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Evidence shows that regular physical exercise reduces physiological reactivity to psychosocial stress. However, previous research mainly focused on the effect of endurance exercise, with only a few studies looking at the effect of resistance exercise. The current study tested whether individuals who regularly participate in either endurance or resistance training differ from untrained individuals in adrenal and cardiovascular reactivity to psychosocial stress. Twelve endurance-trained men, 10 resistance-trained men, and 12 healthy but untrained men were exposed to a standardized psychosocial stressor, the Trier Social Stress Test. Measurements of heart rate, free salivary cortisol levels, and mood were obtained throughout the test and compared among the three groups. Overall, both endurance- and resistance-trained men had lower heart rate levels than untrained men, indicating higher cardiac performance of the trained groups. Trained men also exhibited lower heart rate responses to psychosocial stress compared with untrained men. There were no significant group differences in either cortisol responses or mood responses to the stressor. The heart rate results are consistent with previous studies indicating reduced cardiovascular reactivity to psychosocial stress in trained individuals. These findings suggest that long-term endurance and resistance trainings may be related to the same cardiovascular benefits, without exhibiting strong effects on the cortisol reactivity to stress. published

Contains fulltext : 126635.pdf (Publisher’s version ) (Closed access) Resting-state studies in depressed patients have revealed increased connectivity within the default mode network (DMN) and task-positive network (TPN). This has been associated with heightened rumination, which is the tendency to repetitively think about symptoms of distress. Here, we performed a pharmacological neuroimaging study in healthy volunteers to investigate whether short-term antidepressant administration could reduce DMN connectivity. We recorded resting-state functional magnetic resonance imaging (fMRI) scans in twenty-three healthy volunteers after two week intake of the combined serotonin-norepinephrine reuptake inhibitor (SNRI) duloxetine in a double-blind, placebo-controlled, crossover study. Duloxetine improved mood in part as a result of increased resilience to the mood-worsening effects of scanning and reduced DMN and TPN connectivity. Within the DMN, duloxetine reduced connectivity between the medial prefrontal cortex (MPFC) and the lateral parietal cortex (LPC) and uncoupled the MPFC from the dorsolateral prefrontal cortex (DLPFC). Within the TPN, duloxetine uncoupled the intraparietal sulcus (IPS) from the inferior occipital gyrus. These results show that two-week antidepressant administration reduces DMN and TPN connectivity in healthy volunteers, which may contribute to their antidepressant effects in depression.

Sounds can modulate visual perception as well as neural activity in retinotopic cortex. Most studies in this context investigated how sounds change neural amplitude and oscillatory phase reset in visual cortex. However, recent studies in macaque monkeys show that congruence of audio-visual stimuli also modulates the amount of stimulus information carried by spiking activity of primary auditory and visual neurons. Here, we used naturalistic video stimuli and recorded the spatial patterns of functional MRI signals in human retinotopic cortex to test whether the discriminability of such patterns varied with the presence and congruence of co-occurring sounds. We found that incongruent sounds significantly impaired stimulus decoding from area V2 and there was a similar trend for V3. This effect was associated with reduced inter-trial reliability of patterns (i.e. higher levels of noise), but was not accompanied by any detectable modulation of overall signal amplitude. We conclude that sounds modulate naturalistic stimulus encoding in early human retinotopic cortex without affecting overall signal amplitude. Subthreshold modulation, oscillatory phase reset and dynamic attentional modulation are candidate neural and cognitive mechanisms mediating these effects., Highlights ► Multivariate decoding of video identity from fMRI signals in V1V3. ► Decoding accuracy in V2 is significantly reduced for incongruent sounds. ► Reduced decoding accuracy is associated with reduced inter-trial reliability. ► No modulation of univariate signal amplitude by sounds. ► Noise levels in sensory areas are affected by multisensory congruence.

Item does not contain fulltext It is unknown how antidepressants reverse mood-congruent memory bias, a cognitive core factor causing and maintaining depression. Using a double-blind, placebo-controlled, cross-over design, we investigated the effect of a short-term treatment (14 days) with the dual reuptake inhibitor duloxetine on neural correlates of mood-congruent and mood-incongruent memory formation and retrieval in healthy volunteers who underwent a sad mood induction procedure. Duloxetine did not affect acute mood state or memory performance, but interacted with brain processes mediating mood-congruent memory. It decreased activity related to successful memory formation for mood-congruent and -incongruent items in a set of brain regions comprising the putamen and the middle frontal gyrus, as well as the middle and the anterior cingulate cortex. Duloxetine specifically increased amygdala activity related to successful memory retrieval for mood-incongruent items. Here we show that short-term administration of duloxetine affects the neural correlates of emotional memory formation and retrieval in a set of brain regions whose processing is related to affective state and its regulation. While duloxetine suppressed the neural correlates of emotional memory formation in general, it specifically enhanced amygdala processes associated with mood-incongruent memory retrieval. This pattern of results shows how an antidepressant may reduce emotional memory formation and reverse mood-congruent processing biases at retrieval.

