Quantitative study of the somatosensory sensitization underlying cross-modal plasticity

Abstract

Loss of one sensory modality can cause other types to become more perceptive (cross-modal plasticity). To test the hypothesis that the loss of vision changes the perceptual threshold in the somatosensory system, we applied optogenetics to directly manipulate the afferent inputs involved in the whisker-barrel system using a transgenic rat (W-TChR2V4) that expresses channelrhodopsin-2 (ChR2) selectively in the large mechanoreceptive neurons in the trigeminal ganglion (TG) and their peripheral nerve terminals. The licking behavior of W-TChR2V4 rat was conditioned to a blue LED light cue on the whisker area while the magnitude and duration of light pulses were varied. The perceptual threshold was thus quantitatively determined for each rat according to the relationship between the magnitude/duration of light and the reaction time between the LED light cue and the first licking event after it. We found that the perceptual threshold was more significantly reduced than the control non-deprived rats when the rats were visually deprived at postnatal 26–30 days (P26-30, early VD group), but not at P58-66 (late VD group). However, the sensory threshold of a late VD animal was similar to that of a control. Our results suggest the presence of cross-modal plasticity by which the loss of vision at the juvenile period increased the sensitivity of the somatosensory system involved in the touch of whiskers.

Optogenetic study of the response interaction among multi-afferent inputs in the barrel cortex of rats

“…As a result, the optogenetic inputs on the whisker area arrived at the somatosensory cortex synchronously within 20 ms from their onset. This optical characterization of the input-response relationship in S1 as a function of time should be robust because using the same rat line, Go-task conditioning was established and recalled by the whisker area irradiation as a function of the power and duration of the light pulse 26,27 . Indeed, the LFP amplitude was robust by the MAI s throughout every mode 1 experiment and specifically distinct from those by the peri- MAI s (Supplementary Fig.…”

The impact of early-life environment on absence epilepsy and neuropsychiatric comorbidities

“…For example, blind individuals compensate the lack of visual inputs by responding to somatosensory or auditory inputs with improved sensitivity. In rats, which were visually deprived at postnatal 4 weeks (PND26-PND30), but not later (PND58-PND66), increased sensitivity of the somatosensory system involved in the whisker-dependent tactile perception was found ( Abe and Yawo, 2018 ). It has been well-documented that the somatosensory cortex plays a crucial role in the pathogenesis of absence seizures in genetic rodent models ( Ding and Gallagher, 2016 , Meeren et al, 2002 , Polack et al, 2007 ).…”

Cross-modal activation of the primary visual cortex by auditory stimulation in RCS rats: considerations in visual prosthesis

“…The lack of neural activity that occurs as a consequence of loss or damage of a sensory input, typically hearing or sight, induces an important neuronal reorganization in the brain [1]. In blindness, auditory [2] and somatosensory [3] modalities acquire importance as a result of adaptation to the lack of visual sensations. The neurons in the occipital cortex, conceived to process visual information, become activated after auditory or tactile stimuli are presented.…”