Laminar Specific Cortical Plasticity following Mouse Sensory Deprivation
Friday, September 14, 2018 — Poster Session V
- KA Sheth
- E Petrus
- S Dodd
- AP Koretsky
Sensory deprivation produces widespread cortical reorganization. There is evidence in human MRI literature that plasticity in neural circuits can lead to MRI-detectable anatomical changes. Our lab developed an animal model of unilateral sensory deprivation by cutting the infraorbital nerve (ION - whisker) nerve. Previous fMRI and slice electrophysiology studies detected dramatic changes in both the intact and deprived primary somatosensory barrel cortices (S1BCs). The intact S1BC has increased strength and number of feed-forward synapses arriving from the thalamus to layer 4. The deprived S1BC is recruited to intact whisker stimulation, mediated by the corpus callosum. The goals of this project were 1) to determine if increases in synaptic strength/number were reflected in anatomical changes, and 2) if a behavioral phenotype was associated with unilateral whisker denervation. Manganese-enhanced MRI was used to enhance visualization of layer 4 in mouse S1BC, and the thicknesses of both sides were quantified in vivo. Preliminary data show decreased layer thickness in deprived cortex with decreased thalamic input activity to layer 4 compared to sham animals. Behavioral studies with an open field test and subsequent novel object placement assessed both pain/anxiety associated and exploratory behaviors. ION cut mice spent significantly more time with their whisker cut side against the wall than sham mice, suggesting a guarding behavior for their injured side. Additionally, ION mice inspected a novel object more frequently using nose touches compared to sham mice. Our data demonstrates that layer-specific changes in S1BC may hold clues into the mechanisms underlying sensory deprivation induced plasticity.