Journal of Neuroscience Research
October 1, 2009
Irene Riezzo, Daniela Cerretani, Carmela Fiore et al.
47 citations
A single dose of MDMA (20 mg/kg) in rats rapidly disrupts the brain's antioxidant defenses within hours. Reduced and oxidized glutathione ratios decreased, and antioxidant enzyme activities fell significantly after 3 and 6 hours in the frontal cortex. Ascorbic acid levels rose sharply in the striatum, hippocampus, and frontal cortex after 3 and 6 hours. Malonaldehyde, a marker of oxidative damage, increased in the striatum after 3 and 6 hours and in the hippocampus and frontal cortex after 6 hours. Immunohistochemistry revealed strong antivesicular monoamine transporter 2 positivity in frontal sections, basal ganglia, and thalamus, and heat shock protein 70 appeared in the superficial cortical layer after 24 hours, indicating early neurotoxic changes.
Journal of Neuroscience Research
April 1, 2022
Emilija Glavonic, Milos Mitic, Miroslav Adzic
20 citations
Fear-related disorders like phobias and PTSD involve disrupted fear extinction, leading to excessive fear. Exposure therapy, the standard treatment, fails in up to 35% of patients, and adding antidepressants offers no extra benefit. Hallucinogenic drugs, particularly MDMA and ketamine, may enhance therapy by promoting neuroplastic changes in fear circuits and reducing amygdala hyperreactivity. This review examines preclinical and clinical evidence showing these drugs can strengthen fear extinction learning and improve emotional engagement in psychotherapy, potentially outperforming current first-line treatments.
Journal of Neuroscience Research
March 3, 2023
Veronika Langová, Petra Horká, Jan Hubený et al.
10 citations
Ketamine, an NMDA receptor antagonist, disrupted electric signaling and navigation in the weakly electric fish Gnathonemus petersii, a candidate model for schizophrenia. Lower doses increased locomotion and erratic movement, while higher doses reduced electric organ discharges, indicating positive schizophrenia-like symptoms. A low dose of haloperidol did not normalize these symptoms, suggesting further testing with more antipsychotic doses is needed to confirm the model's predictive validity.
Journal of Neuroscience Research
January 1, 2024
Chitra Vinnakota, Anna Schroeder, Xin Du et al.
7 citations
Blocking NMDA receptors with drugs like PCP and ketamine causes psychosis-like symptoms in humans and hyperlocomotion in rodents. Mice lacking the GluN2D subunit of the NMDA receptor show reduced hyperlocomotion in response to these drugs, suggesting this subunit is key for that effect. This study tested male and female mice lacking GluN2D and found they also had blunted locomotor responses to PCP, S-ketamine, and R-norketamine, in both sexes. These knockout mice showed an anxious baseline, and the drugs had anxiolytic effects that varied by sex and genotype. S-ketamine disrupted spatial memory in females and object recognition in both sexes, regardless of genotype. The GluN2D subunit mediates sex-specific and drug-specific behavioral effects of NMDA receptor antagonists.
Journal of Neuroscience Research
January 1, 2026
Hediye Moghadam, Parisa Akbari, Elmira Beirami et al.
Oral consumption of the psilocybin-containing mushroom Psilocybe azurescens at doses of 10, 100, and 250 mg/kg every other day for 14 days increased anxiety- and depressive-like behaviors and disrupted social interaction in male Wistar rats. These behavioral changes were accompanied by elevated neuroinflammation (IL-6 and TNFα) and oxidative stress (ROS and SOD) and reduced neurotrophic factors (BDNF and GDNF) in the hippocampus, prefrontal cortex, and amygdala. The findings suggest that high doses of P. azurescens can induce mood disorders through increased inflammatory responses and oxidative stress alongside decreased neurotrophic factor expression.
Journal of Neuroscience Research
January 1, 2026
Stephanie N Njau, Artemis Zavaliangos-Petropulu, Shantanu Joshi et al.
