Abstract
BackgroundThe ability to communicate anxiety through chemosensory signals has been documented in humans by behavioral, perceptual and brain imaging studies. Here, we investigate in a time-sensitive manner how chemosensory anxiety signals, donated by humans awaiting an academic examination, are processed by the human brain, by analyzing chemosensory event-related potentials (CSERPs, 64-channel recording with current source density analysis).Methodology/Principal FindingsIn the first study cerebral stimulus processing was recorded from 28 non-socially anxious participants and in the second study from 16 socially anxious individuals. Each individual participated in two sessions, smelling sweat samples donated from either female or male donors (88 sessions; balanced session order). Most of the participants of both studies were unable to detect the stimuli olfactorily. In non-socially anxious females, CSERPs demonstrate an increased magnitude of the P3 component in response to chemosensory anxiety signals. The source of this P3 activity was allocated to medial frontal brain areas. In socially anxious females chemosensory anxiety signals require more neuronal resources during early pre-attentive stimulus processing (N1). The neocortical sources of this activity were located within medial and lateral frontal brain areas. In general, the event-related neuronal brain activity in males was much weaker than in females. However, socially anxious males processed chemosensory anxiety signals earlier (N1 latency) than the control stimuli collected during an ergometer training.Conclusions/SignificanceIt is concluded that the processing of chemosensory anxiety signals requires enhanced neuronal energy. Socially anxious individuals show an early processing bias towards social fear signals, resulting in a repression of late attentional stimulus processing.
Highlights
Within all major taxa stress responses to danger are associated with the release of chemical stress signals, which induce physiological stress adaptations within surrounding conspecifics [1,2,3,4,5,6]
Study 1: Non-socially anxious participants The EEG data reveal that the processing of chemosensory anxiety signals engages significantly more neuronal resources than the chemosensory processing of sport sweat
Thereby, the results are in line with recent brain imaging studies [11,12], demonstrating that the processing of chemosensory anxiety or stress signals requires more neuronal resources than the processing of body odor signals sampled in a non-emotional control condition
Summary
Within all major taxa stress responses to danger are associated with the release of chemical stress signals, which induce physiological stress adaptations within surrounding conspecifics [1,2,3,4,5,6]. Chemosensory stress signals of conspecifics augment defensive reflexes (startle) in humans [15,16] and rats [17,18]. The ability to communicate anxiety through chemosensory signals has been documented in humans by behavioral, perceptual and brain imaging studies. We investigate in a time-sensitive manner how chemosensory anxiety signals, donated by humans awaiting an academic examination, are processed by the human brain, by analyzing chemosensory event-related potentials (CSERPs, 64-channel recording with current source density analysis)
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