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Journal of Neurochemistry

ISSN 0022-3042

34 papers in the library · 1,555 citations · publishing 1964-2026

Papers

Lysergic acid diethylamide induces increased signalling entropy in rats’ prefrontal cortex

Journal of Neurochemistry November 3, 2021 Aurora Savino, Charles D. Nichols 18 citations

Psychedelic drugs, including LSD, are being studied as potential treatments for psychiatric disorders like mood and substance use disorders. The 5-HT2A receptor is their main molecular target, and early research indicated effects on neuroplasticity genes. By analyzing RNA-sequencing data from the prefrontal cortex of rats chronically treated with LSD, the authors describe how psychedelics rewire gene co-expression networks, making them less centralized but more complex, with an overall increase in signaling entropy characteristic of highly plastic systems. This molecular-level signaling entropy mirrors the increased brain entropy observed in human neuroimaging studies, suggesting underlying mechanisms for higher-order phenomena. Network topology analysis identified potential transcriptional regulators and implicated different cell types in psychedelic activity.

In vivo determination of 5-hydroxytryptamine receptor-stimulated phosphoinositide turnover in rat brain.

Journal of Neurochemistry August 1, 1989 I Hide, T Kato, S Yamawaki 15 citations

In the intact rat brain, phosphoinositide turnover is stimulated by activation of the 5-HT2 receptor. After prelabeling brain phosphoinositides with [3H]inositol, lithium treatment increased levels of [3H]IP1 and [3H]IP2. The 5-HT agonists 5-MeODMT and quipazine further increased 3H-inositol phosphate levels under lithium pretreatment. This response was blocked by the 5-HT2 antagonist ritanserin but not by the 5-HT1 antagonist (-)-propranolol, indicating that 5-HT2 receptors drive this signaling. The method can be used to study in vivo effects of psychotropic drugs like antidepressants on 5-HT2 receptor-stimulated phosphoinositide turnover.

Bioisosteric analogs of MDMA: Improving the pharmacological profile?

Journal of Neurochemistry September 1, 2024 Ana Sofia Alberto-Silva, Selina Hemmer, Hailey A. Bock et al. 10 citations

Three new chemical variants of MDMA—ODMA, TDMA, and SeDMA—show similar activity at serotonin, dopamine, and norepinephrine transporters but reduced activity at 5-HT2A/2B/2C receptors compared to MDMA. They also differ in liver metabolism, with N-demethylation as the only shared route and no phase II metabolites formed. TDMA showed faster clearance. The analogs interacted more weakly with organic cation transporters and plasma membrane monoamine transporter. These bioisosteres may offer therapeutic alternatives to MDMA with a reduced off-target profile, but further studies are needed to determine if they pose lower risks.

Serotonergic Psychedelics Rapidly Modulate Evoked Glutamate Release in Cultured Cortical Neurons

Journal of Neurochemistry February 28, 2025 Aneta Petrušková, Debarpan Guhathakurta, Enes Yağız Akdaş et al. 8 citations

Serotonergic psychedelics like psilocybin, LSD, and DMT rapidly alter how neurons communicate at synapses. Using live-cell imaging in rat cortical neurons, the drugs reduced the fraction of synaptic vesicles that fuse in response to electrical stimulation within minutes, an effect that faded within 24 hours. DMT only reduced the total recycling pool of vesicles, while LSD and psilocin also shrank the readily releasable pool. Psilocin and DMT increased evoked glutamate release, yet LSD and psilocin lowered presynaptic calcium levels. Psilocin further depressed responses to paired stimuli. These drug-specific modulations of glutamatergic transmission may help explain their distinct therapeutic properties.

Inhibition of reactive oxygen species production accompanying alternatively activated microglia by risperidone in a mouse ketamine model of schizophrenia.

Journal of Neurochemistry September 1, 2024 Risako Fujikawa, Jun Yamada, Shoichiro Maeda et al. 6 citations

In a mouse model of schizophrenia, the antipsychotic risperidone reduced behavioral abnormalities and altered microglial activity and reactive oxygen species (ROS) in the hippocampus. Mice given ketamine showed schizophrenia-like behaviors, increased microglial density, and a shift toward more activated microglial shapes. Risperidone reversed these changes, lowering expression of the ROS-producing enzyme Nox2 and raising antioxidant enzyme levels. In isolated microglia, ketamine boosted ROS production, which risperidone blocked. A NOX2 inhibitor also counteracted ketamine-induced behavioral deficits, suggesting that reducing ROS via microglial modulation may help treat schizophrenia.