In people with treatment-resistant depression, a single low-dose ketamine infusion increased glutamate levels in the dorsal anterior cingulate cortex only in those who responded to treatment, and lower pre-treatment glutamate levels predicted greater improvement in depression scores. GABA levels did not change after treatment. Other brain metabolites linked to neuronal health and metabolism also increased. These findings suggest that ketamine's antidepressant effect involves sustained enhancement of glutamate-related neurotransmission and that baseline glutamate levels may help predict who will benefit from ketamine.
Journal of Neuroscience Research
June 1, 2023
Hei-Yin Hydra Ng, Changwei W Wu, Feng-Ying Huang et al.
Low-gamma band effective connectivity increased globally after an 8-week mindfulness-based stress reduction (MBSR) program, while high-beta band effective connectivity increased only during breathing. Outgoing effective connectivity was stronger during resting, breathing, and body-scan. Changes in effective connectivity of the right lateral prefrontal area predicted mindfulness and emotional regulation abilities, partially supporting the theory that lateral prefrontal areas exert top-down modulatory control, implying that mindfulness training cultivates better emotional regulation.
Journal of Neuroscience Research
May 1, 2021
Emiliano Santarnecchi, Eutizio Egiziano, Sicilia D'Arista et al.
An 8-week mindfulness-based stress reduction (MBSR) training program alters functional and effective connectivity in the dorsal striatum, particularly the putamen, in healthy individuals. After training, local connectivity decreased in the right anterior putamen and insula during spontaneous mind-wandering and in the right cerebellum during meditation. Effective connectivity analysis showed reduced modulation by the anterior cingulate cortex over the anterior putamen and a change in excitatory and inhibitory interactions between the posterior putamen and cerebellum. These connectivity rearrangements may help explain mindfulness-related behavioral effects, especially in pain perception.
Journal of Neuroscience Research
November 20, 2019
C. Philippi, J. Bruss, A. Boes et al.
Damage to specific brain networks, particularly the default mode network (DMN), reduces how often people report mind-wandering. In a study of 29 people with brain injuries and 19 healthy controls, mind-wandering frequency was measured with the Imaginal Processes Inventory. Lesion network mapping, which uses resting-state functional connectivity data from healthy brains to infer networks affected by each injury, showed that reduced mind-wandering was most strongly linked to damage in the left inferior parietal lobule within the DMN. Traditional lesion mapping also associated reduced mind-wandering with damage to several DMN regions including the medial prefrontal cortex, parietal lobule, and inferior frontal gyrus. These results support the DMN's role in spontaneous thought.
Journal of Neuroscience Research
May 1, 2013
Martin A. Santini, Cecilia Ratner, Susana Aznar et al.
Subchronic administration of phencyclidine (PCP) to mice increases the sensitivity of serotonin 2A receptors (5-HT2A Rs) in the frontal cortex. Mice treated with PCP (10 mg/kg) for 10 days, followed by a 5-day washout, showed a stronger head-twitch response and greater expression of immediate-early genes (Arc, c-fos, egr-2) after a challenge with the 5-HT2A R agonist DOI, compared to saline-treated mice. These functional changes occurred without alterations in 5-HT2A R binding or in binding of the 5-HT1A receptor or serotonin transporter. Basal Arc mRNA levels were also elevated in the prefrontal cortex. The findings suggest that PCP-induced changes enhance 5-HT2A R-mediated neurotransmission, which may contribute to behavioral deficits in this schizophrenia model.
Journal of Neuroscience Research
December 1, 1992
F. R. Sharp, M. Butman, S. Wang et al.
The non-competitive NMDA receptor antagonists PCP, MK801, and ketamine produce psychosis in humans and cause abnormal vacuoles in posterior cingulate and retrosplenial rat cortical neurons. The drugs induce hsp70 mRNA and HSP70 heat shock protein in these injured neurons at specific doses (PCP ≥5 mg/kg, MK801 ≥0.1 mg/kg, ketamine >20 mg/kg). This injury occurs in rats aged 30 days or older but not in those 0–20 days old, and is prevented by prior administration of the antipsychotic drugs haloperidol and rimcazole. The authors propose that future studies are needed to determine whether dopamine, sigma, M1, or other receptors mediate the injury.