ISSN 1570-159X
31 papers in the library · 1,424 citations · publishing 2011-2026
Current Neuropharmacology December 10, 2014 Roberta Tittarelli, Giulio Mannocchi, Flaminia Pantano et al. 217 citations
A review organizes information from the internet and scientific literature to help specialists, including emergency department personnel, address the emerging threat of new psychoactive substances (NPS) to public health and public security.
Current Neuropharmacology January 1, 2024 Lisa Burback, Suzette Brémault-phillips, Mirjam J Nijdam et al. 187 citations
Chronic PTSD is a systemic disorder with high allostatic load, shaped by advances in genetics, neurobiology, and brain imaging. Current evidence-based treatments include pharmacological and psychotherapeutic approaches, but outcomes are often suboptimal due to barriers such as comorbidity, emotional dysregulation, suicidality, dissociation, substance use, and trauma-related guilt and shame. These challenges drive emerging novel approaches: early interventions during the Golden Hours, medication augmentation, psychedelics, and brain- and nervous-system-targeted interventions. A phase-oriented treatment framework is recognized to align interventions with the disorder's pathophysiology. Revisions to guidelines and care systems will be needed as innovative treatments gain evidence.
Current Neuropharmacology March 2, 2018 Jonathan Hamill, Jaime E. C. Hallak, Serdar Dursun et al. 179 citations
Ayahuasca is a traditional Amazonian brew made from Banisteriopsis caapi vine and Psychotria viridis leaves, containing beta-carboline alkaloids and the hallucinogen DMT. Originally used by indigenous shamans for spiritual and healing purposes, it has been incorporated into folk medicine and religious ceremonies in Brazil and is now also used recreationally in Europe and North America. This review summarizes ayahuasca's behavioral and physiological effects, safety profile, proposed mechanisms, and potential clinical uses for psychiatric disorders and addictions. The side effect profile appears relatively mild, but more detailed studies are needed. Some researchers advocate relaxing government regulations to allow comprehensive clinical trials.
Current Neuropharmacology March 10, 2016 Eric S. Wohleb, Danielle M. Gerhard, Alex Thomas et al. 148 citations
Major depressive disorder (MDD) is a common neuropsychiatric disease with limited treatment options that take weeks to work. Recent breakthroughs show that drugs like ketamine and scopolamine produce rapid and long-lasting antidepressant effects in MDD patients. Preclinical work in rodents indicates these effects arise from increased extracellular glutamate, elevated BDNF, activation of the mTORC1 cascade, and increased spine synapses in the prefrontal cortex (PFC). Both drugs work through converging molecular and cellular mechanisms in the PFC, antagonizing inhibitory interneurons to disinhibit pyramidal neurons, boosting glutamate. Specific NMDA and muscarinic acetylcholine receptor subtypes on GABAergic interneurons are promising targets for new rapid-acting antidepressants.
Current Neuropharmacology March 25, 2016 Brittany A. Jaso, Mark J. Niciu, Nicolas D. Iadarola et al. 97 citations
Current antidepressants for major depressive disorder work through monoaminergic mechanisms and have a delayed onset and limited efficacy. Glutamate, the main excitatory neurotransmitter, is involved in depression's pathophysiology. Since ketamine, an NMDA receptor antagonist, showed rapid antidepressant effects in 2000, other NMDA receptor antagonists have been studied but with more modest effects. Some have advantages like oral administration and fewer side effects. This article reviews clinical evidence for glutamate receptor modulators: non-competitive NMDA antagonists (ketamine, memantine, dextromethorphan, AZD6765), NR2B-subunit antagonists (traxoprodil, MK-0657), glycine-site partial agonists (D-cycloserine, GLYX-13), and metabotropic glutamate receptor modulators (AZD2066, basimglurant). Preclinical targets like AMPA agonists and mGluR2/3 negative allosteric modulators are also discussed.
Current Neuropharmacology June 19, 2017 Rainer Kraehenmann 90 citations
The overlap between dreaming and psychedelic states suggests that psychedelics temporarily produce dreamlike subjective experiences, which may lead to lasting improvements in psychosocial functioning and well-being. Future clinical research should investigate how the acute dreamlike effects of psychedelics relate to therapeutic outcomes.
