scholarly journals Reward, Context, and Human Behaviour

2007 ◽  
Vol 7 ◽  
pp. 626-640 ◽  
Author(s):  
Clare L. Blaukopf ◽  
Gregory J. DiGirolamo

Animal models of reward processing have revealed an extensive network of brain areas that process different aspects of reward, from expectation and prediction to calculation of relative value. These results have been confirmed and extended in human neuroimaging to encompass secondary rewards more unique to humans, such as money. The majority of the extant literature covers the brain areas associated with rewards whilst neglecting analysis of the actual behaviours that these rewards generate. This review strives to redress this imbalance by illustrating the importance of looking at the behavioural outcome of rewards and the context in which they are produced. Following a brief review of the literature of reward-related activity in the brain, we examine the effect of reward context on actions. These studies reveal how the presence of reward vs. rewardandpunishment, or being conscious vs. unconscious of reward-related actions, differentially influence behaviour. The latter finding is of particular importance given the extent to which animal models are used in understanding the reward systems of the human mind. It is clear that further studies are needed to learn about the human reaction to reward in its entirety, including any distinctions between conscious and unconscious behaviours. We propose that studies of reward entail a measure of the animal's (human or nonhuman) knowledge of the reward and knowledge of its own behavioural outcome to achieve that reward.

2021 ◽  
Author(s):  
Stephanie Noble ◽  
Mandy Mejia ◽  
Andrew Zalesky ◽  
Dustin Scheinost

Inference in neuroimaging commonly occurs at the level of "clusters" of neighboring voxels or connections, thought to reflect functionally specific brain areas. Yet increasingly large studies reveal effects that are shared throughout the brain, suggesting that reported clusters may only reflect the "tip of the iceberg" of underlying effects. Here, we empirically compare power of traditional levels of inference (edge and cluster) with broader levels of inference (network and whole-brain) by resampling functional connectivity data from the Human Connectome Project (n=40, 80, 120). Only network- and whole brain-level inference attained or surpassed "adequate" power (β =80%) to detect an average effect, with almost double the power for network- compared with cluster-level procedures at more typical sample sizes. Likewise, effects tended to be widespread, and more widespread pooling resulted in stronger magnitude effects. Power also substantially increased when controlling FDR rather than FWER. Importantly, there may be similar implications for task-based activation analyses where effects are also increasingly understood to be widespread. However, increased power with broader levels of inference may diminish the specificity to localize effects, especially for non-task contexts. These findings underscore the benefit of shifting the scale of inference to better capture the underlying signal, which may unlock opportunities for discovery in human neuroimaging.


2011 ◽  
Vol 111 (5) ◽  
pp. 1505-1513 ◽  
Author(s):  
Michelle W. Voss ◽  
Lindsay S. Nagamatsu ◽  
Teresa Liu-Ambrose ◽  
Arthur F. Kramer

This is a brief review of current evidence for the relationships between physical activity and exercise and the brain and cognition throughout the life span in non-pathological populations. We focus on the effects of both aerobic and resistance training and provide a brief overview of potential neurobiological mechanisms derived from non-human animal models. Whereas research has focused primarily on the benefits of aerobic exercise in youth and young adult populations, there is growing evidence that both aerobic and resistance training are important for maintaining cognitive and brain health in old age. Finally, in these contexts, we point out gaps in the literature and future directions that will help advance the field of exercise neuroscience, including more studies that explicitly examine the effect of exercise type and intensity on cognition, the brain, and clinically significant outcomes. There is also a need for human neuroimaging studies to adopt a more unified multi-modal framework and for greater interaction between human and animal models of exercise effects on brain and cognition across the life span.


