Longitudinal Problematic Social Media Use in Students and Its Association with Negative Mental Health Outcomes.

Purpose: Social media has become increasingly part of our everyday lives and is influential in shaping the habits, sociability, and mental health of individuals, particularly among students. This study aimed to examine the relationship between changes over time in problematic social media use and mental health outcomes in students. We also investigated whether resilience and loneliness moderated the relationship between social media use and mental health.

Lonely and scrolling during the COVID-19 pandemic: understanding the problematic social media use and mental health link among university students.

Introduction: Undergraduate university students experienced many academic and non-academic stressors during the first year of the coronavirus (COVID-19) pandemic, putting them at a greater risk of negative mental health outcomes. Reports worldwide have shown high incidences of depressive, anxiety, and stress scores among university students at the beginning of the pandemic. Emerging evidence also suggests that to cope with the stress and loneliness of the pandemic, many youth and young adults increased the amount of time they spent on social media platforms.

Coping With the COVID-19 Pandemic: Examining Gender Differences in Stress and Mental Health Among University Students.

The COVID-19 pandemic has imposed a wide variety of unprecedented challenges, many of which appear to be disproportionately affecting the mental health and well-being of young adults. While there is evidence to suggest university students experience high rates of mental health disorders, less is known about the specific impacts of the COVID-19 pandemic on student mental health and how they are coping with this stress. To address this gap, we conducted an online study among undergraduate students ( = 366) to examine the impact of the COVID-19 pandemic on academics, social isolation, and mental health, as well as the extent to which they have been implementing a variety of coping strategies.

Exposure to Chronic Mild Stress Differentially Alters Corticotropin-Releasing Hormone and Arginine Vasopressin mRNA Expression in the Stress-Responsive Neurocircuitry of Male and Female Rats Prenatally Exposed to Alcohol.

Background: Prenatal alcohol exposure (PAE) results in dysregulation of the offspring hypothalamic-pituitary-adrenal (HPA) axis, increasing sensitivity to stressors and vulnerability to stress-related disorders. We have previously shown that exposure to chronic mild stress (CMS) in adulthood significantly increases anxiety-like behaviors (elevated plus maze) in PAE males and females compared to controls. To explore neurobiological mechanisms linking HPA dysregulation and altered anxiety-like behavior, we investigated neuropeptide (corticotropin-releasing hormone [CRH] and arginine vasopressin [AVP]) expression in brain areas involved in the stress neurocircuitry of animals from this previous behavioral study.

Neurocircuitry underlying stress and emotional regulation in animals prenatally exposed to alcohol and subjected to chronic mild stress in adulthood.

Individuals exposed to alcohol during gestation show higher rates of psychopathologies. The hyperresponsivity to stress induced by prenatal alcohol exposure (PAE) may be related to this increased rate of psychopathologies, especially because this population is more likely to be exposed to stressful environments throughout life. However, alcohol-induced changes in the overlapping neurocircuitries that underlie stress and the expression of psychopathologies are not fully understood.

Neurobiology of chronic mild stress: parallels to major depression.

The chronic mild (or unpredictable/variable) stress (CMS) model was developed as an animal model of depression more than 20 years ago. The foundation of this model was that following long-term exposure to a series of mild, but unpredictable stressors, animals would develop a state of impaired reward salience that was akin to the anhedonia observed in major depressive disorder. In the time since its inception, this model has also been used for a variety of studies examining neurobiological variables that are associated with depression, despite the fact that this model has never been critically examined to validate that the neurobiological changes induced by CMS are parallel to those documented in depressive disorder.

Prenatal alcohol exposure and chronic mild stress differentially alter depressive- and anxiety-like behaviors in male and female offspring.

Background: Fetal Alcohol Spectrum Disorder (FASD) is associated with numerous neurobehavioral alterations, as well as disabilities in a number of domains, including a high incidence of depression and anxiety disorders. Prenatal alcohol exposure (PAE) also alters hypothalamic-pituitary-adrenal (HPA) function, resulting in increased responsiveness to stressors and HPA dysregulation in adulthood. Interestingly, data suggest that pre-existing HPA abnormalities may be a major contributory factor to some forms of depression, particularly when an individual is exposed to stressors later in life.

Circadian phase and sex effects on depressive/anxiety-like behaviors and HPA axis responses to acute stress.

Circadian dysregulation in sleep pattern, mood, and hypothalamic-pituitary-adrenal (HPA) axis activity, often occurring in a sexually dimorphic manner, are characteristics of depression. However, the inter-relationships among circadian phase, HPA function, and depressive-like behaviors are not well understood. We investigated behavioral and neuroendocrine correlates of depressive/anxiety-like responses during diurnal ('light') and nocturnal ('dark') phases of the circadian rhythm in the open field (OF), elevated plus maze (EPM), forced swim (FST), and sucrose contrast (SC) tests.