Current Neuropharmacology January 5, 2024 Tamar Glatman Zaretsky, Kathleen M. Jagodnik, Robert Barsic et al. 73 citations
Post-traumatic stress disorder (PTSD) affects an estimated 12 million U.S. adults, and many remain symptomatic despite standard psychological and pharmacological treatments. Psychedelic compounds—including psilocybin, LSD, DMT, ayahuasca, MDMA, and ketamine—are being studied as potential therapies. This comprehensive review summarizes current PTSD treatments and their shortcomings, then examines clinical studies of psychedelic-assisted therapy for PTSD and related disorders. For each drug, the review covers history, psychological and somatic effects, pharmacology, and safety, along with proposed mechanisms for trauma treatment. It concludes with future directions to maximize therapeutic benefit and minimize risk for individuals and communities affected by trauma.
Current Neuropharmacology March 1, 2011 Yoko Hagino, Yukio Takamatsu, Hideko Yamamoto et al. 64 citations
MDMA increases extracellular dopamine and serotonin in the striatum and prefrontal cortex of mice. In mice lacking both dopamine and serotonin transporters, the dopamine increase in the striatum is absent, while the serotonin increase is greatly reduced. In the prefrontal cortex, MDMA raises dopamine levels regardless of transporter knockout. These findings confirm that MDMA acts on both the dopamine and serotonin transporters to elevate these neurotransmitters.
Current Neuropharmacology March 1, 2011 Dominik K. Biezonski, Jerrold S. Meyer 51 citations
High doses of MDMA (Ecstasy) reduce the expression of serotonergic markers in the forebrains of rats and nonhuman primates, and neuroimaging suggests similar reductions in the serotonin transporter (SERT) in heavy human users. These effects have often been interpreted as a loss of serotonergic fibers and terminals. However, this view is challenged because MDMA usually does not trigger glial cell reactions typical of central nervous system damage. This review addresses both sides of the MDMA-neurotoxicity controversy, including recent data from a rat binge model. The findings implicate neuroregulatory mechanisms underlying MDMA-induced serotonergic dysfunction and question the need to invoke degeneration.
Current Neuropharmacology March 1, 2011 Chiharu Sogawa, Norio Sogawa, Kazumi Ohyama et al. 50 citations
Methylone, a synthetic hallucinogenic amphetamine analog similar to MDMA, inhibits the activity of dopamine, norepinephrine, and serotonin transporters in a concentration-dependent manner, with the strongest effect on the norepinephrine transporter, followed by dopamine and then serotonin transporters. Compared to methamphetamine, methylone is less effective at blocking dopamine and norepinephrine transporters but more effective at blocking the serotonin transporter. Methylone alone is not toxic to cells except at high concentrations, but when combined with methamphetamine, it produces a synergistic toxic effect in cells that express monoamine transporters, likely because methylone acts as a transportable substrate that inhibits transporter function.
Current Neuropharmacology August 1, 2013 Patricio Sáez-briones, Alejandro Hernández 41 citations
MDMA (Ecstasy) produces a unique altered state of consciousness called the entactogenic syndrome, described as an open mind state, which may have therapeutic applications in psychotherapy and neuropsychiatric disorders. The pharmacological mechanism involves disruption of monoaminergic neurotransmission, but its full mechanism is not completely understood. Despite many structurally similar molecules, almost no experimental evidence shows that any analogue truly reproduces MDMA's full pharmacological profile, suggesting MDMA may be a pharmacological rarity. This review summarizes MDMA's pharmacology and the evidence from classical MDMA analogues, highlighting the need to develop better analogues.
Current Neuropharmacology November 3, 2016 Julian A Michely, Sascha K. Manier, Achim T. Caspar et al. 36 citations
Two new psychoactive substances, 3-MeO-PCP and 3-MeOPCPy, are metabolized in rat and human liver microsomes through multiple pathways including hydroxylation, O-demethylation, and glucuronidation. Specific cytochrome P450 enzymes (CYP 2B6, 2C19, 2C9, 2D6) catalyze initial metabolic steps. Because only polymorphically expressed enzymes are involved, pharmacogenomic variations may affect metabolism, though clinical data are needed to confirm relevance. Standard urine screening approaches using GC-MS, LC-MSn, and LC-HR-MS/MS can detect intake of both drugs via identified metabolites.
