Interaction between serotonin 5-HT1A receptors and β-endorphins modulates antidepressant response

Interactions between serotonergic and the endogenous opioid systems have been suggested to be involved in the etiopathogenesis of depression and in the mechanism of action of antidepressants. Activation of serotonin 5-HT 1A receptors has been shown to increase plasma β-endorphin (β-END) levels in animal studies and in healthy humans. Objectives: To assess interaction abnormalities between 5-HT 1A receptors and the endogenous opioid system in patients with major depression and the possible modulating effect of citalopram. Methods: The β-END response to the 5-HT 1A receptor agonist, buspirone (30 mg), was measured in 30 patients with major depression and in 30 age-and sex-matched healthy controls before and after an 8-week treatment with citalopram. Pre-treatment score of the Hamilton Rating Scale for Depression (HRSD) was ≥17. Antidepressant response was defined by a 50% decrease in the HRSD. Pre-and post-treatment maximum peak response (Δmax) and the area under the curve (AUC) of β-END response were compared. Three time points were measured (60, 90 and 120 min). We also examined the correlations between the β-END response and the antidepressant response. Buspirone plasma levels were not measured. Results: At baseline, β-END response was similar in patients and controls. After 8 weeks of citalopram treatment depressed patients showed a significant decrease in the β-END response (Δmax: p b .001; AUC: p b .001). A significant correlation between the β-END reduction in the response and the reduction in the HRSD score (r =.656; p b .001) was observed. Conclusions: Changes in interaction between 5-HT 1A receptor system and the endogenous opioid system may play a role both in the mechanism of action and response to antidepressant drugs

Clasificación de ecorregiones y determinación de sitio y condición : manual de aplicación a municipios y predios rurales

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Childhood abuse, the BDNF-Val66Met polymorphism and adult psychotic-like experiences

Background The well-established relationship between childhood adversity and psychosis is likely to involve other factors such as genetic variants that can help us to understand why not everyone exposed to adverse events develops psychotic symptoms later in life. Aims We investigated the influence of childhood abuse and neglect on positive and negative psychotic-like experiences in adulthood and the potential moderating effect of the BDNF-Val66Met polymorphism. Method Psychotic-like experiences and childhood adversity were assessed in 533 individuals from the general population. Results Childhood abuse showed a strong independent effect on the positive dimension of psychotic-like experiences (β = 0.16, s.e. = 0.05, P = 0.002). Furthermore, this association was moderated by the BDNF-Val66Met polymorphism (β = 0.27, s.e. = 0.10, P = 0.004). Conclusions Individuals exposed to childhood abuse are more likely to report positive psychotic-like experiences. Met carriers reported more positive psychotic-like experiences when exposed to childhood abuse than did individuals carrying the Val/Val genotype. Therefore, the observed gene-environment interaction effect may be partially responsible for individual variation in response to childhood abuse

Childhood abuse, the BDNF-Val66Met polymorphism and adult psychotic-like experiences

Background The well-established relationship between childhood adversity and psychosis is likely to involve other factors such as genetic variants that can help us to understand why not everyone exposed to adverse events develops psychotic symptoms later in life. Aims We investigated the influence of childhood abuse and neglect on positive and negative psychotic-like experiences in adulthood and the potential moderating effect of the BDNF-Val66Met polymorphism. Method Psychotic-like experiences and childhood adversity were assessed in 533 individuals from the general population. Results Childhood abuse showed a strong independent effect on the positive dimension of psychotic-like experiences (β = 0.16, s.e. = 0.05, P = 0.002). Furthermore, this association was moderated by the BDNF-Val66Met polymorphism (β = 0.27, s.e. = 0.10, P = 0.004). Conclusions Individuals exposed to childhood abuse are more likely to report positive psychotic-like experiences. Met carriers reported more positive psychotic-like experiences when exposed to childhood abuse than did individuals carrying the Val/Val genotype. Therefore, the observed gene-environment interaction effect may be partially responsible for individual variation in response to childhood abuse