Abstract
It has been demonstrated that sensory deprivation results in homeostatic adjustments recovering neuronal activity of the deprived cortex. For example, deprived vision multiplicatively scales up mEPSC amplitudes in the primary visual cortex, commonly referred to as synaptic scaling. However, whether synaptic scaling also occurs in auditory cortex after auditory deprivation remains elusive. Using periodic intrinsic optical imaging in adult mice, we show that conductive hearing loss (CHL), initially led to a reduction of primary auditory cortex (A1) responsiveness to sounds. However, this was followed by a complete recovery of A1 activity evoked sounds above the threshold for bone conduction, 3 days after CHL. Over the same time course patch-clamp experiments in slices revealed that mEPSC amplitudes in A1 layers 2/3 pyramids scaled up multiplicatively in CHL mice. No recovery of sensory evoked A1 activation was evident in TNFα KO animals, which lack synaptic scaling. Additionally, we could show that the suppressive effect of sounds on visually evoked visual cortex activity completely recovered along with TNFα dependent A1 homeostasis in WT animals. This is the first demonstration of homeostatic multiplicative synaptic scaling in the adult A1. These findings suggest that mild hearing loss massively affects auditory processing in adult A1.
Highlights
Homeostatic plasticity is essential in maintaining a stable firing rate in neurons to compensate for prolonged perturbations of neuronal activity[1,2]
Because intrinsic optical imaging is based on temporally periodic stimulus presentation[25], we used tone sweeps linearly ascending or descending in frequency (1–15 kHz) with 70 dB sound pressure level (SPL), which were repeated with a period of 8 s for 5 min
In this study we investigated the effects of a conductive hearing loss (CHL) in form of bilateral malleus removal on the neuronal activity of A1 in adult mice
Summary
Homeostatic plasticity is essential in maintaining a stable firing rate in neurons to compensate for prolonged perturbations of neuronal activity[1,2]. A prolonged reduction of neuronal activity of cultured neocortical neurons generated compensatory changes returning firing levels back to control values[1] Such homeostatic regulations are typically accompanied by an additional insertion of 2-amino-3-(3-hydroxy-5-methyl-isoxasol-4-yl) propanoic acid receptors (AMPARs) into all synapses of a neuron, leading to multiplicatively scaled up mEPSC (miniature excitatory postsynaptic currents) amplitudes or, “synaptic scaling”[2,3]. By performing electrophysiological single cell recordings in brain slices obtained 3 d after CHL, we found amplitudes of spontaneous mEPSCs of A1 layers 2/3 neurons to be increased multiplicatively, strongly indicating homeostatic synaptic scaling In agreement with this interpretation, sound evoked A1 responsiveness did not recover in TNFα KO animals, which have previously been shown to lack synaptic scaling in vitro and in vivo[10,24]. The present study highlights the ability of adult A1 to undergo homeostatic changes in response to mild hearing loss
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