Deep brain stimulation is an established therapy for Parkinson’s disease, although its mechanism of action remains unclear. Kahan et al. use resting state fMRI and dynamic causal modelling to study changes in ‘effective’ connectivity within the basal ganglia. Analyses implicate subthalamic afferents and the direct pathway in the clinical response., Depleted of dopamine, the dynamics of the parkinsonian brain impact on both ‘action’ and ‘resting’ motor behaviour. Deep brain stimulation has become an established means of managing these symptoms, although its mechanisms of action remain unclear. Non-invasive characterizations of induced brain responses, and the effective connectivity underlying them, generally appeals to dynamic causal modelling of neuroimaging data. When the brain is at rest, however, this sort of characterization has been limited to correlations (functional connectivity). In this work, we model the ‘effective’ connectivity underlying low frequency blood oxygen level-dependent fluctuations in the resting Parkinsonian motor network—disclosing the distributed effects of deep brain stimulation on cortico-subcortical connections. Specifically, we show that subthalamic nucleus deep brain stimulation modulates all the major components of the motor cortico-striato-thalamo-cortical loop, including the cortico-striatal, thalamo-cortical, direct and indirect basal ganglia pathways, and the hyperdirect subthalamic nucleus projections. The strength of effective subthalamic nucleus afferents and efferents were reduced by stimulation, whereas cortico-striatal, thalamo-cortical and direct pathways were strengthened. Remarkably, regression analysis revealed that the hyperdirect, direct, and basal ganglia afferents to the subthalamic nucleus predicted clinical status and therapeutic response to deep brain stimulation; however, suppression of the sensitivity of the subthalamic nucleus to its hyperdirect afferents by deep brain stimulation may subvert the clinical efficacy of deep brain stimulation. Our findings highlight the distributed effects of stimulation on the resting motor network and provide a framework for analysing effective connectivity in resting state functional MRI with strong a priori hypotheses.

Patients with visual extinction following right-hemisphere damage sometimes see and sometimes miss stimuli in the left visual field, particularly when stimuli are presented simultaneously to both visual fields. Awareness of left visual field stimuli is associated with increased activity in bilateral parietal and frontal cortex. However, it is unknown why patients see or miss these stimuli. Previous neuroimaging studies in healthy adults show that prestimulus activity biases perceptual decisions, and biases in visual perception can be attributed to fluctuations in prestimulus activity in task relevant brain regions. Here, we used functional MRI to investigate whether prestimulus activity affected perception in the context of visual extinction following stroke. We measured prestimulus activity in stimulus-responsive cortical areas during an extinction paradigm in a patient with unilateral right parietal damage and visual extinction. This allowed us to compare prestimulus activity on physically identical bilateral trials that either did or did not lead to visual extinction. We found significantly increased activity prior to stimulus presentation in two areas that were also activated by visual stimulation: the left calcarine sulcus and right occipital inferior cortex. Using dynamic causal modelling (DCM) we found that both these differences in prestimulus activity and stimulus evoked responses could be explained by enhanced effective connectivity within and between visual areas, prior to stimulus presentation. Thus, we provide evidence for the idea that differences in ongoing neural activity in visually responsive areas prior to stimulus onset affect awareness in visual extinction, and that these differences are mediated by fluctuations in extrinsic and intrinsic connectivity., Highlights • Prestimulus activity in visual extinction affects perception. • The BOLD signal in two visual areas is indicative of perception in bilateral trials. • Intrinsic and extrinsic connectivity is elevated prior to perceived trials.

