Male and female mice respectively form stronger social aversive memories with same and different sex conspecifics.

Mice offer a wealth of opportunities for investigating brain circuits regulating multiple behaviors, largely due to their genetic tractability. Social behaviors are of translational relevance, considering both mice and humans are highly social mammals, and disruptions in human social behavior are key symptoms of myriad neuropsychiatric disorders. Stresses related to social experiences are particularly influential in the severity and maintenance of neuropsychiatric disorders like anxiety disorders, and trauma and stressor-related disorders.

Effects of the designer drug 4-methylamphetamine on core temperature and serotonin levels in the striatum and hippocampus of rats.

New psychoactive substances (NPS) are typically synthesized in clandestine laboratories in an attempt to chemically modify already federally regulated drugs in an effort to circumvent the law. Drugs derived from a phenethylamine pharmacophore, such as 4-chloroamphetamine and 3,4-methylenedioxymethamphetamine (MDMA), reliably induce thermogenesis and serotonergic deficits in the striatum and hippocampus of rodents. 4-methylamphetamine (4-MA), a relative newcomer to the NPS scene, was originally investigated in the mid-1900 s as a potential anorexigenic agent.

Heterotypic Stressors Unmask Behavioral Influences of PMAT Deficiency in Mice.

Certain life stressors having enduring physiological and behavioral consequences, in part by eliciting dramatic signaling shifts in monoamine neurotransmitters. High monoamine levels can overwhelm selective transporters like the serotonin transporter. This is when polyspecific transporters like plasma membrane monoamine transporter (PMAT, ) are hypothesized to contribute most to monoaminergic signaling regulation.

Heterotypic stressors unmask behavioral influences of PMAT deficiency in mice.

Certain life stressors having enduring physiological and behavioral consequences, in part by eliciting dramatic signaling shifts in monoamine neurotransmitters. High monoamine levels can overwhelm selective transporters like the serotonin transporter. This is when polyspecific transporters like plasma membrane monoamine transporter (PMAT, Slc29a4) are hypothesized to contribute most to monoaminergic signaling regulation.

Black representation in critical care randomized controlled trials: a meta-epidemiological study.

Purpose: The under-representation of Black people within critical care research limits the generalizability of randomized controlled trials (RCTs). This meta-epidemiologic study investigated the proportionate representation of Black people enrolled at USA and Canadian study sites from high impact critical care RCTs.

Source: We searched for critical care RCTs published in general medicine and intensive care unit (ICU) journals between 1 January 2016 and 31 December 2020.

Summarizing studies using constitutive genetic deficiency to investigate behavioural influences of uptake 2 monoamine transporters.

Burgeoning literature demonstrates that monoamine transporters with high transport capacity but lower substrate affinity (i.e., uptake 2) contribute meaningfully to regulation of monoamine neurotransmitter signalling.

Uncovering Functional Contributions of PMAT () to Monoamine Clearance Using Pharmacobehavioral Tools.

Plasma membrane monoamine transporter (PMAT, Slc29a4) transports monoamine neurotransmitters, including dopamine and serotonin, faster than more studied monoamine transporters, e.g., dopamine transporter (DAT), or serotonin transporter (SERT), but with ~400-600-fold less affinity.

Anxiety and stress over COVID-19 pandemic associated with increased eating.

Objective: Stressful experiences can dramatically affect eating. The relatively sudden, global emergence of the COVID-19 pandemic served as a massive stressor to virtually all people, regardless of infection status. This study hypothesized that actual and perceived stressors from the onset of the COVID-19 pandemic, in the categories of recurring disruptions, environmental threat, and social isolation would be positively associated with increased self-reported eating in the United States.

DRD4 polymorphism associated with greater positive affect in response to negative and neutral social stimuli.

