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AbstractIntroductionMuscle sympathetic nerve activity (MSNA) controls the diameter of arterioles in skeletalmuscle, contributing importantly to the beat-to-beat regulation of blood pressure (BP). Although brain imaging studies have shown that bursts of MSNA originate in the rostral ventrolateral medulla, other subcortical and cortical structures—including the dorsolateral prefrontal cortex (dlPFC)—contribute.HypothesisWe tested the hypothesis that MSNA and BP could be modulated by stimulating the dlPFC.MethoddlPFC. In 22 individuals MSNA was recorded via microelectrodes inserted into the common peroneal nerve, together with continuous BP, electrocardiographic, and respiration.Stimulation of the right (n=22) or left dlPFC (n=10) was achieved using transcranial alternating current (tcACS; +2 to −2mA, 0.08 Hz,100 cycles), applied between the nasion and electrodes over the F3 or F4 EEG sites on the scalp.ResultsSinusoidal stimulation of either dlPFC caused cyclicmodulation of MSNA, BP and heart rate, and a significant increase in BP.ConclusionWe have shown, for the first time, that tcACS of the dlPFC in awake humans causes partial entrainment of MSNA, heart rate and BP, arguing for an important role of this higher-level cortical area in the control of cardiovascular function.

AbstractInfancy is a sensitive period of development, during which experiences of parental care are particularly important for shaping the developing brain. In a longitudinal study of N = 95 mothers and infants, we examined links between caregiving behavior (maternal sensitivity observed during a mother–infant free‐play) and infants' neural response to emotion (happy, angry, and fearful faces) at 5 and 7 months of age. Neural activity was assessed using functional Near‐Infrared Spectroscopy (fNIRS) in the dorsolateral prefrontal cortex (dlPFC), a region involved in cognitive control and emotion regulation. Maternal sensitivity was positively correlated with infants' neural responses to happy faces in the bilateral dlPFC and was associated with relative increases in such responses from 5 to 7 months. Multilevel analyses revealed caregiving‐related individual differences in infants' neural responses to happy compared to fearful faces in the bilateral dlPFC, as well as other brain regions. We suggest that variability in dlPFC responses to emotion in the developing brain may be one correlate of early experiences of caregiving, with implications for social‐emotional functioning and self‐regulation.

Willingness to fight and die (WFD) has been developed as a measure to capture willingness to incur costly sacrifices for the sake of a greater cause in the context of entrenched conflict. WFD measures have been repeatedly used in field studies, including studies on the battlefield, although their neurofunctional correlates remain unexplored. Our aim was to identify the neural underpinnings of WFD, focusing on neural activity and interconnectivity of brain areas previously associated with value-based decision-making, such as the ventromedial prefrontal cortex (vmPFC) and the dorsolateral prefrontal cortex (dlPFC). A sample of Pakistani participants supporting the Kashmiri cause was selected and invited to participate in an functional magnetic resonance (fMRI) paradigm where they were asked to convey their WFD for a series of values related to Islam and current politics. As predicted, higher compared to lower WFD was associated with increased ventromedial prefrontal activity and decreased dorsolateral activity, as well as lower connectivity between the vmPFC and the dlPFC. Our findings suggest that WFD more prominently relies on brain areas typically associated with subjective value (vmPFC) rather than integration of material costs (dlPFC) during decision-making, supporting the notion that decisions on costly sacrifices may not be mediated by cost-benefit computation.