Prenatal alcohol exposure: fetal programming and later life vulnerability to stress, depression and anxiety disorders.

Children with fetal alcohol spectrum disorder (FASD) exhibit cognitive, neuropsychological and behavioral problems, and numerous secondary disabilities including depression and anxiety disorders. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is common in depression/anxiety, reflected primarily in increased HPA tone or activity. Prenatal alcohol exposure (PAE) increases HPA tone and results in HPA dysregulation throughout life, paralleling many of the HPA changes in depression/anxiety.

Role of testosterone in mediating prenatal ethanol effects on hypothalamic-pituitary-adrenal activity in male rats.

Prenatal ethanol (E) exposure programs the fetal hypothalamic-pituitary-adrenal (HPA) and -gonadal (HPG) axes such that E rats show HPA hyperresponsiveness to stressors and altered HPG and reproductive function in adulthood. Importantly, prenatal ethanol may differentially alter stress responsiveness in adult male and female offspring compared to their control counterparts. To test the hypothesis that alterations in HPA activity in E males are mediated, at least in part, by ethanol-induced changes in the capacity of testosterone to regulate HPA activity, we explored dose-related effects of testosterone on HPA and HPG function in adult male offspring from prenatal E, pair-fed (PF) and ad libitum-fed control (C) dams.

Prenatal alcohol exposure increases vulnerability to stress and anxiety-like disorders in adulthood.

Children and adults with fetal alcohol spectrum disorder (FASD) have elevated rates of depression and anxiety disorders compared to control populations. The effects of prenatal alcohol exposure (PAE) on anxiety, locomotor activity, and hormonal reactivity in male and female rats tested on the elevated plus maze (EPM), a task commonly used to assess anxiety-like behaviors in rodents, were examined. Pregnant dams were assigned to PAE, pair-fed (PF), or ad libitum-fed control (C) groups.

Disrupting reconsolidation of conditioned withdrawal memories in the basolateral amygdala reduces suppression of heroin seeking in rats.

Recent data from our laboratory have demonstrated that appetitive drug memories undergo protein synthesis-dependent reconsolidation in the basolateral amygdala (BLA), an area important in the formation of emotional memories. We here investigated the importance of the BLA in the reconsolidation of opiate conditioned withdrawal memories. Rats with bilateral cannulas implanted in the BLA were trained to respond for heroin (0.

Motivational control of heroin seeking by conditioned stimuli associated with withdrawal and heroin taking by rats.

The authors investigated the impact of conditioned withdrawal on drug seeking by training rats to work for a heroin infusion on a seeking-taking schedule, which required responding on a seeking lever in order to gain the opportunity to self-administer the drug by a single response on a taking lever. Following the establishment of opiate dependence, a conditioned stimulus (CS) that had been previously paired with naloxone-precipitated withdrawal suppressed heroin seeking in extinction. However, when the rats had prior experience of heroin taking in the presence of the withdrawal CS, drug seeking was elevated in the presence of this stimulus.

Alcohol-induced impulsivity in rats: an effect of cue salience?

Rationale: There is a common assumption that alcohol produces impulsive behaviors, thereby increasing the preference for immediate over delayed rewards. An alternative explanation, provided by alcohol myopia theory, is that alcohol alters attentional processes such that intoxicated individuals respond exclusively to the most salient cues in their environment.

Objectives: We tested these two hypotheses in rats using standard (impulsivity) and modified (cue salience) versions of the delayed reinforcement task.

Early environmental experience alters baseline and ethanol-induced cognitive impulsivity: relationship to forebrain 5-HT1A receptor binding.

The relationship between impulsivity and drug abuse is poorly understood despite evidence that impulsive behaviour both predicts, and is a consequence of, drug use. Moreover, although there are clear individual differences in the propensity to addiction, this relationship has not been investigated with respect to impulsive behaviour. We tested whether early environmental experience would influence behavioural measures of impulsivity, and further, whether this experience would alter impulsive choice following ethanol intoxication.

Adolescent enrichment partially reverses the social isolation syndrome.

Early environmental experience produces profound neural and behavioural effects. For example, animals reared in isolation show increased anxiety, neophobia, and poorer performance in learning and spatial memory tasks. We investigated whether later enrichment reverses some or all of the deficits induced by isolation rearing.

Effects of acute and prolonged opiate abstinence on extinction behaviour in rats.

We examined the role of withdrawal in relapse to drug-seeking and drug-taking by testing the effects of opiate abstinence on extinction behaviour in rats trained to self-administer heroin. Male Long-Evans rats responded for IV heroin under a heterogeneous chain (VI 120 s; FR 1) schedule in which "seeking" responses preceded a "taking" response which produced a drug infusion. Responding was then measured in extinction during acute (6, 12, and 24 hr) and prolonged (3, 6, 12, and 25 day) abstinence.