Hallucinogens
G. Hussein Rassool in Alcohol and Drug Misuse, 2017
Three neurotransmitters (the chemical messengers of brain cells): serotonin, dopamine and norepinephrine are involved and their activities are increased with the use of MDMA (Liechti, and Vollenweider 2001). The functions of serotonin are to regulate mood, sleep, pain, appetite and other behaviours. It is this particular neurotransmitter that is involved in the elevation of mood and feeling of euphoria. There is the suggestion that MDMA can cause neurons that are involved with serotonin transmission in animal studies but there are no conclusive studies in humans regarding this effect. There is evidence to suggest that compared to the nonusers, heavy MDMA users had significant impairments in visual and verbal memory (Mathias 1999). The findings of clinical studies suggest that MDMA may increase the risk of long-term, perhaps permanent, problems with memory and learning and that “heavy MDMA users experience long lasting confusion, depression, and selective impairment of working memory and attention processes” (Morgan 1999; Cohen 2001; Verkes et al. 2001; Kish 2002). However, more studies are needed on the potential effects of MDMA on the developing human nervous system and the developed brain.
Brain Motor Centers and Pathways
Nassir H. Sabah in Neuromuscular Fundamentals, 2020
The basal ganglia have been implicated in a wide range of functions, as evidenced by the distribution of the inputs they receive. Practically all areas of the cerebral cortex project essentially topographically to the dorsal striatum, thence to other nuclei, and back through the feedback loops via the thalamus to the same cortical areas of origin of the given input to the basal ganglia. The dorsal striatum also receives: (i) feedback input from thalamic nuclei, (ii) dopaminergic input from the ventral tegmental area of the midbrain, which is believed to be part of the “reward” system in the brain, and (iii) serotonergic input from the raphe nuclei, which are a group of nuclei in the brainstem that are a major source of serotonin to the rest of the brain. Serotonin is a neurotransmitter that influences many brain functions, including mood, behavior, sleep, memory, and learning.
The Chemistry of the Brain
Gail S. Anderson in Biological Influences on Criminal Behavior, 2019
Many serotonin studies have either experimentally depleted or supplemented tryptophan to reduce or elevate available serotonin. Medically, it is simple to acutely deplete tryptophan in individuals for a short period. A review of such studies has shown that although the results vary, general healthy individuals do not show any change in mood, but healthy individuals who have a familial history of depression do show mood depression, although still within the normal range.32 In depressed patients who are recovered and are on antidepressant treatment that modulates the serotonergic system, at least half experience a regression to full depression, but in those no longer on medications, the response is much smaller.32 It appears clear that blocking serotonin production can depress mood in some people and seems to have a greater effect on people vulnerable to depression. Many studies have also used acute tryptophan depletion to study aggression, and most found increased irritability or aggression with depleted tryptophan, but unlike mood, it did not relate to whether the individual was normally aggressive.32 In other studies, tryptophan was supplemented to increase serotonin synthesis. Many human and animal studies have shown the prosocial benefits of increased serotonin levels, with supplementation reducing irritability and increasing friendly behavior.32
Pindolol potentiates the antidepressant effect of venlafaxine by inhibiting 5-HT1A receptor in DRN neurons of mice
Published in International Journal of Neuroscience, 2021
Serotonin (5-HT) has major roles in the regulation of mood, appetite, sleep and memory in CNS [1]. Decreases in the level of 5-HT, which is synthesized by the serotonergic neurons of the raphe nuclei, results in some psychiatric conditions like major depression (MD). Especially, the dorsal raphe nucleus (DRN) among the raphe nuclei sends serotonergic projections to limbic system and regulate mood. Clarification of synthesis, oscillation and reuptake processes of 5-HT in the DRN has importance to find better and more effective cures of mood disorders. MD is one of the most common psychiatric disorders [2]. It ranks second in the life-long burden of disease in developed countries and is expected to rank first by 2030 [3]. MD is mainly caused by decreased level of 5-HT in neurosynaptic junction between serotonergic raphe nuclei neurons and postsynaptic neurons in brain [4]. Increases in the number of presynaptic somatodendritic 5-HT1A autoreceptors in the raphe nuclei as well as decreases in the number of postsynaptic 5-HT1A receptors augment the risk of MD [5].
Fatal serotonin syndrome: a systematic review of 56 cases in the literature
Published in Clinical Toxicology, 2021
Sanjay Prakash, Chaturbhuj Rathore, Kaushik Rana, Anurag Prakash
Serotonergic agents are typically prescribed for psychiatric disorders [1]. Hence, most of the previous case reports and observations on SS were limited to the patients with psychiatric conditions. Recently, several non-psychiatric drugs have been identified to have serotonergic properties, and numerous cases of SS have been reported in patients with various other underlying conditions or scenarios [57]. Cases of SS have been reported in patients being treated for: cough, infection, headache, chronic musculoskeletal pain, neuropathic pain, and after anesthesia or surgery [57, 58]. In our review, 10 (18%) patients with psychiatric disorders developed fatal SS after the addition of such drugs for the development of new illnesses. This is an important finding of our review, suggesting that certain drugs with serotonergic properties should be used with an extreme caution in patients who are already receiving serotonergic agents.
Machine learning, pharmacogenomics, and clinical psychiatry: predicting antidepressant response in patients with major depressive disorder
Published in Expert Review of Clinical Pharmacology, 2022
William V. Bobo, Bailey Van Ommeren, Arjun P. Athreya
Kautzky and colleagues similarly leveraged clustering and RFs to predict response after 4 weeks of treatment with antidepressants or electroconvulsive therapy (ECT) using 12 SNPs in or near HTR2A (rs643627, rs6313), COMT (rs4680), ST8SIA2 (rs8035760, rs3784723), PPP3CC (rs7430, rs10108011), and BDNF (rs6265, rs11030101, rs11030104, and rs12273363) in 225 depressed participants in the Group for the Study of Resistant Depression (GSRD) cohort [59,60]. MDD diagnoses were confirmed using a modified version of the Mini-International Neuropsychiatric Interview (MINI), version 5.0.0 [61]. SNPs were selected based on literature review. Study drugs included selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), noradrenaline reuptake inhibitors (NARIs), tricyclic and tetracyclic antidepressants, and monoamine reuptake inhibitors (MAOIs). There was no stratification based on antidepressants or intervention types. Response to treatment was defined as achieving a HAMD score ≤17 after one or two adequate trials of antidepressants. The RF model was trained using 10-fold cross-validation, and the trained models were not validated in an external dataset. A four-factor RF model incorporating three SNPs (rs6265, rs6313, and rs7430) and melancholic depressive subtype was associated with a 4-fold higher chance of positive treatment response compared with other patients (OR 4.22, 95% CI 1.43–12.49).
Related Knowledge Centers
- Brainstem
- Central Nervous System
- Cognition
- Memory
- Monoamine Neurotransmitter
- Vomiting
- Mood
- Reward System
- Learning
- Vasoconstriction