Prolonged grief disorder (PGD) is a diagnostic entity now included in the
International Classification of Diseases 11th Revision
(ICD-11) and soon to appear in the
Diagnostic and Statistical Manual ...of Mental Disorders
, fifth edition, text revision (DSM-5-TR). A characteristic feature of PGD is distressing, disabling yearning that persists a year or more after the loss. Other characteristic symptoms include disbelief and lack of acceptance of the loss, emotional detachment from others since the loss, loneliness, identity disturbance, and sense of meaninglessness. In this review, we detail psychiatric views on grief and their evolution over the twentieth century. We then discuss the development of diagnostic formulations for disordered grief, which culminated in PGD's status as a mental disorder in the DSM. After summarizing recent evidence that may suggest that PGD is linked to the neural reward system, we suggest further areas of research. In particular, we note the need for studies that extend the evidence base concerning PGD across cultural and sociodemographic boundaries and that investigate novel treatments.
Addictive substances act on a number of neurotransmitter systems, and the end result of this action is the activation of the reward system in the brain. The cellular and neuronal mechanisms that ...underlie addiction have long been searched for. One of such neurotransmitters is dopamine, a catecholamine synthesized in neurons located mainly in the midbrain.
The available literature was reviewed on the Pubmed platform and from other sources. The analysis included original studies, reviews.
of the study was to review the literature on the relationship between the
gene and the occurrence of substance addiction.
This work presents several currently discussed biological mechanisms, especially at the molecular and genetic level, involved in the process of addiction to various psychoactive substances. They discovered the brain structures that are most at risk, as well as other neurotransmitter systems and receptor proteins through which they can exert their pathological effects. It has also been established that exposure to psychoactive substances causes significant changes in expression in over 100 genes (including genes for dopaminergic, serotonergic and signaling pathways). The DRD2 receptor (present, among others, in the nucleus accumbens) plays an important role in the reward system, in the transmission of information. The weakening of this conductivity is a significant risk factor for the onset of clinical features that are associated with reward system deficiency syndrome. The expression of the D2 receptor gene may take up to 2 isoforms: short D2S and long D2L.
Further research at the molecular level may result in the modification of psychotherapy and pharmacotherapy in terms of their personalization.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Background
Anhedonia and irritability are two prevalent symptoms of major depressive disorder (MDD) that predict greater depression severity and poor outcomes, including suicidality. Although both ...symptoms have been proposed to result from paradoxical reward processing dysfunctions, the interactions between these symptoms remain unclear. Anhedonia is a multifaceted symptom reflecting impairments in multiple dimensions of reward processing (e.g., pleasure, desire, motivation, and effort) across distinct reward types (e.g., food, sensory experiences, social activities, hobbies) that may differentially interact with irritability. This study investigated the complex associations between anhedonia and irritability using network analysis.
Method
Participants (N = 448, Mage = 33.29, SD = 14.58) reported their symptoms of irritability on the Brief Irritability Test (Holtzman et al., 2015) and anhedonia (i.e., pleasure, desire, motivation, and effort dimensions across four reward types) on the Dimensional Anhedonia Rating Scale (Rizvi et al., 2015). A regularized Gaussian Graphical Model was built to estimate the network structure between items.
Results
Irritability was negatively related to willingness to expand effort to obtain food/drinks (estimate = −0.18), social activities (−0.13), and hobbies (−0.12) rewards. Irritability was positively associated with a desire for food/drinks (0.12).
Limitations
Only a small proportion (5.8%) of our sample was clinical and the study design was cross‐sectional.
Conclusion
A specific link between irritability and the effort dimension of the hedonic response across three reward types was identified. Investigating effort expenditure deficits with experimental paradigms may help us understand the mechanisms underlying the comorbidity between irritability and anhedonia in the context of MDD.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
We ubiquitously seek information to make better decisions. Particularly in the modern age, when more information is available at our fingertips than ever, the information we choose to collect ...determines the quality of our decisions. Decision neuroscience has long adopted empirical approaches where the information available to decision-makers is fully controlled by the researchers, leaving neural mechanisms of information seeking less understood. Although information seeking has long been studied in the context of the exploration-exploitation trade-off, recent studies have widened the scope to investigate more overt information seeking in a way distinct from other decision processes. Insights gained from these studies, accumulated over the last few years, raise the possibility that information seeking is driven by the reward system signaling the subjective value of information. In this piece, we review findings from the recent studies, highlighting the conceptual and empirical relationships between distinct literatures, and discuss future research directions necessary to establish a more comprehensive understanding of how individuals seek information as a part of value-based decision-making.
Information seeking is an integral, yet often overlooked aspect of value-based decision-making. Kobayashi and Kable review recent findings on the neural mechanisms of information seeking, highlighting an emerging hypothesis that the reward system represents the subjective value of information.
