Subjects: Psychology >> Developmental Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： The human parental brain could be defined as is the network of regions that support caregiving behaviors to identify and react to infant related stimuli (infant vocals and facial expressions). First, we reviewed the neural circuits that were demonstrated to be involved in establishing and maintaining parent-infant relationships, which included circuits for motivation-reward, empathy, emotion regulation and executive function. And the important brain areas incorporate the orbitofrontal cortex, anterior cingulate cortex, anterior insula, amygdala, and supplementary motor area. Second, the current review summed that human parental brain is sensitive to multiple parenting determinants, including parenting abilities, parental hormones and psychopathology. The growth of parenting abilities and the improvement of oxytocin levels are beneficial to the processing for infant stimuli. Finally, several advices were proposed for future directions: 1) prospective and longitudinal studies across important transition periods for parenting; 2) describing the neural basis of male psychopathologies and exploring targeted interventions and treatments; 3) employing some advanced neuroscience technique (e.g., hyper scanning) to highlight the simultaneous neural activity between mother and father or parents and infants; and 4) conducting parental brain research in Chinese culture.
Subjects: Psychology >> Developmental Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： The integration of various emotional information from different modalities (e.g., face and voice) plays an important role in our interpersonal communication. In order to understand its brain mechanism, more and more researchers found that the interaction between facial expression and vocal emotional information begins in the early stage of perception, and the integration of emotional information content occurs in the late decision-making stage. In the early stage, the primary sensory cortex is responsible for encoding information; while in the late stage, the amygdala, temporal lobe and other advanced brain regions are responsible for cognitive evaluation. In addition, the functional coupling of oscillation activities on multiple frequency bands facilitates the integration of emotional information cross channels. Future research needs to explore whether facial expression and vocal emotional information integration is associated with emotional conflict, and whether inconsistent emotional information has advantages. Lastly, we should find out how the neural oscillations of different frequency bands promotes the integration of facial expression and vocal emotional information, so as to further understand its dynamic basis.
Subjects: Psychology >> Developmental Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： Facial trustworthiness plays a key role in how we express and understand social signals. During social interactions, people quickly judge the trustworthiness of others through subtle facial cues in order to make choices in daily life. The researchers delved into behavioral and ERP studies related to the time course of facial trustworthiness processing, and explored the life-span development of facial trustworthiness, as well as the influence of face emotions and face gender on the evaluation of facial trustworthiness. Further research is needed to improve the ecological validity of stimuli used in facial trustworthiness studies, to expand the study of facial trustworthiness in adolescents and aging population, and to consider the contextual effects on facial trustworthiness assessment.
Subjects: Psychology >> Social Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： Sleep problems may induce fear-related mood disorders such as anxiety, post-traumatic stress disorder (PTSD), and phobias, among others. Studying the cognitive cognitive and neural mechanisms involved in the relationship between sleep problems and fear learning can help enhance the prediction, diagnosis, and treatment of fear-related mood disorders. Previous studies have shown that sleep deprivation affects fear acquisition mainly by inhibiting the activity of the ventral medial prefrontal cortex (vmPFC) and blocking its functional connections with the amygdala, resulting in impaired safe learning that fails to inhibit fear of threatening stimuli, thus enhancing fear acquisition. In contrast, sleep deprivation during the fear memory consolidation phase impairs the activity of the amygdala and hippocampus, thereby impairing fear memory. On the other hand, sleep deprivation during the extinction learning phase results in delayed activation of brain regions associated with extinction learning, which in turn impairs fear extinction memory. Further studies have reported that different stages of sleep have distinct effects on brain regions associated with fear learning; in particular, rapid eye movement (REM) sleep deprivation (insufficient) and complete sleep deprivation have similar effects on the cognitive and neural mechanisms of fear learning. Deprivation of REM sleep suppresses vmPFC activity, enhances amygdala activation, and thus enhances fear acquisition. In addition, reduced functional connectivity in the limbic cortex disrupts fear memory consolidation. Deprivation of REM sleep after extinction learning phase increases amygdala, insula, and dorsal anterior cingulate cortex (dACC) activity and diminishes mPFC, thereby impairing extinction memory. Therefore, after