Abstract

Studies have shown that both serotonin and glutamate receptor systems play a crucial role in the mechanisms underlying drug-induced synesthesia. The specific nature of these mechanisms, however, continues to remain elusive. Here we propose two distinct hypotheses for how synesthesia triggered by hallucinogens in the serotonin-agonist family may occur. One hypothesis is that the drug-induced destabilization of thalamic projections via GABAergic neuronal circuits from sensory areas leads to a disruption of low-level, spontaneous integration of multisensory stimuli. This sort of integration regularly occurs when spatial and temporal attributes match. Destabilization of feedback loops, however, can result in incongruent experiences or binding of random thalamus activation with sensory input in a particular sensory modality. The second hypothesis builds on embodied cognition, cases in which visual images of external stimuli activate task-related neural regions. On this proposal, binding processes that do not normally generate awareness become accessible to consciousness as a result of decreased attentional discrimination among incoming stimuli.