Fear of breast cancer among young Spanish women: Factor structure and psychometric properties of the Champion breast cancer fear scale.

Heightened fear of breast cancer (FBC) has been linked to increased distress following breast cancer diagnosis and to avoidance of mammography screening. To our knowledge, however, no studies have examined the nature of FBC exclusively among young females, even though they are overrepresented in media stories of breast cancer. Given that no instruments are available to assess FBC in the Spanish language, we sought to 1) evaluate the psychometric properties and factor structure of the Champion Breast Cancer Fear Scale (CBCFS), and 2) offer preliminary data on the nature of FBC among young women. Participants (N = 442, mean age = 21.17, range 17-35) completed the translated CBCFS (CBCFS-es) and the Spanish version of the Short Health Anxiety Inventory. The CBCFS-es demonstrated good concurrent validity, internal consistency, and test-retest reliability. Confirmatory factor analysis showed adequate fit to a one-factor solution. The majority of participants reported considerably high levels of FBC, as 25.34% and 59.73% of them scored above the moderate- and high-FBC cut-offs, respectively. Moreover, FBC could not be explained by general concerns regarding health and illness, given that levels of health anxiety were low. Implications for health education, research, and clinical practice are discussed.

Ethical values in college education: a mixed-methods pilot study to assess health sciences students' perceptions.

BACKGROUND: Society demands a university education grounded on ethical principles. Education in ethics values is responsibility of universities but will not be viable unless also adopted by directly responsible agents, the teachers who work with the students. For this reason, our primary research objective was to conduct an in-depth analysis of how Health Sciences students self-perceive the ethical dimension. METHODS: A mixed research methodology with two phases, qualitative and quantitative, allowed us to address our research question from two complementary viewpoints. Conversational interviews were conducted in an intentional and purposive sample to identify a wide range of discursive representations. A questionnaire was designed based on previous studies and the topics of qualitative research. The response format for the questionnaire followed a Likert scale and modulators such as sex, age, degree and the score of a social desirability test were examined. RESULTS: After 24 conversational interviews, three main thematic blocks (coinciding with the three subscales of the questionnaire) were identified: "attitudes for harmony in human relations", "construction of the self" and "rules and regulations". A total of 246 students completed a questionnaire with 39 items. The total scores ranged from 93 to 152 points, with an average score of 122.72 ± 10.64 points. Responsibility, the basic rules of education and respect were perceived as the two most important values, whereas solidarity and social participation as the least important. Results showed a significant positive linear correlation between total score on the questionnaire and age and social desirability. Age was also a significant predictor for the total score and the subscale score "rules and regulations". The students´ responses seemed to be conditioned by the degree of social desirability that they present. CONCLUSIONS: The ad-hoc questionnaire captured the maintenance of high ethical values in our college undergraduate students, which may be directly related to enhanced social desirability. The scores obtained on the questionnaire were correlated with the students' age, which may indicate that values might tend to acquire progressively more importance as students grow older. Further research is warranted to delve deeper on the determinants of professionalism and ethical decision-making in college students.

Unique treatment potential of cannabidiol for the prevention of relapse to drug use: preclinical proof of principle.

Cannabidiol (CBD), the major non-psychoactive constituent of Cannabis sativa, has received attention for therapeutic potential in treating neurologic and psychiatric disorders. Recently, CBD has also been explored for potential in treating drug addiction. Substance use disorders are chronically relapsing conditions and relapse risk persists for multiple reasons including craving induced by drug contexts, susceptibility to stress, elevated anxiety, and impaired impulse control. Here, we evaluated the "anti-relapse" potential of a transdermal CBD preparation in animal models of drug seeking, anxiety and impulsivity. Rats with alcohol or cocaine self-administration histories received transdermal CBD at 24 h intervals for 7 days and were tested for context and stress-induced reinstatement, as well as experimental anxiety on the elevated plus maze. Effects on impulsive behavior were established using a delay-discounting task following recovery from a 7-day dependence-inducing alcohol intoxication regimen. CBD attenuated context-induced and stress-induced drug seeking without tolerance, sedative effects, or interference with normal motivated behavior. Following treatment termination, reinstatement remained attenuated up to ≈5 months although plasma and brain CBD levels remained detectable only for 3 days. CBD also reduced experimental anxiety and prevented the development of high impulsivity in rats with an alcohol dependence history. The results provide proof of principle supporting potential of CBD in relapse prevention along two dimensions: beneficial actions across several vulnerability states and long-lasting effects with only brief treatment. The findings also inform the ongoing medical marijuana debate concerning medical benefits of non-psychoactive cannabinoids and their promise for development and use as therapeutics.

