Mice use their whiskers to explore their surrounding world. Whisker tactile information is conveyed from the trigeminal nerve to the brainstem, then to the thalamus, and then to the primary somatosensory cortex (S1). In S1, each whisker is represented in anatomically defined units in layer 4, the “barrels”. Owing to this one-to-one representation, this area of S1, also called barrel cortex (BC), is an excellent model for studying information processing in the brain. Sensory information in the BC is shaped by long-range inputs from higher order areas such as the posteriomedial thalamic nucleus (POm), as well as by inputs from other cortical areas, such as the contralateral S1 (cS1). Though there have been several studies looking at the different cell types and pathways involved in the processing of somatosensory information coming from long-rage projections, the role of these long-range projections in sensory perception is not clearly known. Previous studies have shown that the cS1 sends projections that inhibit the activity of PNs in the BC by recruiting interneurons (INs) in the superficial layers which then further inhibit the PNs. The effect of this inter-hemispheric inhibition through the transcallosal pathway on the sensory perception of mice is not yet fully known. We aimed to answer this question in our study by employing a perceptual detection task where the principal whisker of a mouse (C2) was deflected using a metallic bar attached to the whisker and an electromagnet placed below the head-restricted mouse. The mouse had to then report the perception of this whisker deflection stimulus by licking a lick-port. By varying the intensities of the whisker deflection stimulus, we could then plot the detection probabilities for each intensity against each intensity presented and calculate the perceptual threshold of that session. By introducing an ipsilateral whisker deflection as a manipulation to study the interhemispheric inhibition at alternate trials, we were able to compare the perceptual threshold of the mice for both the ipsilateral whisker deflection condition and the control condition. With this, we saw a significant decrease in sensory perception with the ipsilateral whisker deflection as compared to control trials. Work from our lab and other studies probing further into the cell types involved have shown that neurogliaform cells (NGCs) receive excitatory inputs from the cS1 and are mainly involved in this transcallosal pathway. Hence, to further study the cellular component of interhemispheric inhibition, we chose to directly activate these NGCs using optogenetic tools and observe the effect this has on the sensory perception of mice. This showed that there is a significant decrease in sensory perception for the trials where NGCs were directly stimulated, similar to the result of the ipsilateral whisker stimuli. Looking at the other pathway of focus in this project, previous work in our lab on the paralemniscal pathway has shown that the POm provides synaptic input to pyramidal neurons (PN) as well as vasoactive intestinal peptide (VIP) interneurons, which inhibit parvalbumin (PV) and somatostatin (SST) interneurons. The latter is a mechanism for disinhibition of PNs (Fig. 2). It was also shown previously that rhythmic whisker stimulation (RWS) of the mouse’s principal whisker at a high frequency led to the activation of the POm and leads to a higher response of the PNs to the same stimulus intensity.