Neuropsychopharmacology, Journal Year: 2024, Volume and Issue: 49(6), P. 993 - 1006
Published: Jan. 17, 2024
Language: Английский
Neuropsychopharmacology, Journal Year: 2024, Volume and Issue: 49(6), P. 993 - 1006
Published: Jan. 17, 2024
Language: Английский
Neuroscience & Biobehavioral Reviews, Journal Year: 2021, Volume and Issue: 130, P. 162 - 177
Published: June 30, 2021
Language: Английский
Citations
48Neuron, Journal Year: 2022, Volume and Issue: 110(10), P. 1728 - 1741.e7
Published: March 15, 2022
Language: Английский
Citations
35Frontiers in Pharmacology, Journal Year: 2022, Volume and Issue: 12
Published: Jan. 27, 2022
Recent clinical and preclinical evidence points towards empathogenic prosocial effects elicited by psychedelic compounds, notably the serotonin 5-HT 2A agonists lysergic acid diethylamide (LSD), psilocybin, N,N-Dimethyltryptamine (DMT), their derivatives. These findings suggest a therapeutic potential of compounds for some behavioural traits associated with autism spectrum disorder (ASD), neurodevelopmental condition characterized atypical social behaviour. In this review, we highlight suggesting that psychedelics may potentially ameliorate atypicalities ASD, including reduced behaviour highly co-occurring anxiety depression. Next, discuss dysregulated neurobiological systems in ASD how they underlie or limit psychedelics. phenomena include: 1) synaptic function, 2) serotonergic signaling, 3) prefrontal cortex activity, 4) thalamocortical signaling. Lastly, studies from 1960s 70s assessed use treatment children ASD. We positive outcomes these studies, enhanced mood behaviour, as well adverse trials, increases aggressive dissociative psychotic states. Despite preliminary evidence, further are needed to determine whether benefits outweigh risks population, if receptor represent target social-behavioural disorders.
Language: Английский
Citations
31Therapeutic Advances in Psychopharmacology, Journal Year: 2022, Volume and Issue: 12
Published: Jan. 1, 2022
Generalized anxiety disorder (GAD), the most frequently diagnosed form of anxiety, is usually treated by cognitive-behavioural approaches or medication; in particular, benzodiazepines (acutely) and serotonin serotonin/noradrenaline reuptake inhibitors (long term). Efficacy, compliance, acceptability are, however, far from ideal, reinforcing interest alternative options. Agomelatine, clinically employed treatment major depression, expresses anxiolytic properties rodents was effective GAD (including severely ill patients) several double-blind, short-term (12 weeks) relapse-prevention (6 months) studies. At active doses, incidence adverse effects no higher than for placebo. Agomelatine possesses a unique binding profile, behaving as melatonin (MT1/MT2) receptor agonist 5-HT2C antagonist, yet recognizing neither monoamine transporters nor GABAA receptors. Extensive evidence supports role receptors induction anxious states, their blockade likely plays primary mediating actions agomelatine, including populations amygdala bed nucleus stria terminalis, well hippocampus. Recruitment MT suprachiasmatic nucleus, thalamic reticular hippocampus appears to fulfil complimentary role. Downstream receptors, modulation stress-sensitive glutamatergic circuits altered release anxiogenic neuropeptides, corticotrophin-releasing factor, vasopressin, may be implicated agomelatine. To summarize, agomelatine exerts its mechanisms clearly distinct those other agents currently management GAD.How helps disorders.• Anxiety disorders have significant negative impact on quality life.• The common type disorder, called generalized associated with nervousness excessive worry.• These symptoms can lead additional like tiredness, sleeplessness, irritability, poor attention.• generally through either therapy medication. However, widely used drugs effects.• well-established antidepressant drug, has shown anxiety-lowering ('anxiolytic') rats been effectively treat minimal side exactly how it acts brain manage not clear.• Thus, this review aims shed light agomelatine's mechanism action treating GAD.• authors reviewed studies treats animals.• They also looked at clinical people study showed that 'blocks' nerve cells, which causing receptor.• Blocking receptor, especially specific regions such cells amygdala, hippocampus, produced reduction seen during treatment.• activates (MT) known keep check, promote sleep, maintain sleep cycle.• should thus tackle disturbances commonly patients Beyond signalling molecules are involved (called 'neurotransmitters' 'neuropeptides') affected agomelatine.• Agomelatine's caused medications This explains therapeutic success effects.
Language: Английский
Citations
31Neuropsychopharmacology, Journal Year: 2024, Volume and Issue: 49(6), P. 993 - 1006
Published: Jan. 17, 2024
Language: Английский
Citations
8