Adolescence: physical changes and neurological development.

This article provides a brief overview of adolescence. It highlights the key physical changes related to puberty and identifies the latest understanding of neurological development in young people. It is also recognised, within the article, that this period of rapid change can have an impact on social and emotional wellbeing. There are conditions that typically have an onset during adolescence, examples of this are offered. The term 'adolescence' is used to describe the stage of development and growth and 'young people' is used throughout to refer to the individuals.

Effects of chronic stress on reinstatement of palatable food seeking: Sex differences and relationship to trait anxiety.

Previous research in our lab has established a causal role for chronic stress exposure in subsequent increases in relapse-like behaviors in male rats with a history of palatable food self-administration. Given that many of the neurobehavioral consequences of stress are sex dependent, we aimed to determine whether sex differences exist with regard to the effects of chronic stress on relapse. Additionally, because high trait anxiety confers vulnerability to stress-related disorders, we examined whether individual differences in trait anxiety were related to differences in relapse-like behavior after chronic stress exposure. Following elevated plus maze testing for classification into high- or low-anxiety phenotypes, male and female rats responded for highly palatable food pellets. During subsequent extinction training, stress was manipulated (0 or 90 min restraint/day for 7 days). Rats were then tested for cue- and pellet priming-induced reinstatement of palatable food seeking. Results showed that female rats displayed higher levels of responding during cue-induced reinstatement tests compared to males, and that a history of chronic stress caused an attenuation of cue-induced reinstatement in female, but not male, rats. Regarding pellet priming-induced reinstatement, there was a three-way interaction such that neither stress history nor anxiety phenotype was related to reinstatement in females, but a history of stress in males caused increased and decreased responding in low- and high-anxiety rats, respectively. These results suggest that biological sex and trait anxiety level may help to explain differences in vulnerability to relapse among individuals exposed to chronic stress. Such information may be useful in designing more personalized and effective treatments for obesity and eating disorders.

Chronic restraint stress during withdrawal increases vulnerability to drug priming-induced cocaine seeking via a dopamine D1-like receptor-mediated mechanism.

BACKGROUND: A major obstacle in the treatment of individuals with cocaine addiction is their high propensity for relapse. Although the clinical scenario of acute stress-induced relapse has been well studied in animal models, few pre-clinical studies have investigated the role of chronic stress in relapse or the interaction between chronic stress and other relapse triggers. METHODS: We tested the effect of chronic restraint stress on cocaine seeking in rats using both extinction- and abstinence-based animal relapse models. Rats were trained to press a lever for I.V. cocaine infusions (0.50 mg/kg/infusion) paired with a discrete tone + light cue in daily 3-h sessions. Following self-administration, rats were exposed to a chronic restraint stress procedure (3 h/day) or control procedure (unstressed) during the first seven days of a 13-day extinction period during which lever presses had no programmed consequences. This was followed by cue- and cocaine priming-induced drug seeking tests. In a separate group of rats, cocaine seeking was assessed during forced abstinence both before and after the same chronic stress procedure. RESULTS: A history of chronic restraint stress was associated with increased cocaine priming-induced drug seeking, an effect attenuated by co-administration of SCH-23390 (10.0 µg/kg; i.p.), a dopamine D1-like receptor antagonist, with daily restraint. Repeated SCH-23390 administration but not stress during extinction increased cue-induced reinstatement. CONCLUSIONS: Exposure to chronic stress during early withdrawal may confer lasting vulnerability to some types of relapse, and dopamine D1-like receptors appear to mediate both chronic stress effects on cocaine seeking and extinction of cocaine seeking.

Chronic restraint stress causes a delayed increase in responding for palatable food cues during forced abstinence via a dopamine D1-like receptor-mediated mechanism.

Relapse to unhealthy eating habits in dieters is often triggered by stress. Animal models, moreover, have confirmed a causal role for acute stress in relapse. The role of chronic stress in relapse vulnerability, however, has received relatively little attention. Therefore, in the present study, we used an abstinence-based relapse model in rats to test the hypothesis that exposure to chronic stress increases subsequent relapse vulnerability. Rats were trained to press a lever for highly palatable food reinforcers in daily 3-h sessions and then tested for food seeking (i.e., responding for food associated cues) both before and after an acute or chronic restraint stress procedure (3h/day×1day or 10days, respectively) or control procedure (unstressed). The second food seeking test was conducted either 1day or 7days after the last restraint. Because chronic stress causes dopamine D1-like receptor-mediated alterations in prefrontal cortex (a relapse node), we also assessed dopaminergic involvement by administering either SCH-23390 (10.0µg/kg; i.p.), a dopamine D1-like receptor antagonist, or vehicle prior to daily treatments. Results showed that chronically, but not acutely, stressed rats displayed increased food seeking 7days, but not 1day, after the last restraint. Importantly, SCH-23390 combined with chronic stress reversed this effect. These results suggest that drugs targeting D1-like receptors during chronic stress may help to prevent future relapse in dieters.

Effects of repeated yohimbine administration on reinstatement of palatable food seeking: involvement of dopamine D1 -like receptors and food-associated cues.

Acute exposure to the pharmacological stressor yohimbine induces relapse to both food and drug seeking in a rat model. However, no systematic studies on the effects of chronic stress on relapse have been conducted. Because chronic stress causes changes in dopamine D1 -like receptor-mediated transmission in prefrontal cortex (a relapse node), we tested the hypothesis that chronic exposure to stress increases vulnerability to relapse via dopamine-mediated mechanisms. Additionally, to determine the role of food-conditioned cues in reinstatement of food seeking, we made discrete food-paired cues either available (CS Present) or not available (CS Absent) during extinction and reinstatement testing. Rats responded for palatable food reinforcers in daily 3-hour sessions, and the behavior was extinguished. To model chronic stress, rats were injected daily with yohimbine (0.0, 2.5, or 5.0 mg/kg; i.p.) during the first 7 days of extinction. Injections were combined with SCH-23390 (0.0, 5.0, or 10.0 µg/kg; i.p.), a D1 -like receptor antagonist. Rats were then tested for reinstatement of food seeking triggered by acute yohimbine (0.0, 1.0, or 2.0 mg/kg; i.p.) and pellet priming. Rats treated previously with chronic yohimbine displayed increased responding following acute yohimbine priming relative to non-chronically stressed rats, but in the CS Absent condition only. Conversely, the lower dose of chronic yohimbine caused an increase in pellet-primed reinstatement, but this effect was more pronounced in the CS Present condition. Importantly, SCH-23390 combined with repeated yohimbine injections attenuated these effects. Thus, chronic stress may increase vulnerability to relapse under specific circumstances via a dopamine D1 -like receptor-mediated mechanism.