CORTICAL CORRELATES OF AUDITORY SENSORY GATING: A SIMULTANEOUS NEAR-INFRARED SPECTROSCOPY EVENT-RELATED POTENTIAL STUDY A.-C. EHLIS,* T. M. RINGEL, M. M. PLICHTA, M. M. RICHTER, M. J. HERRMANN AND A. J. FALLGATTER Laboratory for Psychophysiology and Functional Imaging, Department of Psychiatry, Psychosomatics, and Psychotherapy, University of Wuerzburg, Fuechsleinstraße 15, 97080 Wuerzburg, Germany Abstract—Sensory gating refers to the ability of cerebral networks to inhibit responding to irrelevant environmental stimuli, a mechanism that protects the brain from information overflow. The reduction of the P50 amplitude (an early com- ponent of the event-related potential/ERP in electrophysio- logical recordings) after repeated occurrence of a particular acoustic stimulus is one means to quantitatively assess gat- ing mechanisms. Even though P50 suppression has been extensively investigated, neuroimaging studies on the corti- cal correlates of auditory sensory gating are so far very sparse. Near-infrared spectroscopy (NIRS) is an optical im- aging technique perfectly suitable for the investigation of auditory paradigms, since it involves virtually no noise. We conducted a simultaneous NIRS-ERP measurement to as- sess cortical correlates of auditory sensory gating in hu- mans. The multi-channel NIRS recording indicated a specific activation of prefrontal and temporo-parietal cortices during conditions of increased sensory gating (dual-click trials). Combining the hemodynamic data with an electrophysiolog- ical index of the “gating quality” (gating quotient Q) revealed a positive correlation between the amount of sensory gating and the strength of the hemodynamic response during dual- clicks in the left prefrontal and temporal cortices. The results are in line with previous findings and confirm a possible inhibitory influence of the prefrontal cortex on primary audi- tory cortices. © 2009 IBRO. Published by Elsevier Ltd. All rights reserved. Key words: prefrontal cortex, P50, optical topography. Sensory gating refers to the ability of cerebral networks to transmit only part of the incoming information and filter out irrelevant stimuli (Freedman et al., 1991), a mechanism that protects the human brain from information overflow. If sensory gating is pathologically reduced, disturbances of signal perception and signal processing may result (Freed- man et al., 1987), which has been discussed in the context of schizophrenic illnesses, for example. A well-established possible method of detecting gating mechanisms electro- physiologically is the dual-click P50 paradigm (Adler et al., 1982). Briefly, a first conditioning stimulus (S1) activates inhibitory systems that reduce the response to the second (identical) test stimulus (S2), which is presented very shortly after the first one. The magnitude of the brain’s response to these acoustic stimuli is quantified by the P50 event-related potential (ERP) that usually peaks about 50 ms after presentation of the stimuli. An insufficient reduc- tion of the P50 amplitude after the second as compared to the first stimulus indicates a deficient sensory gating mech- anism. The ratio Q of the mean test/conditioning response amplitudes (Q=A(S2)/A(S1)) has been defined as a mea- sure of sensory gating, with smaller quotients indicating more effective gating mechanisms. While healthy subjects usually show a highly significant suppression of the P50 response to the second stimulus, some clinical groups, and particularly schizophrenic pa- tients, have been shown to have a significantly increased gating quotient Q (e.g. Adler et al., 1982; Nagamoto et al., 1989; Freedman et al., 1996; Thoma et al., 2003; Ringel et al., 2004) indicating deficient sensory gating mechanisms. The underlying brain mechanisms that account for impair- ments in sensory gating are largely unknown, mostly be- cause the exact neural substrates of the P50 wave and their modulation have yet to be elucidated. Detailed knowl- edge of the neuroanatomical correlates of auditory sensory gating would be a precondition for an appropriate under- standing of the functional relevance of the dual-click P50 paradigm and of differences in gating mechanisms be- tween different groups of patients and healthy subjects. Studies that have investigated this issue so far have mainly been conducted with magnetoencephalography (MEG)/electroencephalography (EEG) source localiza- tions and intracranial EEG recordings in epilepsy patients. These studies repeatedly localized the P50 (or the MEG equivalent M50) within the superior temporal gyrus (pri- mary auditory cortex/Heschl’s gyrus; Godey et al., 2001; Edgar et al., 2003; Thoma et al., 2003) with an additional modulation of the P50 response after repeated stimulation in the temporo-parietal and prefrontal brain areas (Grun- wald et al., 2003). Weisser et al. (2001) similarly localized the P50 within the auditory cortex and found an additional mid-frontal source. Though informative, these studies pro- vide information about the neuroanatomical generator(s) of the P50 ERP, but not necessarily about the neural struc- tures involved in the gating mechanism that accounts for the modulation of the P50 component. Observations that might allow more direct conclusions to be made about *Corresponding author. Tel: +49-931-201-77410; fax: +49-931-201- 77550. E-mail address: Ehlis_A@klinik.uni-wuerzburg.de (A.-C. Ehlis). Abbreviations: BOLD, blood oxygenation level-dependent; DLPFC, dorsolateral prefrontal cortex; EEG, electroencephalography; ERP, event-related potential; fMRI, functional magnetic resonance imaging; HHb, deoxygenated hemoglobin; MEG, magnetoencephalography; MRI, magnetic resonance imaging; NIRS, near-infrared spectroscopy; O 2 Hb, oxygenated hemoglobin. Neuroscience 159 (2009) 1032–1043 0306-4522/09 © 2009 IBRO. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.neuroscience.2009.01.015 1032