Atypical child-parent neural synchrony is linked to negative family emotional climate and children's psychopathological symptoms.

[Correction Notice: An Erratum for this article was reported in Vol 79(2) of American Psychologist (see record 2024-62662-005). In the article "Atypical Child-Parent Neural Synchrony Is Linked to Negative Family Emotional Climate and Children's Psychopathological Symptoms," by Haowen Su, Christina B. Young, Zhuo Rachel Han, Jianjie Xu, Bingsen Xiong, Zisen Zhou, Jingyi Wang, Lei Hao, Zhi Yang, Gang Chen, and Shaozheng Qin (American Psychologist, 2024, Vol. 79, No. 2, pp. 210-224, https://doi.org/10.1037/amp0001173), Figure 2 and its caption were corrected to fix a mismatch between the r coefficients and scatterplots. The caption was changed from "(c) Child-parent hippocampal activity concordance was significantly higher for boundary than nonboundary event time series (Z = 2.30, p = .01). (d) Child-parent vmPFC activity concordance was marginally significantly higher for boundary than nonboundary time series (Z = -1.39, p = .08)" to "(c) Child-parent vmPFC activity concordance was marginally significantly lower for boundary than nonboundary time series (Z = -1.39, p = .08). (d) Child- parent hippocampal activity concordance was significantly higher for boundary than nonboundary event time series (Z = 2.30, p = .01)." In addition, in the second sentence of the second paragraph of the "Reduced Child-Parent vmPFC Connectivity With the Hippocampus Links to Negative Family Emotional Climate and Children's Internalizing Symptoms" section, "anxious/depressed" and "internalizing" were switched. All versions of this article have been corrected.] Family emotional climate is fundamental to children's well-being and mental health. Family environments filled with negative emotions may lead to increased psychopathological symptoms in the child through dysfunctional child-parent interactions. Single-brain paradigms have uncovered changes in brain systems and networks related to negative family environments, but how the neurobiological reciprocity between child and parent brains is associated with children's psychopathological symptoms remains unknown. Here, we first investigated the relation between family emotional climate and children's psychopathological symptoms in 395 child-parent dyads. Using a naturalistic movie-watching functional magnetic resonance imaging technique in a subsample of 50 child-parent dyads, we further investigated the neurobiological underpinnings of how family emotional climates are associated with children's psychopathological symptoms through child-parent neural synchrony. Children from negative family emotional climate experienced significantly more severe psychopathological symptoms. In comparison to child-stranger dyads, child-parent dyads exhibited higher intersubject correlations in the dorsal and ventral portions of the medial prefrontal cortex (mPFC), and greater concordance of activity with widespread regions critical for socioemotional skills. Critically, negative family emotional climate was associated with decreased intersubject functional correlation between the ventral-mPFC and the hippocampus during movie watching in child-parent dyads, which further accounted for higher children's internalizing symptoms. Together, our findings provide insights into the neurobiological mechanisms that negative family environments can cause and maintain psychopathological symptoms in children through atypical child-parent neural synchrony. This has important implications for a better understanding of how child-parent connections may mediate the relation between environmental risks and developmental outcomes. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Rapid neural reorganization during retrieval practice predicts subsequent long-term retention and false memory.

Active retrieval can alter the strength and content of a memory, yielding either enhanced or distorted subsequent recall. However, how consolidation influences these retrieval-induced seemingly contradictory outcomes remains unknown. Here we show that rapid neural reorganization over an eight-run retrieval practice predicted subsequent recall. Retrieval practice boosted memory retention following a 24-hour (long-term) but not 30-minute delay, and increased false memory at both delays. Long-term retention gains were predicted by multi-voxel representation distinctiveness in the posterior parietal cortex (PPC) that increased progressively over retrieval practice. False memory was predicted by unstable representation distinctiveness in the medial temporal lobe (MTL). Retrieval practice enhanced the efficiency of memory-related brain networks, through building up PPC and MTL connections with the ventrolateral and dorsolateral prefrontal cortex that predicted long-term retention gains and false memory, respectively. Our findings indicate that retrieval-induced rapid neural reorganization together with consecutive consolidation fosters long-term retention and false memories via distinct pathways.

Brain preparedness: The proactive role of the cortisol awakening response in hippocampal-prefrontal functional interactions.

Upon awakening from nighttime sleep, the stress hormone cortisol in humans exhibits a robust rise within thirty to forty-five minutes. This cortisol awakening response (CAR), a crucial point of reference within the healthy cortisol circadian rhythm, has been linked to various psychological, psychiatric and health-related conditions. The CAR is thought to prepare the brain for anticipated challenges of the upcoming day to maintain one's homeostasis and promote adaptive responses. Using brain imaging with a prospective design and pharmacological manipulation, we investigate the neurobiological mechanisms underlying this preparation function of the CAR across two studies. In Study 1, a robust CAR is predictive of less hippocampal and prefrontal activity, though enhanced functional coupling between those regions during a demanding task hours later in the afternoon. Reduced prefrontal activity is in turn linked to better working memory performance, implicating that the CAR proactively promotes brain preparedness based on improved neurocognitive efficiency. In Study 2, pharmacologically suppressed CAR using Dexamethasone mirrors this proactive effect, which further causes a selective reduction of prefrontal top-down functional modulation over hippocampal activity. These findings establish a causal link between the CAR and its proactive role in optimizing functional brain networks involved in neuroendocrine control, executive function and memory.