Inhibition in the Human Auditory Cortex

• Published in: PloS one Vol. 11; no. 5; p. e0155972
• Main Authors: Inui, Koji, Nakagawa, Kei, Nishihara, Makoto, Motomura, Eishi, Kakigi, Ryusuke
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 24.05.2016; Public Library of Science (PLoS)
• Subjects: Acoustic Stimulation; Adult; Auditory cortex; Auditory Cortex - physiology; Biology and Life Sciences; Cortex (auditory); Cortex (somatosensory); Evoked Potentials, Auditory; Female; Firing pattern; Genetic aspects; Humans; Information processing; Inhibition; Inhibitory Postsynaptic Potentials; Interneurons; Interneurons - physiology; Magnetoencephalography; Magnetoencephalography - methods; Male; Medicine and Health Sciences; Mental disorders; Parvalbumin; Physical Sciences; Physiological aspects; Physiology; Prepulse Inhibition; Research and Analysis Methods; Rodents; Schizophrenia; Sensory integration; Sensory receptors; Somatostatin; Sound pressure; Japan
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0155972

Despite their indispensable roles in sensory processing, little is known about inhibitory interneurons in humans. Inhibitory postsynaptic potentials cannot be recorded non-invasively, at least in a pure form, in humans. We herein sought to clarify whether prepulse inhibition (PPI) in the auditory cortex reflected inhibition via interneurons using magnetoencephalography. An abrupt increase in sound pressure by 10 dB in a continuous sound was used to evoke the test response, and PPI was observed by inserting a weak (5 dB increase for 1 ms) prepulse. The time course of the inhibition evaluated by prepulses presented at 10-800 ms before the test stimulus showed at least two temporally distinct inhibitions peaking at approximately 20-60 and 600 ms that presumably reflected IPSPs by fast spiking, parvalbumin-positive cells and somatostatin-positive, Martinotti cells, respectively. In another experiment, we confirmed that the degree of the inhibition depended on the strength of the prepulse, but not on the amplitude of the prepulse-evoked cortical response, indicating that the prepulse-evoked excitatory response and prepulse-evoked inhibition reflected activation in two different pathways. Although many diseases such as schizophrenia may involve deficits in the inhibitory system, we do not have appropriate methods to evaluate them; therefore, the easy and non-invasive method described herein may be clinically useful.