Auditory aversive generalization learning prompts threat-specific changes in alpha-band activity.

Pairing a neutral stimulus with aversive outcomes prompts neurophysiological and autonomic changes in response to the conditioned stimulus (CS+), compared to cues that signal safety (CS-). One of these changes-selective amplitude reduction of parietal alpha-band oscillations-has been reliably linked to processing of visual CS+. It is, however, unclear to what extent auditory conditioned cues prompt similar changes, how these changes evolve as learning progresses, and how alpha reduction in the auditory domain generalizes to similar stimuli. To address these questions, 55 participants listened to three sine wave tones, with either the highest or lowest pitch (CS+) being associated with a noxious white noise burst. A threat-specific (CS+) reduction in occipital-parietal alpha-band power was observed similar to changes expected for visual stimuli. No evidence for aversive generalization to the tone most similar to the CS+ was observed in terms of alpha-band power changes, aversiveness ratings, or pupil dilation. By-trial analyses found that selective alpha-band changes continued to increase as aversive conditioning continued, beyond when participants reported awareness of the contingencies. The results support a theoretical model in which selective alpha power represents a cross-modal index of continuous aversive learning, accompanied by sustained sensory discrimination of conditioned threat from safety cues.

The Relationship Between Self-Reported Misophonia Symptoms and Auditory Aversive Generalization Leaning: A Preliminary Report.

Misophonia is characterized by excessive aversive reactions to specific "trigger" sounds. Although this disorder is increasingly recognized in the literature, its etiological mechanisms and maintaining factors are currently unclear. Several etiological models propose a role of Pavlovian conditioning, an associative learning process heavily researched in similar fear and anxiety-related disorders. In addition, generalization of learned associations has been noted as a potential causal or contributory factor. Building upon this framework, we hypothesized that Misophonia symptoms arise as a consequence of overgeneralized associative learning, in which aversive responses to a noxious event also occur in response to similar events. Alternatively, heightened discrimination between conditioned threat and safety cues may be present in participants high in Misophonia symptoms, as predicted by associative learning models of Misophonia. This preliminary report (n = 34) examines auditory generalization learning using self-reported behavioral (i.e., valence and arousal ratings) and EEG alpha power reduction. Participants listened to three sine tones differing in pitch, with one pitch (i.e., CS+) paired with an aversive loud white noise blast, prompting aversive Pavlovian generalization learning. We assessed the extent to which overgeneralization versus heightened discrimination learning is associated with self-reported Misophonia symptoms, by comparing aversive responses to the CS+ and other tones similar in pitch. Behaviorally, all participants learned the contingencies between CS+ and noxious noise, with individuals endorsing elevated Misophonia showing heightened aversive sensitivity to all stimuli, regardless of conditioning and independent of hyperacusis status. Across participants, parieto-occipital EEG alpha-band power reduction was most pronounced in response to the CS+ tone, and this difference was greater in those with self-reported Misophonia symptoms. The current preliminary findings do not support the notion that overgeneralization is a feature of self-reported emotional experience in Misophonia, but that heightened sensitivity and discrimination learning may be present at the neural level.

Open science in psychophysiology: An overview of challenges and emerging solutions.

The present review is the result of a one-day workshop on open science, held at the Annual Meeting of the Society for Psychophysiological Research in Washington, DC, September 2019. The contributors represent psychophysiological researchers at different career stages and from a wide spectrum of institutions. The state of open science in psychophysiology is discussed from different perspectives, highlighting key challenges, potential benefits, and emerging solutions that are intended to facilitate open science practices. Three domains are emphasized: data sharing, preregistration, and multi-site studies. In the context of these broader domains, we present potential implementations of specific open science procedures such as data format harmonization, power analysis, data, presentation code and analysis pipeline sharing, suitable for psychophysiological research. Practical steps are discussed that may be taken to facilitate the adoption of open science practices in psychophysiology. These steps include (1) promoting broad and accessible training in the skills needed to implement open science practices, such as collaborative research and computational reproducibility initiatives, (2) establishing mechanisms that provide practical assistance in sharing of processing pipelines, presentation code, and data in an efficient way, and (3) improving the incentive structure for open science approaches. Throughout the manuscript, we provide references and links to available resources for those interested in adopting open science practices in their research.

Altered sulcogyral patterns of orbitofrontal cortex in a large cohort of patients with schizophrenia.