Current Neuropharmacology October 20, 2022 Alessio Mosca, Stefania Chiappini, Andrea Miuli et al. 30 citations
Ibogaine and noribogaine, psychedelic substances from plants of the Apocynaceae family, show some efficacy in treating substance use disorders, particularly opiate detoxification. However, their use carries concerning risks of cardiotoxicity and mortality. A meta-analysis of side effects found a significant risk of developing headaches after treatment. The evidence, drawn from case reports, randomized controlled trials, open-label studies, surveys, and observational studies, remains unclear on overall efficacy and toxicity. Further research is needed to evaluate therapeutic benefits and safety.
Current Neuropharmacology December 2, 2016 Laura Orsolini, Paul St John‐smith, Daniel Mcqueen et al. 28 citations
Multiple evolutionary mechanisms—optimal foraging, costly signaling, and reproduction at the expense of health—may jointly explain the recent spread and diffusion of the novel psychoactive substances (NPS) market, representing a reason for concern.
Current Neuropharmacology January 1, 2024 Michel Sabé, Chaomei Chen, Wissam El-Hage et al. 25 citations
A scientometric analysis of 42,170 publications on posttraumatic stress disorder (PTSD) from 1945 to 2022 identified four major research trends: war veterans and refugees, treatment of PTSD/neuroimaging, evidence syntheses, and somatic symptoms of PTSD. The largest cluster focused on evidence synthesis for genetic predisposition and environmental exposures leading to PTSD. War-related trauma research has shifted from battlefield in-person exposure to drone operator trauma and is being outpaced by civilian trauma research, including the COVID-19 pandemic, postpartum, and grief disorder. Recent trends show a burst in PTSD treatment research involving Mhealth, virtual reality, and psychedelic drugs. The USA dominates collaboration networks, with a recent surge of publications from China. Compared to other psychiatric disorders, there is a lack of high-quality randomized controlled trials for pharmacological and nonpharmacological treatments.
Current Neuropharmacology January 1, 2024 Mortimer Mamelak 24 citations
Rodent models of psychological stress mirror many features of major depressive disorder, linking activation of the hypothalamic-pituitary axis to oxidative stress, neuroinflammation, dominance of cholinergic neurotransmission, increased REM sleep pressure, impaired glycolysis and brain glucose utilization, reduced energy production, and decreased glutamate/GABA-glutamine cycling. Rapidly acting antidepressants like scopolamine, ketamine, and ECT raise extracellular glutamate; scopolamine and ketamine increase glutamate/GABA-glutamine cycling in both men and rodents, providing short-term relief. Nightly use of gammahydroxybutyrate (GHB), a GABAB agonist, may achieve more permanent results and possibly prevent depression by inhibiting cholinergic neurotransmission, relieving REM sleep pressure, and generating NADPH and succinate to boost energy and glutamate synthesis.
Current Neuropharmacology January 1, 2025 Gianluca Rosso, Giacomo d'Andrea, Stefano Barlati et al. 23 citations
Among patients with treatment-resistant depression who continued esketamine nasal spray for at least six months, 76.2% responded or achieved remission. Of those who had not responded by six months, a subset improved by twelve months. Side effects occurred in 71.8% of patients at six months, decreasing to 42% at twelve months; the most common were sedation and dissociation. Only two patients stopped treatment due to tolerability issues. The findings suggest esketamine is effective and safe for mid- to long-term treatment, with a novel observation of late clinical response in some patients. Results require confirmation in larger samples and longer observation periods.
Current Neuropharmacology October 20, 2025 Vassilis Martiadis, Fabiola Raffone, Danilo Atripaldi et al. 21 citations
A single dose of esketamine quickly reduced suicidal thoughts and depression in people with treatment-resistant depression. Preliminary evidence suggests that men and women may respond differently, indicating that personalized treatment approaches could improve results. More research is needed to confirm these gender differences, examine long-term effects, and understand the biological reasons behind them.
Current Neuropharmacology January 14, 2021 Stefania Chiappini, Andrea Miuli, Alessio Mosca et al. 19 citations
Benzydamine, an over-the-counter anti-inflammatory drug, is being diverted and used recreationally at high dosages (500–1500 mg) for its hallucinogenic properties. A systematic review of eleven articles from 1997–2019, including case reports, surveys, and case series, along with analysis of European adverse drug reaction reports from 2005–2020, found three reported abuse cases. The findings suggest healthcare professionals should be aware of potential misuse and that emergency physicians should consider benzydamine abuse when patients present with psychotic symptoms.