Nicotine causes opposite effects on alcohol intake: Evidence in an animal experimental model of abstinence and relapse from alcohol.

INTRODUCTION: Tobacco and alcohol are frequently co-abused, but the mechanism underlying this interaction is not well understood. Experimental data on the influence of nicotine upon alcohol consumption are not conclusive. METHODS: To elucidate the role of nicotine in alcohol consumption, alcohol-experienced rats were submitted to consecutive phases of forced abstinence from alcohol, followed by relapses, in which their alcohol consumption was measured in a 2-bottle choice test. Rats were assigned to one of 4 groups: (a) "Control," which received daily saline injections during both the abstinence and relapse phases, (b) "Nic. All," which received nicotine injections during both phases, (c) "Nic. Abst.," which received nicotine during the abstinence phase only, and (d) "Nic. Rel.," which received nicotine during the relapse phase only. The nicotine doses (0.4, 0.6, and 0.8 mg/kg) were administered in an escalating fashion. Alcohol consumption was measured 3 times per day. RESULTS: Overall, the rats treated daily with nicotine during both the abstinence and relapse phases (Nic. All) significantly increased their alcohol intake compared with the rats treated daily with vehicle alone (Control). Similarly, rats treated with nicotine during the alcohol abstinence phase only (Nic. Abst.) also increased their alcohol consumption. However, rats treated with nicotine during the alcohol relapse phase only (Nic. Rel.) decreased their alcohol intake. In addition, a more exhaustive analysis showed critical differences in patterns of alcohol consumption during the first hour and the first day of alcohol access. DISCUSSION: Taken together, we provide evidence that depending on the timing of exposure, the same dose of nicotine can have opposite effects on alcohol consumption.

Administration of MDMA to ethanol-deprived rats increases ethanol operant self-administration and dopamine release during reinstatement.

Recreational use of (±)-3,4-methylenedioxymethamphetamine (MDMA, ecstasy) is often associated with other drugs, among which ethanol (EtOH) is one of the most common. However, little is known about how neurochemical sensitization produced by MDMA can modulate EtOH abuse. In this study we used EtOH operant self-administration tasks to investigate the effect of several low doses (0.33, 1.0 and 3.0 mg/kg) of MDMA in Dark Agouti rats. Motor activity was recorded after each MDMA administration. Changes in extracellular dopamine in the nucleus accumbens following a single EtOH injection (1.5 g/kg i.p.) were measured using intracerebral microdialysis in vivo after 1 wk of abstinence from EtOH, in order to mimic the dopaminergic response associated with reinstatement into EtOH consumption. Animals exposed to higher doses of MDMA (1.0 and 3.0 mg/kg) showed significantly enhanced EtOH self-administration during reinstatement and an increased EtOH-induced dopamine efflux. MDMA treatment acutely elevated motor activity after each administration in a dose-dependent manner. These findings suggest that repeated administration of MDMA, a relatively common drug of abuse, even at low doses, can alter subsequent vulnerability to EtOH consumption.

The pharmacology of the endocannabinoid system: functional and structural interactions with other neurotransmitter systems and their repercussions in behavioral addiction.