Impulsivity is a feature of many brain disorders. Although often defined as the predisposition to act with an inadequate degree of deliberation, forethought or control, it has proven difficult to measure. This may in part be because, increasingly, impulsivity is recognized as a multifaceted construct, with impulsive decisions potentially arising due to a number of underlying mechanisms. Indeed, in certain contexts, a ‘functional’ degree of impulsivity may promote effective, motivated behavior in healthy participants. Although many tasks have been developed to study impulsivity, few examine decisions made rapidly, for time-sensitive rewards: In this context, a degree of impulsivity may be adaptive. In the current study we examine behavior in 59 adults on a manual ‘Traffic Light’ task which requires participants to take risks under time pressure, if they are to maximize reward. We show that behavioral variables that index rapid anticipatory responding in this paradigm are correlated with a specific self-report measure of impulsivity: ‘lack of premeditation’ on the UPPS Impulsive Behavior Scale. Participants who scored more highly on this subscale performed better on the task. Moreover, anticipatory behavior reduced significantly with age (18-79 years), an effect that continued to be upheld after correction for potential age differences in the ability to judge the timing of responses. Based on these findings, we argue that the Traffic Light task provides a parametric method to study a ‘functional’ aspect of impulsivity in health and disease: namely, rapid decision-making in pursuit of risky, time-sensitive rewards.

Contains fulltext : 95925.pdf (Publisher’s version ) (Closed access) Objective: Enhanced memory for emotionally charged events helps us to remember potentially vital information. There are large interindividual differences in emotional-memory enhancement, but little is known about their neurobiological basis. Recently, a functional deletion variant of the gene that codes for the alpha2b-adrenoceptor (ADRA2B) has been shown to affect memory for emotional experiences. Initial neuroimaging evidence linked this behavioral effect to increased amygdala activity, but its influence on successful memory processing remains unknown. Therefore, the aim of this study was to investigate the effect of the common deletion in the ADRA2B gene on neural activity related to specific mnemonic processing, successful memory formation, and retrieval. Methods: Twenty-three noncarriers (10 males) and 28 deletion carriers (13 males) with a mean age of 24 years were investigated while performing an emotional-learning task with sad and happy scenes. Functional magnetic resonance imaging was acquired both during memory formation and retrieval. Results: Although there were no differences in memory performance between groups, the common deletion variant of ADRA2B was related to enhanced activity in the amygdala and inferior frontal gyrus during successful emotional memory formation, but not retrieval. Deletion carriers showed a larger differential response in these brain regions between later-remembered and later-forgotten stimuli than nondeletion carriers did. Conclusion: Our results demonstrate that the ADRA2B polymorphism influences emotional memory formation but not memory retrieval in the amygdala and left inferior frontal gyrus. Hum Brain Mapp, 2011. (c) 2011 Wiley Periodicals, Inc.

Item does not contain fulltext BACKGROUND: Anhedonia and lack of motivation are core symptoms of major depressive disorder (MDD). Neuroimaging studies in MDD patients have shown reductions in reward-related activity in terminal regions of the mesolimbic dopamine (DA) system, such as the ventral striatum. Monoamines have been implicated in both mesolimbic incentive processing and the mechanism of action of antidepressant drugs. However, not much is known about antidepressant effects on mesolimbic incentive processing in humans, which might be related to the effects on anhedonia. METHODS: To investigate the short-term effects of antidepressants on reward-related activity in the ventral striatum, we investigated the effect of the combined serotonin-norepinephrine reuptake inhibitor duloxetine. Healthy volunteers underwent functional magnetic resonance imaging in a randomized, double-blind, placebo-controlled, crossover study. After taking duloxetine (60 mg once a day) or placebo for 14 days, participants completed a monetary incentive delay task that activates the ventral striatum during reward anticipation. RESULTS: Our results (n = 19) show enhanced ventral striatal responses after duloxetine administration compared with placebo. Moreover, this increase in ventral striatal activity was positively correlated with duloxetine plasma levels. CONCLUSIONS: This is the first study to demonstrate that antidepressants augment neural activity in mesolimbic DA incentive processing circuits in healthy volunteers. These effects are likely caused by the increase in monoamine neurotransmission in the ventral striatum. Our findings suggest that antidepressants may alleviate anhedonia by stimulating incentive processing.

Spontaneous fluctuations in resting state activity can change in response to experience-dependent plasticity and learning. Visual learning is fast and can be elicited in an MRI scanner. Here, we showed that a random dot motion coherence task can be learned within one training session. While the task activated primarily visual and parietal brain areas, learning related changes in neural activity were observed in the hippocampus. Crucially, even this rapid learning affected resting state dynamics both immediately after the learning and 24 h later. Specifically, the hippocampus changed its coupling with the striatum, in a way that was best explained as a consolidation of early learning related changes. Our findings suggest that long-lasting changes in neuronal coupling are accompanied by changes in resting state activity., Highlights • Early learning of sensory task changes hippocampal activity. • Coupling changes between hippocampus and striatum. • Resting-state changes are consolidated during sleep. • Stochastic DCM is a tool for resting state analysis.