Aims/Background:
Inhibition deficits are consistently shown in a broad spectrum of neuropsychiatric conditions, such as schizophrenia, implicating altered dopamine neurotransmission. This results in impaired ‘sensorimotor gating’, a physiological measure of inhibitory brain processes. We investigated the neural networks underlying sensorimotor gating.
Methods:
Sensorimotor gating was measured using prepulse inhibition (PPI) of the acoustic startle eye-blink response through bipolar EMG from the left orbicularis oculi muscle and functional magnetic resonance imaging (fMRI). fMRI images were acquired using sparse temporal sampling techniques to minimize stray masking noise interfering with the auditory processing. Trial types: (A) startle probes alone (baseline), (B/C) startle probes preceded by a prepulse at 120 or 480 ms and (D) ‘scanner-noise only’. Significant BOLD contrasts were assessed using one-sample t-tests [P > 0.001 (uncorrected) and exploratory data analyses at P > 0.01].
Results:
Data from 16 healthy volunteers (9 men:7 women, age: 23 ± 4 years) were included. Cortical peak BOLD activation was confirmed for the superior temporal (STG), inferior frontal (IFG), precentral gyri and quadrangularis lobule for the baseline vs. scanner-noise only. No changes were detected for the STG and IFG in baseline vs. 120 or 480 ms prepulse condition, whereas increased right IFG activation was confirmed for the short vs. long lead interval contrast. Explorative analyses suggested concurrent decrease of activation in the right anterior STG in the 120 vs. 480 ms condition. When correlating the electromyographically recorded PPI effect with hemodynamic responses, the activation was mediated by thalamic activation (bilateral).
Conclusions:
Thalamic activation mediates auditory PPI. The potential relationship with impaired sensorimotor gating in clinical populations remains to be investigated.