Addiction is a chronic, recurring and complex disorder. It is characterized by anomalous behaviors that are linked to permanent or long-lasting neurobiological alterations. Furthermore, the endocannabinoid system has a crucial role in mediating neurotransmitter release as one of the main neuromodulators of the mammalian central nervous system. The purpose of the present review is to instruct readers about the functional and structural interactions between the endocannabinoid system and the main neurotransmitter systems of the central nervous system in the context of drug addiction. With this aim, we have systematically reviewed the main findings of most of the existing literature that explores cross-talk in the five brain areas that are most traditionally implicated in addiction: amygdala, prefrontal cortex, nucleus accumbens, hippocampus and ventral tegmental area (VTA). The neurotransmission systems influenced by the pharmacology of the endocannabinoid system in these brain areas, which are reviewed here, are gamma-aminobutyric acid (GABA), glutamate, the main biogenic amines (dopamine, noradrenaline and serotonin), acetylcholine and opioids. We show that all of these neurotransmitter systems can be modulated differentially in each brain area by the activation or deactivation of cannabinoid CB1 brain receptors. Specifically, most of the studies relate to the hippocampus and nucleus accumbens. Moreover, the neurotransmitter with the fewest number of related studies is acetylcholine (excepting in the hippocampus), whereas there is a large number that evaluates GABA, glutamate and dopamine. Finally, we propose a possible interpretation of the role of the endocannabinoid system in the phenomenon of addiction.

Changed accumbal responsiveness to alcohol in rats pre-treated with nicotine or the cannabinoid receptor agonist WIN 55,212-2.

Alcohol, nicotine, and cannabinoid acutely increase the activity of the mesolimbic dopamine (DA) pathway. Although polysubstance consumption is a common pattern of abuse in humans, little is known about dopamine release following pre-exposure to these drugs. The purpose of this study was to test whether alcohol-induced dopamine release into the nucleus accumbens (NAc) shell is modified by different pre-treatments: water (i.g.), alcohol (1 g/kg, i.g.), nicotine (0.4 mg/kg, s.c.), and WIN 55,212-2 (1 mg/kg, s.c.). Male Wistar rats were treated (i.g.) for 14 days with either water or alcohol. In the following 5 days rats were injected (s.c.) with vehicle, nicotine, or WIN 55,212-2. Finally, a cannula was surgically implanted into the NAc shell and alcohol-induced extracellular dopamine release was monitored in freely moving rats. Alcohol (1 g/kg; i.g.) only increased the release of dopamine when animals were previously treated with water. This DA increase was markedly inhibited by (subchronic) treatment (5 days) with nicotine or WIN 55-212-2 as well as by previous (chronic) exposure to alcohol (14 days). These data demonstrate that pre-treatment with nicotine and the cannabinoid agonist WIN 55,212-2 is able to change the sensitivity of the NAc shell in response to a moderate dose of alcohol. Therefore, cannabinoid and nicotine exposure may have important implications on the rewarding effects of alcohol, because these drugs lead to long-lasting changes in accumbal dopamine transmission.

Effects of the cannabinoid CB1 receptor antagonist rimonabant on distinct measures of impulsive behavior in rats.

RATIONALE: Pathological impulsivity is a prominent feature in several psychiatric disorders, but detailed understanding of the specific neuronal processes underlying impulsive behavior is as yet lacking. OBJECTIVES: As recent findings have suggested involvement of the brain cannabinoid system in impulsivity, the present study aimed at further elucidating the role of cannabinoid CB(1) receptor activation in distinct measures of impulsive behavior. MATERIALS AND METHODS: The effects of the selective cannabinoid CB(1) receptor antagonist, rimonabant (SR141716A) and agonist WIN55,212-2 were tested in various measures of impulsive behavior, namely, inhibitory control in a five-choice serial reaction time task (5-CSRTT), impulsive choice in a delayed reward paradigm, and response inhibition in a stop-signal paradigm. RESULTS: In the 5-CSRTT, SR141716A dose-dependently improved inhibitory control by decreasing the number of premature responses. Furthermore, SR141716A slightly improved attentional function, increased correct response latency, but did not affect other parameters. The CB(1) receptor agonist WIN55,212-2 did not change inhibitory control in the 5-CSRTT and only increased response latencies and errors of omissions. Coadministration of WIN55,212-2 prevented the effects of SR141716A on inhibitory control in the 5-CSRTT. Impulsive choice and response inhibition were not affected by SR141716A at any dose, whereas WIN55,212-2 slightly impaired response inhibition but did not change impulsive choice. CONCLUSIONS: The present data suggest that particularly the endocannabinoid system seems involved in some measures of impulsivity and provides further evidence for the existence of distinct forms of impulsivity that can be pharmacologically dissociated.

