Is inhibitory brain circuitry involved in cross-modal sensory perception? In many research articles, a vague description of a inhibitory circuitry in the brain is mentioned. This is presented as an inhibitory mechanism that prevents input from one sensory modality to excite another region (for example touch exciting visual cortex) or in general prevents any signal not coming from the visual nerve to excite the visual cortex. And that preventing test subjects from their sight (blindfolding for a longer period) interferes with those inhibitory circuits and deactivates them. The results are presented here where subjects started having hallucinations and perceiving things even though totally blindfolded. I am interested to know if there is some active research about those inhibitory circuits in the brain and if they are well understood. 

I am trying to find out if normally sighted or normally hearing people could get visual/auditory information from both the original sense and through the skin via an electrotactile pattern through a sensory substitution device, to see if passive learning can be achieved.
As far as I know, there is just one article that explicitly mentions the generation of cross-modal qualia, i.e., visual qualia in response to tactile stimulation (Ortiz et al., 2011). Before continuing about this article I do wish to emphasize it is a single, isolated study that hasn't been supported by other studies at the time of this writing. Moreover, the journal PlosONE is not my favorite and a bit of a strange journal to throw such an important observation in. I would have trusted this work more if published into a more appropriate journal for such strong claims, such as J Neurosci. Having said that:

The authors trained 18 blind subjects and 10 sighted, blindfolded controls for 3 months, on a daily basis using a tactile vision-substitution device; a vibrotactile display equipped with a camera. They deployed a grating acuity task and 7 out of 18 subjects reported 'seeing' visual qualia after 3 months, i.e., these subjects started seeing the gratings instead of feeling them. It was only blind folks that reported this, not any of the sighted controls. Those blind folks reporting qualia showed increased activation of the primary visual cortex upon using the tactile device. The authors conclude that recruitment of the deafferented V1 in blind people led them to 'see' the tactile stimuli after sufficient training (Ortiz et al., 2011).

You are right that it is believed that a disintegration of inhibitory circuits in the cortex is believed to underlie crossmodal cortical recruitment of (e.g.) the visual cortex to tactile stimulation (Stronks et al., 2015). Chronic visual deprivation is believed to reduce the inhibitory circuits, while visual stimulation is believed to enhance them. For example, tetanic stimulation of inhibitory neurons (presumably through GABAA) resulted in more long-term potentiation of inhibitory responses in young rats than in adult rats (Komatsu, 1994). This is in line with the theory that shaping of the brain is critically dependent on sensory input in early life, i.e., inhibitory circuits are thought to be actively developed through experience, resulting in containment of visual processing in the visual cortices and tactile processing in the somatosensory cortex etc. Note, however, that even V1 has shown to be multimodal even in normally sighted folks, i.e., while V1 is dedicated to visual processing, it is not exclusively devoted to it. One theory about synesthesia is that the development of inhibitory circuits is compromised, leading to crossmodal activation in folks without any sensory disability. This theory has made people conclude that babies are all synesthetes (e.g., Wagner &amp; Dobkins, 2009).         

References
- Komatsu, J Neurosci (1994); 14(11): 6489-99
- Ortiz et al., PlosONE (2011); 6(8): e23264
- Stronks et al., Brain Res (2015); 1624: 140–52)
- Wagner &amp; Dobkins, JOV (2009); 9: 699