Willingness to fight and die (WFD) has been developed as a measure to capture willingness to incur costly sacrifices for the sake of a greater cause in the context of entrenched conflict. WFD measures have been repeatedly used in field studies, including studies on the battlefield, although their neurofunctional correlates remain unexplored. Our aim was to identify the neural underpinnings of WFD, focusing on neural activity and interconnectivity of brain areas previously associated with value-based decision-making, such as the ventromedial prefrontal cortex (vmPFC) and the dorsolateral prefrontal cortex (dlPFC). A sample of Pakistani participants supporting the Kashmiri cause was selected and invited to participate in an functional magnetic resonance (fMRI) paradigm where they were asked to convey their WFD for a series of values related to Islam and current politics. As predicted, higher compared to lower WFD was associated with increased ventromedial prefrontal activity and decreased dorsolateral activity, as well as lower connectivity between the vmPFC and the dlPFC. Our findings suggest that WFD more prominently relies on brain areas typically associated with subjective value (vmPFC) rather than integration of material costs (dlPFC) during decision-making, supporting the notion that decisions on costly sacrifices may not be mediated by cost-benefit computation. ; This work was supported by the Minerva Program and the Air Force Office of Scientific Research of the U.S. Department of Defense (AFOSR FA9550-14-1-0030 DEF) and the BIAL Foundation (Grant #163/14) and the Ministerio de Ciencia, Innovación y Universidades (RTI2018-093550-B-I00).

Altres ajuts: This work was supported by the Minerva Program and the Air Force Office of Scientific Research of the U.S. Department of Defense (AFOSR FA9550-14-1-0030 DEF) and the BIAL Foundation (Grant #163/14). ; Willingness to fight and die (WFD) has been developed as a measure to capture willingness to incur costly sacrifices for the sake of a greater cause in the context of entrenched conflict. WFD measures have been repeatedly used in field studies, including studies on the battlefield, although their neurofunctional correlates remain unexplored. Our aim was to identify the neural underpinnings of WFD, focusing on neural activity and interconnectivity of brain areas previously associated with value-based decision-making, such as the ventromedial prefrontal cortex (vmPFC) and the dorsolateral prefrontal cortex (dlPFC). A sample of Pakistani participants supporting the Kashmiri cause was selected and invited to participate in an functional magnetic resonance (fMRI) paradigm where they were asked to convey their WFD for a series of values related to Islam and current politics. As predicted, higher compared to lower WFD was associated with increased ventromedial prefrontal activity and decreased dorsolateral activity, as well as lower connectivity between the vmPFC and the dlPFC. Our findings suggest that WFD more prominently relies on brain areas typically associated with subjective value (vmPFC) rather than integration of material costs (dlPFC) during decision-making, supporting the notion that decisions on costly sacrifices may not be mediated by cost-benefit computation.

While it is widely accepted that motor sequence learning (MSL) is supported by a prefrontal-mediated interaction between hippocampal and striatal networks, it remains unknown whether the functional responses of these networks can be modulated in humans with targeted experimental interventions. The present proof-of-concept study employed a multimodal neuroimaging approach, including functional magnetic resonance (MR) imaging and MR spectroscopy, to investigate whether individually-tailored theta-burst stimulation of the dorsolateral prefrontal cortex can modulate responses in the hippocampus and the basal ganglia during motor learning. Our results indicate that while stimulation did not modulate motor performance nor task-related brain activity, it influenced connectivity patterns within hippocampo-frontal and striatal networks. Stimulation also altered the relationship between the levels of gamma-aminobutyric acid (GABA) in the stimulated prefrontal cortex and learning-related changes in both activity and connectivity in fronto-striato-hippocampal networks. This study provides the first experimental evidence, to the best of our knowledge, that brain stimulation can alter motor learning-related functional responses in the striatum and hippocampus. ; This work was supported by the Belgian Research Foundation Flanders (FWO; G099516N) and internal funds from KU Leuven. GA also received support from FWO (G0D7918N, G0B1419N, 1524218N) and Excellence of Science (EOS, 30446199, MEMODYN, with SPS and DM). MAG, ND and MPV received salary support from these grants. MAG is funded by a predoctoral fellowship from FWO (1141320N). Financial support for author BRK was provided by the European Union's Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement (703490) and a postdoctoral fellowship from FWO (132635). This study applies tools developed under National Institutes of Health (NIH) Grants R01- EB-016089, R01-023963, and P41-EB015909; RAEE also receives salary support from these grants. NAJP receives salary support from NIH Grant R00-MH-107719. EMR received salary support from the Air Force Office of Scientific Research (AFOSR, Virginia, USA; FA9550-16-1-0191).