Despite the robustness of DRD4 polymorphism associations with brain-based behavioral characteristics in candidate gene research, investigations have minimally explored associations between these polymorphisms and emotional responses. In particular, the prevalent single nucleotide polymorphism (SNP) -521C/T (rs1800955) in the promoter region of DRD4 remains unexplored relative to emotions. Here, two independent samples were evaluated using different emotion elicitation tasks involving social stimuli: Study 1 (N = 120) evoked positive and negative emotional responses to validated film clips; Study 2 (N = 122) utilized Cyberball to simulate social rejection and acceptance.

Salt as a non-caloric behavioral modifier: A review of evidence from pre-clinical studies.

Though excess salt intake is well-accepted as a dietary risk factor for cardiovascular diseases, relatively little has been explored about how it impacts behavior, despite the ubiquity of salt in modern diets. Given the challenges of manipulating salt intake in humans, non-human animals provide a more tractable means for evaluating behavioral sequelae of high salt. By describing what is known about the impact of elevated salt on behavior, this review highlights how underexplored salt's behavioral effects are.

High Salt Intake Lowers Behavioral Inhibition.

Stress-related neuropsychiatric (e.g., anxiety, depression) and cardiovascular diseases are frequently comorbid, though discerning the directionality of their association has been challenging.

Age- and Sex-Specific Plasticity in Dopamine Transporter Function Revealed by Food Restriction and Exercise in a Rat Activity-Based Anorexia Paradigm.

Eating disorders such as anorexia typically emerge during adolescence, are characterized by engagement in compulsive and detrimental behaviors, and are often comorbid with neuropsychiatric disorders and drug abuse. No effective treatments exist. Moreover, anorexia lacks adolescent animal models, contributing to a poor understanding of underlying age-specific neurophysiological disruptions.

Neuroinflammation Contributes to High Salt Intake-Augmented Neuronal Activation and Active Coping Responses to Acute Stress.

High dietary salt intake increases risk of stress-related neuropsychiatric disorders. Here, we explored the contribution of high dietary salt intake-induced neuroinflammation in key stress-responsive brain regions, the hypothalamic paraventricular nucleus and basolateral amygdala, in promoting exaggerated neuronal activation and coping behaviors in response to acute psychogenic stress. Mice that underwent high dietary salt intake exhibited increased active stress coping behaviors during and after an acute swim stress, and these were reduced by concurrent administration of minocycline, an inhibitor of microglial activation, without affecting body fluid hyperosmolality caused by high dietary salt intake.

Basolateral amygdala Thy1-expressing neurons facilitate the inhibition of contextual fear during consolidation, reconsolidation, and extinction.

Disrupted fear inhibition is a characteristic of many anxiety disorders. Investigations into the neural mechanisms responsible for inhibiting fear will improve understanding of the essential circuits involved, and facilitate development of treatments that promote their activity. Within the basolateral amygdala (BLA), Thy1-expressing neuron activity has been characterized by us and others as promoting fear inhibition to discrete fear cues by influencing consolidation of cued fear learning or cued fear extinction.

Extreme enhancement or depletion of serotonin transporter function and serotonin availability in autism spectrum disorder.

A variety of human and animal studies support the hypothesis that serotonin (5-hydroxytryptamine or 5-HT) system dysfunction is a contributing factor to the development of autism in some patients. However, many questions remain about how developmental manipulation of various components that influence 5-HT signaling (5-HT synthesis, transport, metabolism) persistently impair social behaviors. This review will summarize key aspects of central 5-HT function important for normal brain development, and review evidence implicating perinatal disruptions in 5-HT signaling in the pathophysiology of autism spectrum disorder.

Constitutive plasma membrane monoamine transporter (PMAT, Slc29a4) deficiency subtly affects anxiety-like and coping behaviours.

Originally, uptake-mediated termination of monoamine (e.g., serotonin and dopamine) signalling was believed to only occur via high-affinity, low-capacity transporters ("uptake ") such as the serotonin or dopamine transporters, respectively.

High salt intake enhances swim stress-induced PVN vasopressin cell activation and active stress coping.

