European Journal of Neuroscience
August 19, 2022
Zen Juen Lau, Tam Pham, Shen‐hsing Annabel Chen et al.
225 citations
EEG complexity measures, which quantify the predictability and irregularity of neural signals, are increasingly used as biomarkers for psychopathologies like depression and schizophrenia. This review explains these measures in accessible terms, categorizing them into those assessing predictability and regularity. It synthesizes findings across consciousness research, mood and anxiety disorders, schizophrenia, neurodevelopmental and neurodegenerative conditions, and lifespan changes, addressing theoretical and methodological issues that cause data discrepancies. The review also provides guidance on selecting and interpreting these metrics for psychological and neuropsychiatric research.
European Journal of Neuroscience
November 16, 2007
Susan Schenk, Lincoln S. Hely, Barbara Lake et al.
113 citations
MDMA self-administration was studied in previously drug-naïve rats. Acquisition varied widely, with about 60% of rats learning to self-administer MDMA over 15 days, a lower rate and slower onset than for cocaine. Responding depended on dose, and breakpoints under a progressive ratio schedule increased with dose. Rats that self-administered MDMA showed lower densities of serotonin transporter sites (SERT) across brain regions, comparable to reductions from experimenter-administered MDMA. The findings indicate MDMA has high abuse liability and that long-term self-administration may cause lasting deficits in serotonin neurotransmission.
European Journal of Neuroscience
July 1, 2004
Paul Brown, Eugene A. Kiyatkin
105 citations
MDMA (ecstasy) causes a moderate, prolonged increase in brain and muscle temperature in rats under quiet resting conditions. When rats interact socially with a female or have chronically occluded jugular veins, the drug-induced brain hyperthermia is dramatically amplified (89% and 188% greater, respectively). At a warm environmental temperature of 29 °C, MDMA pushes brain temperature above 41 °C, leading to fatalities in 83% of tested animals. The findings suggest that metabolic brain activation combined with impaired heat dissipation makes MDMA use under 'party' conditions far more dangerous than standard laboratory settings.
European Journal of Neuroscience
September 1, 1999
Viktor L. Arvanov, Xiaofu Liang, Angelo Russo et al.
64 citations
Hallucinogenic compounds, including the phenethylamine DOB (a selective serotonin 5-HT2A,2C receptor agonist) and the indoleamine LSD (which binds to multiple serotonin, dopamine, and adrenergic receptors), inhibit NMDA receptor-mediated currents and synaptic responses in pyramidal cells of prefrontal cortical slices, while non-hallucinogenic congeners do not. This inhibition is mimicked by serotonin when 5-HT1A and 5-HT3 receptors are blocked, and is prevented by 5-HT2A receptor antagonists. At low concentrations, LSD and DOB partially depress the NMDA response and block serotonin's inhibitory effect, indicating partial agonist action. The inhibition depends on a Ca2+/calmodulin-dependent protein kinase II pathway, not protein kinase C. The findings suggest hallucinogens may alter sensory, perceptual, affective, and cognitive processes by modulating NMDA receptors through 5-HT2A receptor partial agonism.
European Journal of Neuroscience
May 1, 2006
Christopher Bishop, Jennifer L. Taylor, Donald M. Kuhn et al.
63 citations
In a rat model of Parkinson's disease, the serotonin-releasing drugs MDMA and fenfluramine reduced the abnormal involuntary movements (dyskinesia) caused by chronic L-DOPA treatment. This antidyskinetic effect was blocked by a drug that inhibits the serotonin 5-HT1A receptor, suggesting that these compounds work at least partly through that receptor. The findings indicate that boosting serotonin activity may help manage L-DOPA-induced dyskinesia without compromising the therapeutic benefit of L-DOPA.
European Journal of Neuroscience
April 1, 2000
H. S. Fischer, Gerald Zernig, Dieter S. Schatz et al.
54 citations
MDMA (ecstasy) increases the release of the neurotransmitter acetylcholine in rat striatal brain slices in a dose-dependent manner, with a half-maximal effect at about 30 µM. This effect requires calcium and is blocked by tetrodotoxin, indicating it depends on neuronal firing. Blocking glutamate, dopamine D2, serotonin 5-HT1, 5-HT2, 5-HT3C, or muscarinic acetylcholine receptors did not alter MDMA's effect, but blocking histamine H1 receptors completely abolished the acetylcholine release. The findings suggest MDMA directly activates histamine H1 receptors to stimulate striatal cholinergic neurons, revealing a previously unknown neurochemical pathway for MDMA's acute effects.
European Journal of Neuroscience
July 1, 2007
Sameera Dasari, Kert Viele, Amy Turner et al.
40 citations
Para-chlorophenylalanine (PCPA) and MDMA ('ecstasy') each delay development and reduce movement and feeding in larval fruit flies. PCPA blocks serotonin synthesis and MDMA depletes serotonin in mammalian neurons, so the experiments targeted the serotonergic system. PCPA lowered serotonin and dopamine levels in the larval brain, while MDMA did not reduce serotonin. The central nervous system remained sensitive to externally applied serotonin, but PCPA reduced that sensitivity, suggesting serotonin receptor regulation depends on neural activity. MDMA enhanced the central response to serotonin, indicating a possible agonist action or release of serotonin from neurons. Heart responses to serotonin were unchanged by either drug.
