The study of synesthesia has grown exponentially over the past few decades and as a result there is some level of ambiguity as to the scope of what defines it. Gail Martino and Lawrence Mark propose that synesthesia can be categorized into strong or weak. The former refers to those who experience “a vivid image in one sensory in response to stimulation in another”, whereas the latter is characterized as “cross-sensory correspondence[s] expressed through language, perceptual similarity and perceptual interactions during information processing” (Martino and Marks, 2001). This view implies that even the subtlest forms of cross-modal interactions that take place in the individual, albeit associating certain sounds to sight, deserve some credibility as being a form of synesthesia. Such a wide scope implies that far more people can experience some type of synesthesia even if its not necessarily the more exaggerated and rare forms like lexical-gustatory and grapheme color.
These rare forms of synesthesia, typically referred to as developmental, tend to persist “since birth or early childhood and remain relatively stable and systematic over time” (Brogaard 2013). However, recent evidence suggests that synesthesia is not solely developmental in the alleged “4% of the general population” (Brang and Ramachandran 2007). For the purpose of this paper I will look at studies in which serotonin appears to play a key role across not only developmental synesthesia, but also drug-induced and acquired, suggesting that there are underlying mechanisms which make synesthesia readily accessible to more people than what was once believed.
Brang and his colleague Ramachandran propose that “serotonin S2a receptors are the ‘synesthesia receptors’ in the brain,” supported by their observations that activating and inhibiting the S2a receptors resulted in activation of synesthesia or lack there of (p. 903). One piece of evidence they use to support their hypothesis is that “LSD produces synesthesia,” and in the process activates S2a receptors. Furthermore, Prozac caused hyperactivation in the S1 receptors of two subjects, which caused inhibition of both S2a receptors and consequently their synesthesia. Conversely, the administration of melatonin allowed for a subject to experience grapheme-color synesthesia, in which S1 activation was lowered allowing for the “dis-inhibit[ion] of S2a receptors leading to synesthesia” (p. 903). These conclusions thus support the notion that the uptake of serotonin in the S2a receptors has some correlation to synesthetic experience, yet it is unclear which S2a receptors were specifically looked at.
Berit Brogaard recently conducted a study that looked at Brang and Ramachandran’s serotonin hypothesis across drug-induced and acquired forms of synesthesia. Brogaard states that “it has been shown in several studies...