2021 ◽  
Vol 5 ◽  
pp. 239821282110554
Author(s):  
Vasileia Kotoula ◽  
Toby Webster ◽  
James Stone ◽  
Mitul A Mehta

Acute ketamine administration has been widely used in neuroimaging research to mimic psychosis-like symptoms. Within the last two decades, ketamine has also emerged as a potent, fast-acting antidepressant. The delayed effects of the drug, observed 2–48 h after a single infusion, are associated with marked improvements in depressive symptoms. At the systems’ level, several studies have investigated the acute ketamine effects on brain activity and connectivity; however, several questions remain unanswered around the brain changes that accompany the drug’s antidepressant effects and how these changes relate to the brain areas that appear with altered function and connectivity in depression. This review aims to address some of these questions by focusing on resting-state brain connectivity. We summarise the studies that have examined connectivity changes in treatment-naïve, depressed individuals and those studies that have looked at the acute and delayed effects of ketamine in healthy and depressed volunteers. We conclude that brain areas that are important for emotional regulation and reward processing appear with altered connectivity in depression whereas the default mode network presents with increased connectivity in depressed individuals compared to healthy controls. This finding, however, is not as prominent as the literature often assumes. Acute ketamine administration causes an increase in brain connectivity in healthy volunteers. The delayed effects of ketamine on brain connectivity vary in direction and appear to be consistent with the drug normalising the changes observed in depression. The limited number of studies however, as well as the different approaches for resting-state connectivity analysis make it very difficult to draw firm conclusions and highlight the importance of data sharing and larger future studies.


2019 ◽  
Vol 5 (3) ◽  
pp. 222-242 ◽  
Author(s):  
Nicole A. Crowley ◽  
Nigel C. Dao ◽  
Sarah N. Magee ◽  
Alexandre J. Bourcier ◽  
Emily G. Lowery-Gionta

2019 ◽  
Vol 16 (6) ◽  
pp. 544-558 ◽  
Author(s):  
Carla Petrella ◽  
Maria Grazia Di Certo ◽  
Christian Barbato ◽  
Francesca Gabanella ◽  
Massimo Ralli ◽  
...  

Neuropeptides are small proteins broadly expressed throughout the central nervous system, which act as neurotransmitters, neuromodulators and neuroregulators. Growing evidence has demonstrated the involvement of many neuropeptides in both neurophysiological functions and neuropathological conditions, among which is Alzheimer’s disease (AD). The role exerted by neuropeptides in AD is endorsed by the evidence that they are mainly neuroprotective and widely distributed in brain areas responsible for learning and memory processes. Confirming this point, it has been demonstrated that numerous neuropeptide-containing neurons are pathologically altered in brain areas of both AD patients and AD animal models. Furthermore, the levels of various neuropeptides have been found altered in both Cerebrospinal Fluid (CSF) and blood of AD patients, getting insights into their potential role in the pathophysiology of AD and offering the possibility to identify novel additional biomarkers for this pathology. We summarized the available information about brain distribution, neuroprotective and cognitive functions of some neuropeptides involved in AD. The main focus of the current review was directed towards the description of clinical data reporting alterations in neuropeptides content in both AD patients and AD pre-clinical animal models. In particular, we explored the involvement in the AD of Thyrotropin-Releasing Hormone (TRH), Cocaine- and Amphetamine-Regulated Transcript (CART), Cholecystokinin (CCK), bradykinin and chromogranin/secretogranin family, discussing their potential role as a biomarker or therapeutic target, leaving the dissertation of other neuropeptides to previous reviews.


Author(s):  
Armin Schnider

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Alan M. Daniel ◽  
Brenda G. Rushing ◽  
Karla Y. Tapia Menchaca

AbstractUnderstanding the emotional reaction to loss, or frustration, is a critical problem for the field of mental health. Animal models of loss have pointed to the opioid system as a nexus of frustration, physical pain, and substance abuse. However, few attempts have been made to connect the results of animal models of loss to human behavior. Allelic differences in the human mu opioid receptor gene, notably the A118G single nucleotide polymorphism, have been linked to individual differences in pain sensitivity, depressive symptoms, and reward processing. The present study explored the relationship between A118G and behavior in two frustrating tasks in humans. Results showed that carriers of the mutant G-allele were slower to recover behavior following a reward downshift and abandoned a frustrating task earlier than those without the mutation. Additionally, G-carriers were more sensitive to physical pain. These results highlight the overlap between frustration and pain, and suggest that genetic variation in opioid tone may contribute to individual differences in vulnerability and resilience following emotional disturbances.