clinical treatment, quality of sleep, particularly REM sleep, should be ensured at night. In addition to reinforcing recently acquired memories, REM sleep is involved in integrating new information into existing knowledge structures, reorganizing these structures, and generalizing recently acquired memories; therefore, improving REM sleep can promote fading retention and generalization. In contrast, the slow-wave sleep (SWS) stage facilitates fear extinction learning through target memory reactivation, which allows the hippocampus to re-code threatening stimuli and accelerate the consolidation of new safety information in the amygdala. During the SWS stage, participants are not conscious and therefore do not have to directly face the threatening stimulus, thus avoiding some of the drawbacks of traditional extinction therapy applied during wakefulness for patients with fear-related mood disorders, such as anxiety disorders and (PTSD). Clinically relevant studies have found that individuals with insomnia also exhibit delayed activation of the fear extinction brain regions, with related activation occurring only during extinction recall. At the same time, individuals with insomnia have stronger learned fear which causes their insomnia and can easily develop into pathological anxiety or PTSD. Furthermore, sleep immediately following exposure therapy can optimize the therapeutic effect and may even promote extinction generalization; therefore, sleep should be used in combination with traditional exposure therapy. Future research should be conducted to further the study of the neural mechanisms by which sleep affects fear generalization and the effect of circadian rhythm disruption on fear extinction, as well as clarifying the problems in the translation of animal sleep studies to human sleep studies.
Subjects: Psychology >> Social Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： Pain and reward are two basic motivational factors that regulate human perception and behavior, and can provide individuals with different behavioral motivations and subjective value experiences. Both pain avoidance sand reward seeking are essential for survival. Pain can be categorized into acute and chronic pain, and reward can be differentiated into a motivational component in the anticipatory phase and a hedonic component in the experiential phase. Acute pain increases the motivational component of reward and increases or decreases the hedonic component of reward, whereas chronic pain decreases the motivational component of reward and, and generally, decreases the hedonic component of reward.The neural mechanisms by which pain affects reward are mainly related to changes in the dopamine and opioid systems and neural activity in the medial prefrontal cortex(mPFC). Acute pain affects reward processing through neural mechanisms related to increased dopamine release, functional changes in the opioid system, and modulation of the mPFC. On the other hand, chronic pain leads to abnormal changes in the dopamine system, opioid system, and functional connectivity of the mPFC -voxel nucleus in the reward circuit, and reduces activation of brain regions associated with reward processing. These changes in neural mechanisms suggest that adaptive changes in reward circuits based on pain experience can predict the chronicity of pain. Further analysis revealed that the different effects of acute and chronic pain on reward processing are due to the following four factors: First, different symptom expressions in acute and chronic pain; second, different activities of the dopamine and opioid systems in acute and chronic pain; third, different mechanisms of neural activity in the neural in acute and chronic pain; and fourth, different mechanisms of reward processing in acute and chronic pain caused. In acute pain conditions, activation of brain regions that overlap with reward circuits is enhanced, thereby enhancing the motivational and hedonic components of reward processing; in chronic pain conditions, activation of these brain regions is abnormal, reducing the motivational and hedonic components of reward processing. Owing to the inconsistencies between current findings and previous studies, many issues should be addressed and resolved in the future: First, the issue of reproducibility of studies and comparability of results must/should be addressed by standardizing the relevant experimental operations and using uniform experimental paradigms and measures. Second, the immediate neural activity changes in the neural corresponding with the effects of acute pain and chronic pain on reward processing can be further explored. Next, the differences between acute pain and chronic pain can be examined, and based on these differences, the question of whether different types of chronic pain have different effects on reward processing and different changes in reward processing circuits can be investigated, the effects of different types of chronic pain on reward processing neural circuits can be measured separately, and the transition from acute pain to chronic pain can be prevented. Finally, the effects of different types of chronic pain on reward processing can be explored based on the co-morbidity of chronic pain and mood disorders, and further, the effects of different types of chronic pain on reward processing can be explored. Based on this, the relationship between different degrees of deficits, different types of chronic pain, and mood disorders should be clarified.
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