1,720,984 research outputs found
Sleep and the pharmacotherapy of alcohol use disorder: unfortunate bedfellows. A systematic review with meta-analysis
No full textBackground: Sleep disorders are commonly associated with acute and chronic use of alcohol, and with abstinence. To date, there are four approved drugs to treat Alcohol Use Disorder (AUD): disulfiram, acamprosate, naltrexone and nalmefene. These AUD therapies reduce the craving and risk of relapse into heavy drinking, but little is known about their effect on sleep. As recent evidences indicate a crucial role of sleep disorders in AUD, claiming that sleep problems may trigger alcohol abuse and relapses, it is fundamental to clarify the impact of those drugs on the sleep quality of AUD patients. This systematic review aims to answer the question: how does the pharmacotherapy for AUD affect sleep?
Methods: We searched PubMed, EMBASE, CINAHL plus, Cochrane and SCOPUS using sleep- and AUD pharmacotherapy- related keywords. The articles included were appraised using the CASP checklists and the risk of bias was assessed following the Cochrane Risk of Bias assessment tool. Finally, we pooled sleep outcomes in a meta-analysis to measure the overall effect.
Results and conclusion: We included 26 studies: only three studies focused on sleep as a main outcome, two with polysomnography (objective measurement) and one with subjective self-reported sleep, while all the other studies reported sleep problems among the adverse effects (subjective report). The only study available on disulfiram showed reduced REM sleep. Acamprosate showed no/little effect on self-reported sleep, but improved sleep continuity and architecture measured by polysomnography. The two opioidergic drugs naltrexone and nalmefene had mainly detrimental effect on sleep, giving increased insomnia and/or somnolence compared with placebo, although not always significant. The meta-analysis confirmed significantly increased somnolence and insomnia in the naltrexone group, compared with the placebo.
Overall, the currently available evidences show more sleep problems with the opioidergic drugs (especially naltrexone), while acamprosate seems to be well tolerated or even beneficial. Acamprosate might be a more suitable choice when patients with AUD report sleep problems. Due to the paucity of information available, and with the majority of results being subjective, more research on this topic is needed to further inform the clinical practice, ideally with more objective measurements such as polysomnography
Long-term imipramine withdrawal induces a depressive-like behaviour in the forced swimming test
No full textChronic antidepressant treatments enhance dopaminergic neurotransmission in the mesolimbic dopamine system. We suggested that this potentiation might underlie both the antidepressant therapeutic effect and the antidepressant-induced switch from depression to mania. In a recent study we have shown a reversal of the imipramine-induced dopaminergic supersensitivity after 40 days of chronic imipramine withdrawal. We interpreted this result suggesting that the mood-switches observed in bipolar patients following antidepressant treatment and subsequent withdrawal, i.e. mania followed by rebound depression, might depend upon parallel changes in the mesolimbic dopamine system sensitivity. On this basis, one might predict a depressive-like behaviour after long-term interruption of a chronic treatment with imipramine. To test this hypothesis we examined the behaviour of rats treated with chronic imipramine 40 days after treatment interruption in an animal model of depression, the forced swimming test. The results show that animals treated with chronic imipramine, 40 days after treatment interruption, display a depressive-like behaviour in the forced swimming test, as indicated by their increased immobility with respect to the control group
Chronic valproate fails to prevent imipramine-induced behavioural sensitization to the dopamine D2-like receptor agonist quinpirole
No full textBased on experimental evidence suggesting a relationship between dopamine and mania, we proposed the antidepressant-induced dopaminergic supersensitivity as a model of antidepressant-related mania. We have previously shown the ability of carbamazepine, but not lithium, to prevent this phenomenon. Here we show that sodium valproate (50mg/kg/day for 3weeks) fails to prevent imipramine (20mg/kg/day for 3weeks)-induced sensitization to the locomotor response to the dopamine D2-like receptor agonist quinpirole (0.15mg/kg). Since lithium, carbamazepine and valproate are all considered poorly effective in the treatment of antidepressant-related mania, the validity of the proposed model should be disproved by the carbamazepine results, to which, however, a pharmacokinetic mechanism might have concurred
Nicotine-induced increase of dopaminergic mesoaccumbal neuron activity is prevented by acute restraint stress. In vivo electrophysiology in rats
No full textTwo-day-old newborns learn to discriminate accelerated-decelerated biological kinematics from constant velocity motion