2021 ◽  
Vol 16 ◽  
pp. 263310552110187
Author(s):  
Christopher D Link

Numerous studies have identified microbial sequences or epitopes in pathological and non-pathological human brain samples. It has not been resolved if these observations are artifactual, or truly represent population of the brain by microbes. Given the tempting speculation that resident microbes could play a role in the many neuropsychiatric and neurodegenerative diseases that currently lack clear etiologies, there is a strong motivation to determine the “ground truth” of microbial existence in living brains. Here I argue that the evidence for the presence of microbes in diseased brains is quite strong, but a compelling demonstration of resident microbes in the healthy human brain remains to be done. Dedicated animal models studies may be required to determine if there is indeed a “brain microbiome.”


2021 ◽  
Vol 22 (13) ◽  
pp. 6858
Author(s):  
Fanny Gaudel ◽  
Gaëlle Guiraudie-Capraz ◽  
François Féron

Animals strongly rely on chemical senses to uncover the outside world and adjust their behaviour. Chemical signals are perceived by facial sensitive chemosensors that can be clustered into three families, namely the gustatory (TASR), olfactory (OR, TAAR) and pheromonal (VNR, FPR) receptors. Over recent decades, chemoreceptors were identified in non-facial parts of the body, including the brain. In order to map chemoreceptors within the encephalon, we performed a study based on four brain atlases. The transcript expression of selected members of the three chemoreceptor families and their canonical partners was analysed in major areas of healthy and demented human brains. Genes encoding all studied chemoreceptors are transcribed in the central nervous system, particularly in the limbic system. RNA of their canonical transduction partners (G proteins, ion channels) are also observed in all studied brain areas, reinforcing the suggestion that cerebral chemoreceptors are functional. In addition, we noticed that: (i) bitterness-associated receptors display an enriched expression, (ii) the brain is equipped to sense trace amines and pheromonal cues and (iii) chemoreceptor RNA expression varies with age, but not dementia or brain trauma. Extensive studies are now required to further understand how the brain makes sense of endogenous chemicals.


2021 ◽  
Vol 22 (13) ◽  
pp. 6839
Author(s):  
Ali H. El-Far ◽  
Yaser H. A. Elewa ◽  
Elsayeda-Zeinab A. Abdelfattah ◽  
Abdel-Wahab A. Alsenosy ◽  
Mustafa S. Atta ◽  
...  

D-galactose (D-gal) administration causes oxidative disorder and is widely utilized in aging animal models. Therefore, we subcutaneously injected D-gal at 200 mg/kg BW dose to assess the potential preventive effect of thymoquinone (TQ) and curcumin (Cur) against the oxidative alterations induced by D-gal. Other than the control, vehicle, and D-gal groups, the TQ and Cur treated groups were orally supplemented at 20 mg/kg BW of each alone or combined. TQ and Cur effectively suppressed the oxidative alterations induced by D-gal in brain and heart tissues. The TQ and Cur combination significantly decreased the elevated necrosis in the brain and heart by D-gal. It significantly reduced brain caspase 3, calbindin, and calcium-binding adapter molecule 1 (IBA1), heart caspase 3, and BCL2. Expression of mRNA of the brain and heart TP53, p21, Bax, and CASP-3 were significantly downregulated in the TQ and Cur combination group along with upregulation of BCL2 in comparison with the D-gal group. Data suggested that the TQ and Cur combination is a promising approach in aging prevention.


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