these functional changes reveal that damage to the auditory periphery results in a selective down-regulation of normal adult inhibitory GABAergic function in the IC.…”

Section: Inferior Colliculusmentioning

confidence: 99%

Inhibitory neurotransmission, plasticity and aging in the mammalian central auditory system

Caspary

Ling

Turner

et al. 2008

Journal of Experimental Biology

436

355

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SummaryAging and acoustic trauma may result in partial peripheral deafferentation in the central auditory pathway of the mammalian brain. In accord with homeostatic plasticity, loss of sensory input results in a change in pre-and postsynaptic GABAergic and glycinergic inhibitory neurotransmission. As seen in development, age-related changes may be activity dependent. Age-related presynaptic changes in the cochlear nucleus include reduced glycine levels, while in the auditory midbrain and cortex, GABA synthesis and release are altered. Presumably, in response to age-related decreases in presynaptic release of inhibitory neurotransmitters, there are age-related postsynaptic subunit changes in the composition of the glycine (GlyR) and GABA A (GABA A R) receptors. Age-related changes in the subunit makeup of inhibitory pentameric receptor constructs result in altered pharmacological and physiological responses consistent with a net down-regulation of functional inhibition. Age-related functional changes associated with glycine neurotransmission in dorsal cochlear nucleus (DCN) include altered intensity and temporal coding by DCN projection neurons. Loss of synaptic inhibition in the superior olivary complex (SOC) and the inferior colliculus (IC) likely affect the ability of aged animals to localize sounds in their natural environment. Age-related postsynaptic GABA A R changes in IC and primary auditory cortex (A1) involve changes in the subunit makeup of GABA A Rs. In turn, these changes cause age-related changes in the pharmacology and response properties of neurons in IC and A1 circuits, which collectively may affect temporal processing and response reliability. Findings of age-related inhibitory changes within mammalian auditory circuits are similar to age and deafferentation plasticity changes observed in other sensory systems. Although few studies have examined sensory aging in the wild, these age-related changes would likely compromise an animal's ability to avoid predation or to be a successful predator in their natural environment.Key words: aging, central auditory system, GABA A receptor, glycine receptor, inhibitory neurotransmission, plasticity. THE JOURNAL OF EXPERIMENTAL BIOLOGY 1782important in determining the location of sound, echolocation and extracting information from voiced and unvoiced communication signals (Carr et al., 1986;Portfors and Wenstrup, 2001).The complex processing that occurs at the level of the MGB and the A1 is beyond the scope of the present review. Coding in the auditory cortex has been recently reviewed (Wang, 2007;Rauschecker, 2005). As seen in the visual cortex, in the auditory cortex, acoustically complex hierarchical analysis has been described for awake-behaving primates (Rauschecker, 2005;Steinschneider et al., 2008). A1 has been shown to undergo agerelated plastic changes, including down-regulation of inhibitory coding, similar to that observed at lower levels of the auditory pathway and in visual cortex. Similar to age-related changes, activity-dependant changes have be...

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Threshold shifts and enhancement of cortical evoked responses after noise exposure in rats

Cited by 91 publications

References 21 publications

Deafness associated changes in two-pore domain potassium channels in the rat inferior colliculus

Deafness associated changes in two-pore domain potassium channels in the rat inferior colliculus

Enduring effects of early structured noise exposure on temporal modulation in the primary auditory cortex

Inhibitory neurotransmission, plasticity and aging in the mammalian central auditory system

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