Current Neuropharmacology March 1, 2011 Z K Binienda, M A Beaudoin, B T Thorn et al. 10 citations
Fast Fourier Transform (FFT) analysis of electrocorticogram (ECoG) recordings in conscious rats reveals that different drugs alter brainwave frequencies in distinct ways. Domoic acid administration links slow-wave delta and theta activity with behavioral seizure type. Ibogaine pretreatment before cocaine increases power in the alpha(1) band, suggesting serotonergic involvement, and lowers the threshold for cocaine-induced electrographic seizures by increasing delta and theta power. Two weeks of daily cocaine reduces slow-wave ECoG activity 24 hours after the last injection, mirroring reduced frontal cortex metabolism in chronic human users. Gamma-hydroxybutyrate (GHB) at 400 and 800 mg/kg increases energy across all except beta(2) bands, producing EEG patterns resembling absence seizures in human petit mal epilepsy.
Current Neuropharmacology January 16, 2025 Sen Wang, Chaoli Huang, Mengyu Wang et al. 4 citations
Depression affects about 300 million people worldwide, and its underlying mechanisms remain unclear. Changes in oligodendrocytes and myelin are implicated in depression pathology. Conventional antidepressants take weeks to work and fail for about one-third of patients. Ketamine provides rapid, sustained antidepressant effects in treatment-resistant patients. Reduced myelination is linked to depression, so repairing myelin damage may be a key mechanism behind ketamine's prolonged effects. This review summarizes the relationship between demyelination and depression and discusses how ketamine might exert antidepressant effects by repairing myelin, offering new insights into the role of myelination in antidepressant mechanisms.
Current Neuropharmacology February 20, 2025 Alessio Mosca, Stefania Chiappini, Gianluca Mancusi et al. 3 citations
Abusing certain over-the-counter medications can trigger psychotic symptoms such as paranoia, hallucinations, and thought disorders. Antihistamines, dextromethorphan, and other OTC drugs are implicated. Dextromethorphan misuse is especially linked to chronic psychosis, while other substances more often cause acute substance-induced psychosis. The review analyzed 46 relevant studies from an initial pool of 2,677 articles, highlighting the need for greater awareness and interventions to address OTC drug misuse and its psychiatric consequences.
Current Neuropharmacology January 9, 2026 Maria Antonietta De Luca, Cristina Miliano, Amanda Roxburgh et al. 1 citation
Tablets sold as MDMA frequently contain psychoactive adulterants that vary by region and year, potentially increasing central nervous system harm. A review of studies from 2020 to 2025 covering Continental Europe, the UK, the USA, and Australia found that co-administration of MDMA with common adulterants can exacerbate noxious neurological and psychiatric effects. The composition of tablets differs across these regions, and interactions between MDMA and adulterants may explain some adverse effects seen in users. Expanding drug checking and public health efforts is essential to inform users, first responders, and healthcare professionals about these risks.
Current Neuropharmacology May 15, 2025 Yuanyuan Ding, Shiya Liu, Kaixin Wang et al. 1 citation
General anesthesia induces unconsciousness by disrupting communication between the fronto-parietal networks, which are brain regions critical for attention, executive function, and cognitive control. This review synthesizes findings from functional neuroimaging and neurophysiological studies showing that loss of fronto-parietal connectivity underlies the transition from wakefulness to anesthesia-induced unconsciousness. The authors explain the mechanisms at both neuronal and molecular levels, and discuss how these insights advance understanding of the neural correlates of consciousness and could inform development of anesthetic agents with more targeted effects on conscious states. The review bridges consciousness research and anesthetic pharmacology, offering a framework for future studies on neural mechanisms controlling conscious state transitions.
Current Neuropharmacology April 7, 2025 Marika Alborghetti, Luana Lionetto, Ginevra Lombardozzi et al. 1 citation
In patients with treatment-resistant depression receiving intranasal esketamine (56 mg) alongside another antidepressant, those taking antidepressants that inhibit cytochrome-P450 isoforms (paroxetine, fluoxetine, duloxetine, venlafaxine) had significantly higher serum esketamine levels 20 minutes after dosing and over 72 hours compared to patients on sertraline, citalopram, escitalopram, or vortioxetine. Salivary esketamine levels were several-fold higher than serum levels at all time points and showed high variability. These pharmacokinetic differences did not affect clinical outcomes, but changes in systolic blood pressure positively correlated with serum esketamine levels, suggesting dose reduction may be warranted for patients with cardiovascular comorbidity on those CYP450-inhibiting antidepressants. Small subgroup sizes limit strong conclusions.