Seeing Less Helps The Brain Hear More

Crossmodal Induction of Thalamocortical Potentiation Leads to Enhanced Information Processing in the Auditory Cortex
Emily Petrus, et al.
Neuron 81(3):664–673, 5 February 2014


Visual deprivation improves frequency selectivity of A1 neurons
•Visual deprivation improves sound discrimination performance by A1 neurons
•Visual deprivation strengthens thalamocortical synapses in A1, but not in V1
•Crossmodal changes are more effectively recruited than unimodal changes in adult

Sensory systems do not work in isolation; instead, they show interactions that are specifically uncovered during sensory loss.
To identify and characterize these interactions, we investigated whether visual deprivation leads to functional enhancement in primary auditory cortex (A1).
We compared sound-evoked responses of A1 neurons in visually deprived animals to those from normally reared animals.

Here, we show that visual deprivation leads to improved frequency selectivity as well as increased frequency and intensity discrimination performance of A1 neurons.
Furthermore, we demonstrate in vitro that in adults visual deprivation strengthens thalamocortical (TC) synapses in A1, but not in primary visual cortex (V1).
Because deafening potentiated TC synapses in V1, but not A1, crossmodal TC potentiation seems to be a general property of adult cortex.
Our results suggest that adults retain the capability for crossmodal changes whereas such capability is absent within a sensory modality. Thus, multimodal training paradigms might be beneficial in sensory-processing disorders.

journalistic version:
Seeing Less Helps The Brain Hear More
February 05, 2014
A few days in the dark can improve an animal’s hearing, scientists report this week in the journal Neuron.
This temporary loss of visual input seems to trigger favorable changes in areas of the brain that process auditory information.

Even when blindness occurs after that critical period in early childhood.


Critical period

A disinhibitory microcircuit initiates critical-period plasticity in the visual cortex
Sandra J. Kuhlman, et al.
Nature (2013)
Published online  25 August 2013
Early sensory experience instructs the maturation of neural circuitry in the cortex.
This has been studied extensively in the primary visual cortex, in which loss of vision to one eye permanently degrades cortical responsiveness to that eye, a phenomenon known as ocular dominance plasticity (ODP).

A critical period for auditory thalamocortical connectivity
Nature Neuroscience  14, 1189–1194 (2011)
Tania Rinaldi Barkat, et al.
Neural circuits are shaped by experience during periods of heightened brain plasticity in early postnatal life.
Exposure to acoustic features produces age-dependent changes through largely unresolved cellular mechanisms and sites of origin.
We isolated the refinement of auditory thalamocortical connectivity by in vivo recordings and day-by-day voltage-sensitive dye imaging in an acute brain slice preparation.
Passive tone-rearing modified response strength and topography in mouse primary auditory cortex (A1) during a brief, 3-d window, but did not alter tonotopic maps in the thalamus.
Gene-targeted deletion of a forebrain-specific cell-adhesion molecule (Icam5) accelerated plasticity in this critical period.
Consistent with its normal role of slowing spinogenesis, loss of Icam5 induced precocious stubby spine maturation on pyramidal cell dendrites in neocortical layer 4 (L4), identifying a primary locus of change for the tonotopic plasticity.
The evolving postnatal connectivity between thalamus and cortex in the days following hearing onset may therefore determine a critical period for auditory processing.

Manipulating critical period closure across different sectors of the primary auditory cortex
Nature Neuroscience 11, 957 – 965 (2008)
Etienne de Villers-Sidani, Kimberly L Simpson, Y-F Lu, Rick C S Lin & Michael M Merzenich
During early brain development and through ‘adult’ experience-dependent plasticity, neural circuits are shaped to represent the external world with high fidelity.
When raised in a quiet environment, the rat primary auditory cortex (A1) has a well-defined ‘critical period’, lasting several days, for its representation of sound frequency. The addition of environmental noise extends the critical period duration as a variable function of noise level. It remains unclear whether critical period closure should be regarded as a unified, externally gated event that applies for all of A1 or if it is controlled by progressive, local, activity-driven changes in this cortical area. We found that rearing rats in the presence of a spectrally limited noise band resulted in the closure of the critical period for A1 sectors representing the noise-free spectral bands, whereas the critical period appeared to remain open in noise-exposed sectors, where the cortex was still functionally and physically immature.

Critical period plasticity in local cortical circuits
Nature Reviews Neuroscience 6, 877-888 (November 2005)
Takao K. Hensch
Neuronal circuits in the brain are shaped by experience during ‘critical periods’ in early postnatal life.
In the primary visual cortex, this activity-dependent development is triggered by the functional maturation of local inhibitory connections and driven by a specific, late-developing subset of interneurons. Ultimately, the structural consolidation of competing sensory inputs is mediated by a proteolytic reorganization of the extracellular matrix that occurs only during the critical period. The reactivation of this process, and subsequent recovery of function in conditions such as amblyopia, can now be studied with realistic circuit models that might generalize across systems.

Box 1 | Critical periods: gateway to lifelong plasticity