European Journal of Neuroscience
July 1, 2006
40 citations
Repeated exposure to MDMA (ecstasy) produces a sensitized locomotor response in rats only when the drug is experienced in the same environment where the response is later tested. Recording from over 200 striatal neurons showed that sensitized rats had a decreased baseline firing rate in neurons later excited by MDMA, leading to a greater percentage increase from baseline on challenge day. This suggests that contextual associations are critical for the expression of behavioral sensitization to MDMA and that the striatum is involved in the neurobehavioral changes from repeated use.
European Journal of Neuroscience
July 15, 2004
Patricia Robledo, Victoria Mendizábal, Jordi Ortuño et al.
40 citations
The rewarding effects of MDMA do not require µ-opioid receptors, unlike those of opioids, ethanol, nicotine, and THC. In mice lacking µ-opioid receptors, MDMA still produced a conditioned place preference and increased dopamine release in the nucleus accumbens, while decreasing dopamine metabolites DOPAC and HVA. Basal dopamine and metabolite levels were similar between knockout and wild-type mice. The findings indicate that MDMA's effects on dopamine neurons are independent of µ-opioid receptor activation.
European Journal of Neuroscience
July 1, 2006
Linda Ferrington, Eszter Kirilly, Douglas E. Mcbean et al.
21 citations
A single dose of MDMA causes long-term loss of serotonin nerve terminals and disrupts the normal coupling between brain blood flow and glucose use. Three weeks after MDMA pretreatment in rats, serotonin transporter density fell by about 46% and paroxetine binding by 47%. Brain glucose use decreased widely, but blood flow did not change, indicating lost cerebrovascular constrictor tone. A subsequent MDMA dose increased glucose use but decreased blood flow overall; in half of pretreated rats, random focal hyperemia suggested a failure of autoregulation during MDMA-induced hypertension. The findings suggest that prior MDMA exposure does not protect against acute cerebrovascular dysfunction and may, in some individuals, increase stroke risk.
European Journal of Neuroscience
May 21, 2024
Nur Damla Korkmaz, Ugur Cikrikcili, Merve Akan et al.
19 citations
Classical psychedelics such as psilocybin, LSD, and mescaline alter perception, emotion, and cognition by activating serotonin 5-HT2A receptors. After early research was halted in 1967 due to legal restrictions, studies resumed in the 1990s. Psilocybin-assisted psychotherapy has shown promise for treating anxiety and depression in cancer patients, as well as treatment-resistant depression and substance addictions. The article discusses the historical development, therapeutic applications, and ethical considerations of psychedelic therapy for depression, trauma disorders, and substance use disorders.
European Journal of Neuroscience
October 4, 2024
Victorita E Ivan, David P Tomàs-Cuesta, Ingrid M Esteves et al.
4 citations
Psychedelic drugs such as psilocybin reduce the place specificity of neurons in the retrosplenial cortex of mice navigating a treadmill, making neural activity less tied to distinct locations. The stability of place-related activity across trials also decreases, and functional correlations among simultaneously recorded neurons are lowered. These effects are blocked by the serotonin 2A receptor antagonist ketanserin, indicating that the 5-HT2A receptor mediates them. The findings suggest that psychedelics increase the entropy of neural signaling, which may contribute to the disorientation often reported by humans after taking psychedelics.
European Journal of Neuroscience
November 1, 2025
Paolo La‐torraca‐vittori, Livio Tarchi, Elisa Arrigo et al.
1 citation
Lysergic acid diethylamide (LSD) reduces local brain activity and connectivity in sensory and association regions, with effects linked to specific neurotransmitter receptors. In 15 healthy adults, fMRI scans under LSD versus placebo showed decreased amplitude of low-frequency fluctuations (ALFF) in somatosensory, visual, default mode, and frontoparietal networks, and decreased regional homogeneity (ReHo) in sensory and subcortical areas. Test-retest reliability was high for ALFF and moderate for ReHo. LSD-induced changes correlated negatively with densities of D2 and 5-HT1A receptors, suggesting the drug engages neurochemical processes beyond its primary 5-HT2A target. These preliminary results indicate complex, dynamic mechanisms underlying LSD's neural effects.
European Journal of Neuroscience
December 1, 2025
Nina Kleditzsch, James J Gattuso, Anthony J. Hannan et al.
Psilocybin, the active compound in psychedelic mushrooms, is being studied as a treatment for depression. Its metabolite psilocin binds to serotonin receptors and the serotonin transporter (5-HTT). In mice lacking 5-HTT, psilocybin failed to cause hyperactivity or head twitches, suggesting 5-HTT might be involved. To test this, researchers gave mice the selective 5-HTT inhibitor escitalopram before psilocybin. Escitalopram did not block psilocybin's effects on movement or head twitches. This indicates that acute blockade of 5-HTT does not directly mediate these behaviors, and the earlier findings in knockout mice likely stem from developmental changes or altered serotonin levels rather than acute transporter function.