The prefrontal cortex (PFC) plays an important role in the integration of cognitive and affective behavior and regulating autonomic and neuroendocrine functions. This region of the brain, which may be considered analogous to the RAM memory of a computer, is important for translating stressful experience into adaptive behavior. The PFC responds to stress and modulates the response to stress through regulation of the hypothalamic paraventricular nucleus (PVN) which, in turn, controls sympathoadrenal and hypothalamic-pituitary-adrenal (HPA) activity. Interestingly, the latter convey the signals that link the CNS with the immune system. The present review highlights findings that contribute to elucidate the involvement of the PFC in the control of behavioral and neuroendocrine responses to chronic stress. It also considers the implications of these regulatory links for disorders of the nervous and immune systems. ; Authors' work was in part supported by grants from the Portuguese J.J. Cerqueira et al. / Brain, Behavior, and Immunity 22 (2008) 630–638 635 government Foundation for Science and Technology (FCT)—Project PTDC/SAU-NEU/72699/2006—and Calouste Gulbenkian Foundation—Project ...

Abstract
Integrating and predicting the intentions and actions of others are critical components of social interactions, but the behavioral and neural bases of such mechanisms under altered perceptual conditions are poorly understood. In the present study, we recruited expert violinists and age-matched controls with no musical training and asked them to evaluate simplified dynamic stimuli of violinists playing in a piano or forte communicative intent while undergoing functional magnetic resonance imaging. We show that expertise is needed to successfully understand and evaluate communicative intentions in spatially and temporally altered visual representations of musical performance. Frontoparietal regions—such as the dorsolateral prefrontal cortex and the inferior parietal lobule and sulcus—and various subregions of the cerebellum—such as cerebellar lobules I-IV, V, VI, VIIb, VIIIa, X—a re recruited in the process. Functional connectivity between these brain areas reveals widespread organization, particularly in the dorsolateral prefrontal cortex, inferior frontal gyrus, inferior parietal sulcus, and in the cerebellum. This network may be essential to successfully assess communicative intent in ambiguous or complex visual scenes.

Research suggests that altered emotion processing may be one important pathway linking social risk factors and depressive symptoms. We examined the extent to which neural response to negatively valenced social information might help to account for the relationship between social risk and depressive symptoms in youth. Forty‐nine youth were scanned while identifying the emotional valence of words that connoted social status. They also completed questionnaires assessing self‐reported social risk factors and depressive symptoms. Mediation analysis revealed that reduced dorsolateral prefrontal cortex activity in response to negative social status words explained the positive association between social risk and depressive symptoms. These findings suggest that social risk factors present during adolescence may contribute to depressive symptoms by influencing the neural substrates of emotion processing.

AbstractThe ability to keep information active in working memory is one of the cornerstones of cognitive development. Prior studies have demonstrated that regions which are important for working memory performance in adults, such as dorsolateral prefrontal cortex (DLPFC), ventrolateral prefrontal cortex (VLPFC), and superior parietal cortex, become increasingly engaged across school‐aged development. The primary goal of the present functional MRI study was to investigate the involvement of these regions in the development of working memory manipulation relative to maintenance functions under different loads. We measured activation in DLPFC, VLPFC, and superior parietal cortex during the delay period of a verbal working memory task in 11–13‐year‐old children and young adults. We found evidence for age‐related behavioral improvements in working memory and functional changes within DLPFC and VLPFC activation patterns. Although activation profiles of DLPFC and VLPFC were similar, group differences were most pronounced for right DLPFC. Consistent with prior studies, right DLPFC showed an interaction between age and condition (i.e. manipulation versus maintenance), specifically at the lower loads. This interaction was characterized by increased activation for manipulation relative to maintenance trials in adults compared to children. In contrast, we did not observe a significant age‐dependent load sensitivity. These results suggest that age‐related differences in the right DLPFC are specific to working memory manipulation and are not related to task difficulty and/or differences in short‐term memory capacity.

