Abstract
The neurochemical mechanisms that contribute to synaesthesia are poorly understood, but multiple models implicate serotonin and GABA in the development of this condition. Here we used psychophysical tasks to test the predictions that synaesthetes would display behavioral performance consistent with reduced GABA and elevated serotonin in primary visual cortex. Controls and synaesthetes completed the orientation-specific surround suppression (OSSS) and tilt-after effect (TAE) tasks, previously shown to relate to GABA and serotonin levels, respectively. Controls and synaesthetes did not differ in the performance parameter previously associated with GABA or in the magnitude of the TAE. However, synaesthetes did display lower contrast difference thresholds in the OSSS task than controls when no surround (NS) was present. These results are inconsistent with the hypothesized roles of GABA and serotonin in this condition, but provide preliminary evidence that synaesthetes exhibit enhanced contrast discrimination.
Highlights
Grapheme-color synaesthesia is an unusual neurological condition in which letters and numerals reliably elicit involuntary color experiences
It has been argued that disinhibition theories of synaesthesia (Grossenbacher and Lovelace, 2001; Cohen Kadosh and Henik, 2007), which propose that synaesthesia arises from disinhibited feedback from higher cortical areas, predict that synaesthesia is characterized by reduced GABA concentrations in synaesthesia-relevant regions (Hubbard et al, 2011; Specht, 2012)
Elsewhere we have argued that cortical hyperexcitability in primary visual cortex in synaesthetes does not play a causal role in the online experience of synaesthesia; rather, it may have only contributed to the expression of synaesthesia at an early developmental stage (Terhune et al, 2011)
Summary
Grapheme-color synaesthesia is an unusual neurological condition in which letters and numerals reliably elicit involuntary color experiences (for a review, see Ward, 2013). Γ-aminobutyric acid (GABA) and serotonin (5-HT), have been proposed to contribute to synaesthesia by different models (Grossenbacher and Lovelace, 2001; Cohen Kadosh and Henik, 2007; Brang and Ramachandran, 2008; Brogaard, 2013). Both play fundamental, but differential, roles in visual processing and are strong candidates for exploring the neurochemistry of synaesthesia. A number of studies have provided direct or indirect evidence in support of disinhibition models (e.g., Cohen Kadosh et al, 2009; Terhune et al, 2011), but none have directly evaluated the prediction of reduced GABA in the synaesthetic brain
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