Parvalbumin immunoreactivity in the auditory cortex of a mouse model of presbycusis

Campo, H.N. Martin del; Measor, Kevin; Razak, Khaleel A.

doi:10.1016/j.heares.2012.08.017

Cited by 67 publications

(59 citation statements)

References 55 publications

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“…Once the animal was anesthetized, a midline sagittal incision was made along the scalp to expose the skull, and the right temporalis muscle was displaced. A dental drill was used to remove the skull overlying the right auditory cortex identified using previously published methods (Martin del Campo et al 2012). Location of core auditory cortex was identified using vasculature, and confirmed with extracellular recordings in response to sounds.…”

Section: Methodsmentioning

confidence: 99%

“…Postnatal day (P) 40 mice (n=5 mice per group) were euthanized with isoflurane and the auditory cortex was dissected based on coordinates (Paxinos and Franklin, 2004) and previous electrophysiological and dye-placement studies (Martin del Campo et al, 2012). The tissues were flash-frozen on dry ice and stored at −80° C. Gelatin gel zymography was performed as previously described with minor modifications (Sidhu et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

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Matrix metalloproteinase-9 deletion rescues auditory evoked potential habituation deficit in a mouse model of Fragile X Syndrome

Lovelace

Wen

Reinhard

et al. 2016

Neurobiology of Disease

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Sensory processing deficits are common in autism spectrum disorders, but the underlying mechanisms are unclear. Fragile X Syndrome (FXS) is a leading genetic cause of intellectual disability and autism. Electrophysiological responses in humans with FXS show reduced habituation with sound repetition and this deficit may underlie auditory hypersensitivity in FXS. Our previous study in Fmr1 knockout (KO) mice revealed an unusually long state of increased sound-driven excitability in auditory cortical neurons suggesting that cortical responses to repeated sounds may exhibit abnormal habituation as in humans with FXS. Here, we tested this prediction by comparing cortical event related potentials (ERP) recorded from wildtype (WT) and Fmr1 KO mice. We report a repetition-rate dependent reduction in habituation of N1 amplitude in Fmr1 KO mice and show that matrix metalloproteinase −9 (MMP-9), one of the known FMRP targets, contributes to the reduced ERP habituation. Our studies demonstrate a significant up-regulation of MMP-9 levels in the auditory cortex of adult Fmr1 KO mice, whereas a genetic deletion of Mmp-9 reverses ERP habituation deficits in Fmr1 KO mice. Although the N1 amplitude of Mmp-9/Fmr1 DKO recordings was larger than WT and KO recordings, the habituation of ERPs in Mmp-9/Fmr1 DKO mice is similar to WT mice implicating MMP-9 as a potential target for reversing sensory processing deficits in FXS. Together these data establish ERP habituation as a translation relevant, physiological pre-clinical marker of auditory processing deficits in FXS and suggest that abnormal MMP-9 regulation is a mechanism underlying auditory hypersensitivity in FXS.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Matrix metalloproteinase-9 deletion rescues auditory evoked potential habituation deficit in a mouse model of Fragile X Syndrome

Lovelace

Wen

Reinhard

et al. 2016

Neurobiology of Disease

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“…However, only limited information exists on the role of PV in the auditory system. Several recent studies have reported age-related and region-specific changes in the expression of PV-positive neurons in a variety of mammalian species: an age-related decline of calcium binding protein-positive neurons in the dorsal cochlear nucleus of CBA/CaJ mice [13], a decrease in the percentage of PV-expressing neurons in the superficial layers of the auditory cortex of C57Bl/6 mice [17] or an increase of PV-positive neurons in the inferior colliculus of old Long Evans rats and a pronounced decline in the number of PV-positive neurons in the auditory cortex of aged Fischer 344 rats [19]. The assessment of the function of PV in mice has been facilitated by using genetically modified mice deficient for this protein [23].…”

Section: Introductionmentioning

confidence: 99%

The effect of parvalbumin deficiency on the acoustic startle response and prepulse inhibition in mice

Popelář

Rybalko

Burianová

et al. 2013

Neuroscience Letters

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h i g h l i g h t s• PV−/− mice had smaller ASR amplitudes in response to relatively weak startling stimuli (80-90 dB SPL) in comparison with PV+/+ mice.• PPI of the ASR in PV−/− mice was less effective than in PV+/+ mice.• Mean ABR audiograms were found to be similar in both genotypes.The strength of the acoustic startle response (ASR) to short bursts of broadband noise or tone pips (4, 8 and 16 kHz) and the prepulse inhibition (PPI) of the ASR elicited by prepulse tones (4, 8 and 16 kHz) were measured in parvalbumin-deficient (PV−/−) mice and in age-matched PV+/+ mice as controls. Hearing thresholds as determined from recordings of auditory brainstem responses were found to be similar in both genotypes. The ASRs to broadband noise and tones of low and middle frequencies were stronger than the ASRs in response to high-frequency tones in both groups. In PV−/− mice, we observed smaller ASR amplitudes in response to relatively weak startling stimuli (80-90 dB sound pressure level (SPL)) of either broadband noise or 8-kHz tones compared to those recorded in PV+/+ mice. For these startling stimuli, PV−/− mice had higher ASR thresholds and longer ASR latencies. PPI of the ASR in PV−/− mice was less effective than in PV+/+ mice, for all tested prepulse frequencies (4, 8 or 16 kHz) at 70 dB SPL. Our findings demonstrate no effect of PV deficiency on hearing thresholds in PV−/− mice. However, the frequency-specific differences in the ASR and the significant reduction of PPI of ASR likely reflect specific changes of neuronal circuits, mainly inhibitory, in the auditory centers in PV-deficient mice..

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“…However, regulatory compensation of Ca ++ homeostasis in the aging auditory pathway may have other levels of complexity. The auditory cortex is unique in that changes in parvalbumin levels are not homogeneous, but rather fi eld-and corticallayer specifi c (Martin del Campo et al 2012 ). Although parvalbumin expression is increased in deep cortical layers, it tends to diminish in GABAergic interneurons (Ouda and Syka 2012 ;Ouellet and de Villers-Sidani 2014 ), with no apparent neuronal loss.…”

Section: Cellular Mechanisms Of Age-related Hearing Loss In the Centrmentioning

confidence: 99%

Cellular Mechanisms of Age-Related Hearing Loss

Melgar–Rojas

Alvarado

Fuentes–Santamaría

et al. 2015

Oxidative Stress in Applied Basic Research and Clinical Practice

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Parvalbumin immunoreactivity in the auditory cortex of a mouse model of presbycusis

Cited by 67 publications

References 55 publications

Matrix metalloproteinase-9 deletion rescues auditory evoked potential habituation deficit in a mouse model of Fragile X Syndrome

Matrix metalloproteinase-9 deletion rescues auditory evoked potential habituation deficit in a mouse model of Fragile X Syndrome

The effect of parvalbumin deficiency on the acoustic startle response and prepulse inhibition in mice

Cellular Mechanisms of Age-Related Hearing Loss

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