© The Author(s) 2021. Motor sequence learning (MSL) is supported by dynamical interactions between hippocampal and striatal networks that are thought to be orchestrated by the prefrontal cortex. In the present study, we tested whether individually-tailored theta-burst stimulation of the dorsolateral prefrontal cortex (DLPFC) prior to MSL can modulate multivoxel response patterns in the stimulated cortical area, the hippocampus and the striatum. Response patterns were assessed with multivoxel correlation structure analyses of functional magnetic resonance imaging data acquired during task practice and during resting-state scans before and after learning/stimulation. Results revealed that, across stimulation conditions, MSL induced greater modulation of task-related DLPFC multivoxel patterns than random practice. A similar learning-related modulatory effect was observed on sensorimotor putamen patterns under inhibitory stimulation. Furthermore, MSL as well as inhibitory stimulation affected (posterior) hippocampal multivoxel patterns at post-intervention rest. Exploratory analyses showed that MSL-related brain patterns in the posterior hippocampus persisted into post-learning rest preferentially after inhibitory stimulation. These results collectively show that prefrontal stimulation can alter multivoxel brain patterns in deep brain regions that are critical for the MSL process. They also suggest that stimulation influenced early offline consolidation processes as evidenced by a stimulation-induced modulation of the reinstatement of task pattern into post-learning wakeful rest. ; Belgian Research Foundation Flanders (FWO; G099516N); KU Leuven; FWO (G0D7918N, G0B1419N, 1524218N); Excellence of Science (EOS, 30446199, MEMODYN); European Union's Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement (703490); FWO (132635) postdoctoral fellowship; Air Force Office of Scientific Research (AFOSR, Virginia, USA; FA9550-16-1-0191).

To reveal post-traumatic stress disorder (PTSD) genetic risk influences on tissue-specific gene expression, we use brain and non-brain transcriptomic imputation. We impute genetically regulated gene expression (GReX) in 29,539 PTSD cases and 166,145 controls from 70 ancestry-specific cohorts and identify 18 significant GReX-PTSD associations corresponding to specific tissue-gene pairs. The results suggest substantial genetic heterogeneity based on ancestry, cohort type (military versus civilian), and sex. Two study-wide significant PTSD associations are identified in European and military European cohorts; ZNF140 is predicted to be upregulated in whole blood, and SNRNP35 is predicted to be downregulated in dorsolateral prefrontal cortex, respectively. In peripheral leukocytes from 175 marines, the observed PTSD differential gene expression correlates with the predicted differences for these individuals, and deployment stress produces glucocorticoid-regulated expression changes that include downregulation of both ZNF140 and SNRNP35. SNRNP35 knockdown in cells validates its functional role in U12-intron splicing. Finally, exogenous glucocorticoids in mice downregulate prefrontal Snrnp35 expression.

To reveal post-traumatic stress disorder (PTSD) genetic risk influences on tissue-specific gene expression, we use brain and non-brain transcriptomic imputation. We impute genetically regulated gene expression (GReX) in 29,539 PTSD cases and 166,145 controls from 70 ancestry-specific cohorts and identify 18 significant GReX-PTSD associations corresponding to specific tissue-gene pairs. The results suggest substantial genetic heterogeneity based on ancestry, cohort type (military versus civilian), and sex. Two study-wide significant PTSD associations are identified in European and military European cohorts; ZNF140 is predicted to be upregulated in whole blood, and SNRNP35 is predicted to be downregulated in dorsolateral prefrontal cortex, respectively. In peripheral leukocytes from 175 marines, the observed PTSD differential gene expression correlates with the predicted differences for these individuals, and deployment stress produces glucocorticoid-regulated expression changes that include downregulation of both ZNF140 and SNRNP35. SNRNP35 knockdown in cells validates its functional role in U12-intron splicing. Finally, exogenous glucocorticoids in mice downregulate prefrontal Snrnp35 expression.