In the article the problem of compliance to treatment is discussed considering pharmacodynamics of different classes of psychotropic drugs. Use of antipsychotics is associated with a high risk of ...non-compliance. Antipsychotics can inhibit the endogenous reward system and decreasing its tone reduce adherence to treatment. Both antidepressants and anxiolytics increase the tone of the reward system. But if for antidepressants an increase in adherence is associated with the activation of the reward system limited by related clinical effects, for anxiolytics high adherence to treatment is associated to the rapid development of specific effect and an indirect increase in the tone of the reward system with an increase general subjective satisfaction with treatment. The tolerance associated with the chronic use of benzodiazepine anxiolytics secondarily worsens the situation leading to the development of pathological addiction.
Dopamine is involved in physiological processes like learning and memory, motor control and reward, and pathological conditions such as Parkinson’s disease and addiction. In contrast to the extensive ...studies on neurons, astrocyte involvement in dopaminergic signaling remains largely unknown. Using transgenic mice, optogenetics, and pharmacogenetics, we studied the role of astrocytes on the dopaminergic system. We show that in freely behaving mice, astrocytes in the nucleus accumbens (NAc), a key reward center in the brain, respond with Ca2+ elevations to synaptically released dopamine, a phenomenon enhanced by amphetamine. In brain slices, synaptically released dopamine increases astrocyte Ca2+, stimulates ATP/adenosine release, and depresses excitatory synaptic transmission through activation of presynaptic A1 receptors. Amphetamine depresses neurotransmission through stimulation of astrocytes and the consequent A1 receptor activation. Furthermore, astrocytes modulate the acute behavioral psychomotor effects of amphetamine. Therefore, astrocytes mediate the dopamine- and amphetamine-induced synaptic regulation, revealing a novel cellular pathway in the brain reward system.
•Astrocytes in the Nucleus Accumbens respond to synaptic dopamine in vivo•Astrocytes mediate the synaptic regulation induced by dopamine and amphetamine•Amphetamine-induced enhancement in locomotion activity is modulated by astrocytes
Corkrum et al. report that astrocyte activity is required for dopamine- and amphetamine-evoked synaptic regulation and amphetamine-induced locomotor effects. Their study reveals astrocytes as active components of dopaminergic signaling and the brain reward system.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
In this brief, a reinforcement learning-based control approach for nonlinear systems is presented. The proposed control approach offers a design scheme of the adjustable policy learning rate (APLR) ...to reduce the influence imposed by negative or large advantages, which improves the learning stability of the proximal policy optimization (PPO) algorithm. Besides, this brief puts forward a Lyapunov-fuzzy reward system to further promote the learning efficiency. In addition, the proposed control approach absorbs the Lyapunov stability concept into the design of the Lyapunov reward system and a particular fuzzy reward system is set up using the knowledge of the cart-pole inverted pendulum and fuzzy inference system (FIS). The merits of the proposed approach are validated by simulation examples.
This narrative review aims to pinpoint mental and behavioral effects of starvation, which may be triggered by hypoleptinemia and as such may be amenable to treatment with leptin receptor agonists. ...The reduced leptin secretion results from the continuous loss of fat mass, thus initiating a graded triggering of diverse starvation related adaptive functions. In light of leptin receptors located in several peripheral tissues and many brain regions adaptations may extend beyond those of the hypothalamus-pituitary-end organ-axes. We focus on gastrointestinal tract and reward system as relevant examples of peripheral and central effects of leptin. Despite its association with extreme obesity, congenital leptin deficiency with its many parallels to a state of starvation allows the elucidation of mental symptoms amenable to treatment with exogenous leptin in both ob/ob mice and humans with this autosomal recessive disorder. For starvation induced behavioral changes with an intact leptin signaling we particularly focus on rodent models for which proof of concept has been provided for the causative role of hypoleptinemia. For humans, we highlight the major cognitive, emotional and behavioral findings of the Minnesota Starvation Experiment to contrast them with results obtained upon a lesser degree of caloric restriction. Evidence for hypoleptinemia induced mental changes also stems from findings obtained in lipodystrophies. In light of the recently reported beneficial cognitive, emotional and behavioral effects of metreleptin-administration in anorexia nervosa we discuss potential implications for the treatment of this eating disorder. We postulate that leptin has profound psychopharmacological effects in the state of starvation.
•Hypoleptinemia may trigger major mental and behavioral effects of starvation.•Leptin may have profound psychopharmacological effects in the state of starvation.•Leptin receptor agonists can potentially be used to treat anorexia nervosa.•Mental and behavioural effects of starvation overlap with the symptomatology observed in patients with anorexia nervosa.•Results from food restriction studies in rodents match with observations in humans.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
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