No full textAlready in uterus the hand moves with the typical accelerated-decelerated kinematics of goal-directed actions and, from the twenty-second week of pregnancy, the unborn shows the ability to modulate the velocity of the movement depending on the nature of the target. According to the direct matching hypothesis, this motor knowledge may be sufficient to attune neonates' motion perception-like adults'-to biological kinematics. Using dots configuration motions which varied with respect to the kinematics of goal-directed actions, we observed that two-day-old human newborns did not show any spontaneous preference for either biological accelerated-decelerated motion or non-biological constant velocity motion when these were simultaneously presented in a standard preferential looking paradigm. In contrast, newborns preferred the biological kinematics after the repeated visual presentation of the different motions in a standard infant-control visual habituation paradigm. We propose that present results indicate that the relationship between perception and action does not require only action development but also the accumulation of sufficient perceptual experience. They also suggest a fast plasticity of the sensorimotor system in linking an already acquired motor knowledge with a newly experienced congruent visual stimulation
Dopamine D3 receptor antisense ODN potentiates imipramine-induced dopaminergic behavioural supersensitivity
No full textChronic antidepressant treatments result in the potentiation of dopaminergic transmission in the mesolimbic dopamine system revealed as an increased motor response to dopamine D2-like agonists. On thebasis of the involvement of this system in the control of motivation and reward-related behaviour, which are impaired in depression, it has been suggested that such supersensitivity might play an important role in the mechanism of action of these drugs. Several studies have provided evidence suggesting a role of dopamine D3 receptors in mediating antidepressant-induced increased motor response to dopamine agonists. To test this hypothesis, we studied the effect of the intracerebroventricular infusion of a dopamine D3 receptor antisense oligodeoxynucleotide (10 lg/3 ll, 2–3 daily injections) on the expression of imipramine-induced supersensitivity (20 mg/kg daily intraperitoneal injections for 21 days) to the motor effect of the dopamine D2-like receptor agonist quinpirole (a single 0.3 mg/kg subcutaneous injection 24–48 h after imipramine withdrawal). The results show that a treatment previously shown to reduce the synthesis of dopamine D3 receptors, rather than resulting in an inhibitory effect, potentiated the ability of imipramine to induce dopaminergic motor supersensitivity. The present results suggest that increased dopamine D3 receptor expression following antidepressant treatments is not involved in the mechanism of dopaminergic supersensitivity, and are consistent with evidence supporting an inhibitory role for dopamine D3 receptors in motor activity, both in normal and in sensitized subjects
Dopamine D3 receptor antisense oligodeoxynucleotide potentiates imipramine-induced dopaminergic behavioural supersensitivity
No full textChronic antidepressant treatments result in the potentiation of dopaminergic transmission in the mesolimbic dopamine system revealed as an increased motor response to dopamine D2-like agonists. On the basis of the involvement of this system in the control of motivation and reward-related behaviour, which are impaired in depression, it has been suggested that such supersensitivity might play an important role in the mechanism of action of these drugs. Several studies have provided evidence suggesting a role of dopamine D3 receptors in mediating antidepressant-induced increased motor response to dopamine agonists. To test this hypothesis, we studied the effect of the intracerebroventricular infusion of a dopamine D3 receptor antisense oligodeoxynucleotide (10 mu g/3 mu l, 2-3 daily injections) on the expression of imipramine-induced supersensitivity (20mg/kg daily intraperitoneal injections for 21 days) to the motor effect of the dopamine D2-like receptor agonist quinpirole (a single 0.3 mg/kg subcutaneous injection 24-48 h after imipramine withdrawal). The results show that a treatment previously shown to reduce the synthesis of dopamine D3 receptors, rather than resulting in an inhibitory effect, potentiated the ability of imipramine to induce dopaminergic motor supersensitivity. The present results suggest that increased dopamine D3 receptor expression following antidepressant treatments is not involved in the mechanism of dopaminergic supersensitivity, and are consistent with evidence supporting an inhibitory role for dopamine D3 receptors in motor activity, both in normal and in sensitized subjects
Long-term imipramine treatment withdrawal induces depressive-like behavior in the forced swimming test
No full text
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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