Auditory evoked potentials recorded in monkeys with hallucinatory-like behaviors induced by bromocriptine.

Objective Bromocriptine and other dopamine D2 receptor agonists can affect a range of behaviors in nonhuman primates, particularly those behaviors associated with motor and mental function, such as suppressant behaviors and hallucinatory-like behaviors in monkeys. Besides bromocriptine, the dysfunction of the rapid eye movement sleep (REM) mechanism may also contribute to hallucinations. Dissociation of wakefulness, REM, and non-REM (NREM) can cause a series of psychotic symptoms. Methods We simultaneously recorded auditory evoked potentials (AEP) from five cerebral regions in monkeys during normal and psychotomimetic states to investigate and compare state-dependent changes in AEP. Results Phase reversal of peak-to-baseline amplitude of 250 ms component (PBA250) in dorsolateral prefrontal cortex was common characteristic of hallucinatory-like and REM, and that hallucinatory-like and REM shared the equivalent modulatory orderliness of the PBA250 in dorsolateral prefrontal cortex. This result suggests that hallucinatory-like and REM share an equivalent electrophysiological modulatory in dorsolateral prefrontal cortex. Conclusion These results reveal that emergence of the N250 in dorsolateral prefrontal cortex is an exclusive marker that may help to discern whether hallucinatory-like behaviors is exhibited, which suggests that dorsolateral prefrontal cortex may be the most pivotal region for exhibition of hallucinatory-like behaviors.