Purpose: Stress contributes to many psychiatric disorders; however, responsivity to stressors can vary depending on previous or current stress exposure. Relatively innocuous heterotypic (differing in type) stressors can summate to result in exaggerated neuronal and behavioral responses. Here we investigated the ability of prior high dietary sodium chloride (salt) intake, a dehydrating osmotic stressor, to enhance neuronal and behavioral responses of mice to an acute psychogenic swim stress (SS).

A film set for the elicitation of emotion in research: A comprehensive catalog derived from four decades of investigation.

Emotions are highly influential to many psychological processes. Indeed, research employing emotional stimuli is rapidly escalating across the field of psychology. However, challenges remain regarding discrete evocation of frequently co-elicited emotions such as amusement and happiness, or anger and disgust.

Hippocampal GABA Receptors Constrain Generalized Contextual Fear.

Many anxiety disorders are characterized by generalization of fear responses to neutral or ambiguous stimuli. Therefore, a comprehensive understanding of the mechanisms contributing to generalized fear is essential for formulating successful treatments for anxiety disorders. Previous research shows that GABA-mediated presynaptic inhibition has a critical role in cued fear generalization, as animals with genetically deleted presynaptic GABA receptors cannot discriminate between CS+ and CS- tones.

A Novel Interaction between Tryptophan Hydroxylase 2 (TPH2) Gene Polymorphism (rs4570625) and BDNF Val66Met Predicts a High-Risk Emotional Phenotype in Healthy Subjects.

Poor inhibitory processing of negative emotional content is central to many psychiatric disorders, including depression and anxiety. Moreover, increasing evidence suggests that core aspects of emotion-inhibitory processing are largely inherited and as such may represent a key intermediate or risk-related phenotype for common affective diseases (e.g.

Perspectives on fear generalization and its implications for emotional disorders.

Although generalization to conditioned stimuli is not a new phenomenon, renewed interest in understanding its biological underpinning has stemmed from its association with a number of anxiety disorders. Generalization as it relates to fear processing is a temporally dynamic process in which animals, including humans, display fear in response to similar yet distinct cues or contexts as the time between training and testing increases. This Review surveys the literature on contextual fear generalization and its relation to several views of memory, including systems consolidation, forgetting, and transformation hypothesis, which differentially implicate roles of the hippocampus and neocortex in memory consolidation and retrieval.

Corticosterone may interact with peripubertal development to shape adult resistance to social defeat.

Studies of social stress in adult mice have revealed two distinct defeat-responsive behavioral phenotypes; "susceptible" and "resistant," characterized by social avoidance and social interaction, respectively. Typically, these phenotypes are observed at least 1day after the last defeat in adults, but may extend up to 30days later. The current study examined the impact of peripubertal social defeat on immediate (1day) and adult (30day) social stress phenotypes and neuroendocrine function in male C57BL/6 mice.

Activity of the anterior cingulate cortex and ventral hippocampus underlie increases in contextual fear generalization.

Memories for context become less specific with time resulting in animals generalizing fear from training contexts to novel contexts. Though much attention has been given to the neural structures that underlie the long-term consolidation of a context fear memory, very little is known about the mechanisms responsible for the increase in fear generalization that occurs as the memory ages. Here, we examine the neural pattern of activation underlying the expression of a generalized context fear memory in male C57BL/6J mice.

Grin1 deletion in CRF neurons sex-dependently enhances fear, sociability, and social stress responsivity.

The corticotropin releasing factor (CRF) system plays a critical role in responses to stressful stimuli, and is expressed in many areas of the brain involved in processing fear, anxiety, and social behaviors. To better understand the mechanisms by which the CRF system modulates responses to stressful events and social stimuli, we employed a mouse model that selectively disrupts NMDA receptor function via NMDA receptor subunit NR1 (Grin1) knockout specifically in Cre-expressing CRF neurons. These animals (Cre+/(fGrin1+)) were compared with littermates lacking Cre expression (Cre-/(fGrin1+)).