Abnormalities in prenatal brain development contribute to schizophrenia vulnerability. Orbitofrontal cortex sulcogyral patterns are largely determined during prenatal development, and four types of orbitofrontal cortex sulcogyral patterns have been classified in humans. Altered orbitofrontal cortex patterns have been reported in individuals with schizophrenia using magnetic resonance imaging; however, sample sizes of previous studies were small-medium effects for detection, and gender manifestation for orbitofrontal cortex sulcogyral patterns is unclear. The present study investigated orbitofrontal cortex patterns of 155 patients with schizophrenia and 375 healthy subjects. The orbitofrontal cortex sulcogyral pattern distributions of schizophrenia were significantly different compared with healthy subjects in the left hemisphere (χ2 = 14.55, p = 0.002). In female schizophrenia, post-hoc analyses revealed significantly decreased Type I expression (χ2 = 6.76, p = 0.009) and increased Type II expression (χ2 = 11.56, p = 0.001) in the left hemisphere. The present study suggested that female schizophrenia showed altered orbitofrontal cortex patterns in the left hemisphere, which may be related to neurodevelopmental abnormality.

Electrophysiological assessment of auditory stimulus-specific plasticity in schizophrenia.

BACKGROUND: Disrupted neuroplasticity may be an important aspect of the neural basis of schizophrenia. We used event-related brain potentials (ERPs) to assay neuroplasticity after auditory conditioning in chronic schizophrenia patients (SZ) and matched healthy control subjects (HC). METHODS: Subjects (15 HC, 14 SZ) performed an auditory oddball task during electroencephalogram recording before and after auditory tetanic stimulation (Pre/Post Blocks). Each oddball block consisted of 1000-Hz and 1500-Hz standards and 400-Hz targets. During tetanic conditioning, 1000-Hz tones were presented at 11 Hz for 2.4 min. We analyzed the standard trials, comparing the ERPs evoked by the tetanized stimuli (1000 Hz tones: TS+) and untetanized stimuli (1500 Hz tones: TS-) in the Post Blocks with ERPs from the Pre Blocks (averaged into Baseline ERPs). RESULTS: In Post Block 1 in HC, TS+ tones evoked a negative shift (60-350 msec) at right temporal electrodes relative to Baseline. No pre-/post-tetanus effects were found in SZ. In Post Block 2 in HC, TS+ tones evoked a positive shift (200-300 msec) at bilateral frontal electrodes. In SZ, TS+ tones evoked a positive shift (100-400 msec) at right frontotemporal electrodes. No pre-/post-tetanus effects were found in either subject group for the TS- tones. The right temporal Post Block 1 and 2 effects were correlated in SZ, suggesting a trade-off in the expression of these effects. CONCLUSIONS: These results suggest that stimulus-specific auditory neuroplasticity is abnormal in schizophrenia. The electrophysiologic assessment of stimulus-specific plasticity may yield novel targets for drug treatment in schizophrenia.

Reduction of prelimbic inhibitory gating of auditory evoked potentials after fear conditioning.

Inhibitory gating (IG) is a basic central nervous system process for filtering repetitive sensory information. Although IG deficits coincide with cognitive and emotional dysfunction in a variety of neuropsychiatric disorders, limited research has been completed on the basic, functional nature of IG. Persistent IG occurs in rat prelimbic medial prefrontal cortex (mPFC), a crucial site for modulating emotional learning. To investigate the interaction of affect and IG, we recorded local field potentials (LFP) directly from prelimbic mPFC and examined the influence of tone-shock fear conditioning (FC) on IG. Behavioral reactions during IG were observed before and after FC, and increase of orienting response after FC indicated induction of tone-shock association. After FC, some components of LFP response exhibited short-term weakening of IG. On a subsequent day of recording, IG strengthened for all LFP components, but individual components differed in their particular changes. Affective regulation of IG represents an important factor influencing within-subject IG variability, and these results have implications for understanding the role of rapid, implicit neural coding involved in emotional learning and affective disruption in psychiatric disease.

Sensory gating: a translational effort from basic to clinical science.

Sensory gating (SG) is a prevalent physiological process important for information filtering in complex systems. SG is evaluated by presenting repetitious stimuli and measuring the degree of neural inhibition that occurs. SG has been found to be impaired in several psychiatric disorders. Recent animal and human research has made great progress in the study of SG, and in this review we provide an overview of recent research on SG using different methods. Animal research has uncovered findings that suggest (1) SG is displayed by single neurons and can be similar to SG observed from scalp recordings in humans, (2) SG is found in numerous brain structures located in sensory, motor and limbic subregions, (3) SG can be significantly influenced by state changes of the organism, and (4) SG has a diverse pharmacological profile accented by a strong influence from nicotine receptor activation. Human research has addressed similar issues using deep electrode recordings of brain structures. These experiments have revealed that (1) SG can be found in cortical regions surrounding hippocampus, (2) the order of neural processing places hippocampal involvement during a later stage of sensory processing than originally thought, and (3) multiple subtypes of gating exist that could be dependent on different brain circuits and more or less influenced by alterations in organismal state. Animal and human research both have limitations. We emphasize the need for integrative approaches to understand the process and combine information between basic and clinical fields so that a more complete picture of SG will emerge.