Subchronic cannabinoid agonist (WIN 55,212-2) treatment during cocaine abstinence alters subsequent cocaine seeking behavior.

The co-abuse of marijuana with cocaine is widespread, but it has not been until recently that the relationship between the behavioral effects of cannabinoids and cocaine has begun to be unveiled in animal models. Male Wistar rats were trained to intravenously self-administer cocaine until a stable baseline was reached. Rats then were subjected to a 5-day cocaine deprivation period during which they were treated daily with the cannabinoid receptor agonist WIN 55,212-2 (R-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate) (0, 0.3, 1, and 3 mg/kg; i.p.). Following this subchronic treatment, rats were tested, in counterbalanced order, in a test of anxiety (elevated plus-maze), as well as extinction and cue-induced reinstatement tests, the latter conducted according to a between-within procedure. Subchronic administration of WIN 55,212-2 was found to produce dose-dependent alterations of performance in the extinction, reinstatement, and anxiety tests with the lowest dose of WIN 55,212-2 producing the highest resistance to extinction and reinstatement, and the highest dose of WIN 55,212-2 producing the highest anxiolytic activity. Subchronic treatment with WIN 55,212-2 in rats without a history of cocaine self-administration did not affect anxiety levels. The results suggest an important role of the cannabinoid system in neuronal processes underlying cocaine seeking behavior. However, further studies will be necessary to understand possible implications of these findings for a role of the cannabinoid system as a treatment target for human cocaine abuse.

The CB1 cannabinoid receptor antagonist rimonabant chronically prevents the nicotine-induced relapse to alcohol.

Preclinical and clinical research shows that the cannabinoid brain receptor type 1 (CB(1)) modulates alcohol- and nicotine-related behaviors. Throughout the nicotine-induced relapse to alcohol, the rats were pre-treated for 10 days with the CB(1) cannabinoid receptor antagonist rimonabant (0, 0.03, 0.3 and 3.0 mg/kg i.p.). In this condition, a long-lasting nicotine-induced relapse to alcohol was observed, and this effect was reversed in a dose-dependent manner with rimonabant. Surprisingly, rats that were not exposed to nicotine developed tolerance to the effects of rimonabant from the sixth day. Also, 3.0 mg/kg of rimonabant reduced the responses for sucrose. Evaluation in the Elevated Plus-Maze after nicotine treatment did not reveal anxiogenic effects. Finally, at the conclusion of rimonabant treatment, a rapid reinstatement of alcohol consumption was detected. These results suggest that rimonabant can prevent the relapse to alcohol, even when an interaction with nicotine exists-the most frequent situation in human alcohol abuse.

Long-lasting increase of alcohol relapse by the cannabinoid receptor agonist WIN 55,212-2 during alcohol deprivation.

Alcoholism is characterized by successive relapses. Recent data have shown a cross-talk between the cannabinoid system and ethanol. In this study, male Wistar rats with a limited (30 min sessions), intermittent, and extended background of alcohol operant self-administration were used. The relapse to alcohol after 1 week of alcohol deprivation was evaluated. Two weeks later, the animals were treated with the cannabinoid agonist WIN 55,212-2 (R-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate) (0, 0.4, 2.0, and 10.0 mg/kg, s.c.) during a similar alcohol deprivation period, and alcohol relapse during 2 weeks was assessed. A conditioned place preference (CPP) paradigm was used to study the rewarding properties of the cannabinoid agonist. Locomotor activity was also recorded. All doses of WIN 55,212-2 produced aversion in the CPP paradigm. The doses of 2.0 and 10.0 mg/kg resulted in an important suppression of spontaneous locomotor activity and a progressive weight loss during the next 2 weeks. The single alcohol deprivation was followed by a transient increase in their responding for alcohol from a range of 20-24 lever presses at baseline to a range of 38-48 responses in the first and second days (alcohol deprivation effect). However, the administration of WIN 55,212-2 during ethanol deprivation produced similar increased responses for alcohol but in a long-term way (at least over 2 weeks). These findings suggest that noncontingent chronic exposure to cannabinoids during alcohol deprivation can potentiate the relapse into alcohol use, indicating that functional changes in the cannabinoid brain receptor may play a key role in ethanol relapse.