The loss of one sensory modality often results in functional enhancement of the remaining senses;this phenomenon is called cross-modal plasticity. The loss of vision specifically can result in better tactile acuity, pitch discriminatin and sound localization in blind individuals. This enhancement can also happen quite quickly, only a few days of blindfold experience can lead to improved Braille reading in normally sighted individuals. These cross-modal changes are correlated with functional recruitment of the visual cortex for processing the remaining senses. While this is beneficial to those affected, it may hinder therapeutic interventions to recover the lost sense. For example, the success of cochlear implants for early deaf people is quite low because extensive cortical reorganization no longer can effectively process auditory stimuli. Our lab reported that depriving rodents of vision alters excitatory synaptic transmission in barrel and auditory cortices. However, regulation of excitatory synaptic transmission represents only half the story of how plasticity mechanisms enhance the remaining senses following visual deprivation. The balance of excitation and inhibition are crucial for normal function in any neuronal circuit. For this reason we hypothesize that changes in excitatory synaptic transmission should also be complemented by inhibitory changes. In addition, this study aims to delineate the molecular mechanisms behind excitatory and inhibitory cross-modal plasticity. By using transgenic mouse models targeting specific activity-regulated gene products (i.e. Arc/Arg3.1 KO and BDNF-KIV KI), which show altered plasticity mechanisms and specifically target excitatory and inhibitory synapses, we can identify if these molecules are important for cross-modal reorganization of neural circuits. Finally, using channel rhodopsin activated parvalbumin neurons, we will investigate the role of this set of inhibitory neurons in cross-modal plasticity. Results from this work will directly impact our understanding of how spared sensory modalities become enhanced following the loss of one sense.

Public Health Relevance

Cross-modal reorganization of sensory cortex determines the success rate of neuroprosthetic treatments for individuals who are born without, or lose a sense. Given that neuroprosthetics (such as cochlear implants) are unsuccessful in those with extensive cross-modal reorganization, the mechanism behind this plasticity must be understood. By improving our understanding of this type of plasticity, we can explore the possibility of overcoming this obstacle in helping people re-gain sensory experience.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31NS079058-03
Application #
8663325
Study Section
Special Emphasis Panel (ZRG1)
Program Officer
Gnadt, James W
Project Start
2012-06-01
Project End
2014-06-06
Budget Start
2014-06-01
Budget End
2014-06-06
Support Year
3
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Johns Hopkins University
Department
Neurosciences
Type
Schools of Arts and Sciences
DUNS #
City
Baltimore
State
MD
Country
United States
Zip Code
21218
Petrus, Emily; Rodriguez, Gabriela; Patterson, Ryan et al. (2015) Vision loss shifts the balance of feedforward and intracortical circuits in opposite directions in mouse primary auditory and visual cortices. J Neurosci 35:8790-801
Petrus, Emily; Lee, Hey-Kyoung (2014) BACE1 is necessary for experience-dependent homeostatic synaptic plasticity in visual cortex. Neural Plast 2014:128631
Petrus, Emily; Isaiah, Amal; Jones, Adam P et al. (2014) Crossmodal induction of thalamocortical potentiation leads to enhanced information processing in the auditory cortex. Neuron 81:664-73
Whitt, Jessica L; Petrus, Emily; Lee, Hey-Kyoung (2014) Experience-dependent homeostatic synaptic plasticity in neocortex. Neuropharmacology 78:45-54