THE EFFECT OF AN ECTOSYLVIAN EPILEPTOGENIC FOCUS INDUCED BY TOPICAL APPLICATION OF MESCALINE ON NITROGENOUS COMPOUNDS IN THE NEOCORTEX OF CAT

Journal of Neurochemistry November 1, 1966 G Badiu, N Mison-Crighel 4 citations

Topical application of mescaline to the neocortex induced an epileptiform spiking focus and altered nitrogenous compounds across the entire cerebral cortex. Within two minutes, before spiking began, ammonia levels rose significantly in all neocortical areas, especially at the focus and the homolateral marginal gyrus; free amide nitrogen decreased and non-protein nitrogen increased throughout the cortex. At thirty minutes, during focus development, ammonia remained elevated with a slight decline, free amide nitrogen was reduced in all neocortical areas, and protein nitrogen decreased in both marginal gyri while lipid nitrogen fell in the focus and both marginal gyri.

N,N‐Dimethyltryptamine ( DMT ) Acutely Exposed to Mouse Ventral Tegmental Area I h ‐Negative Neurons Alters the Firing Rate and Conductance in a Sex‐Dependent Manner

Journal of Neurochemistry May 1, 2026 Jannik Nicklas Eliasen, Amir Rezagholizadeh, Helene Påbøl Jacobsen et al.

Dimethyltryptamine (DMT), a classic psychedelic with potential anti-depressive and anti-addictive properties, alters the electrical activity of certain neurons in the ventral tegmental area (VTA) of the mouse brain, with effects differing by sex. In an ex vivo study on I_h-negative neurons, a low concentration (500 nM) of DMT had no effect on electrophysiological properties in either sex. A high concentration (90 μM) increased action potential firing and changed membrane conductance at subthreshold potentials, but only in female neurons. DMT also raised cytosolic calcium levels in both sexes at the high concentration. The findings suggest that DMT activates mechanisms in females beyond the calcium changes seen in males, highlighting the importance of sex and dose in understanding its therapeutic potential.

Combined Neuroprotective Effects of N,N‐Dimethyltryptamine and Ventral Root Reimplantation Following Spinal Root Avulsion in Rats

Journal of Neurochemistry January 29, 2026 Paola Andrea Caro Aponte, Edison Huertas Montoya, Ítalo Odone Mazali et al.

A combinatorial therapy combining surgical root reimplantation, a fibrin sealant biopolymer, and a low dose of dimethyltryptamine (DMT) extracted from Mimosa tenuiflora roots rescued motor neurons and reduced glial reactivity in a rat model of ventral root avulsion. Proximal axotomy caused 78% motor neuron loss, glial reactivity, and synaptic detachment. Daily DMT at 1 mg/kg for two weeks significantly increased motor neuron survival, reduced glial reactivity, and preserved pre-synaptic boutons. Combining DMT with surgical reimplantation further potentiated these effects and upregulated GDNF expression, suggesting a synergistic neuroprotective benefit. DMT shows promise as a neuroprotective agent for CNS/PNS interface injuries.

Microdosing ketamine in Drosophila does not block serotonin reuptake, but causes complex behavioral changes mediated by glutamate and serotonin receptors

Journal of Neurochemistry February 7, 2024 Kelly E. Dunham, Kani H. Khaled, Leah Weizman et al.

Ketamine, when given at very low (micro) doses, increases movement and feeding in fruit fly larvae, but through a different mechanism than standard antidepressants such as SSRIs. At 1 mM, ketamine did not alter serotonin levels yet still boosted locomotion and feeding, whereas low doses of the SSRIs escitalopram and fluoxetine inhibited the serotonin transporter (dSERT) and similarly increased these behaviors. At a high dose (100 mM), ketamine blocked dSERT and raised serotonin, but reduced movement and feeding due to anesthetic effects. Experiments with mutant flies and other drugs suggest ketamine's behavioral effects come from NMDA receptor antagonism (which increases feeding) and serotonin receptor activation (which increases locomotion), not from acting on the serotonin transporter like SSRIs.