Experimental neurology
February 1, 1984
K Rasmussen, J Heym, B L Jacobs
125 citations
Serotonergic neurons in the nucleus centralis superior (NCS) of freely moving cats fire most rapidly during active waking (mean 2.94 spikes/s), slow down during slow-wave sleep (mean 1.38 spikes/s), and are least active during REM sleep (mean 0.46 spikes/s). Their activity does not increase with transient muscle movements but decreases just before and during sleep spindles. Most NCS serotonergic neurons are excited by sudden sounds or lights. A serotonin-like drug reduces their firing by about 44%. A subset of these neurons shows much smaller changes across sleep-wake states and is inhibited, rather than excited, by sensory stimuli. These patterns are compared with serotonergic neurons in other brain regions.
Experimental neurology
May 1, 2021
Fabrizio Schifano, Stefania Chiappini, Andrea Miuli et al.
49 citations
Several new psychoactive substances (NPS) can trigger serotonin syndrome, a dangerous condition of excessive serotonin activity marked by altered mental status, neuromuscular effects, and autonomic hyperactivity. A systematic review of three retrospective studies, two case series, and five case reports identified implicated substances including psychedelic phenethylamines (2C-I, 25I-NBOMe, 5-IT) and synthetic cathinones (mephedrone, MDPV, methylone, butylone, NRG3, AMT, MXP), as well as the antidepressant bupropion when misused at high doses or combined with other serotonergic drugs. Most substances were taken orally, though nasal insufflation and sublingual administration occurred. Psychiatric history was negative for most subjects. Clinicians should recognize NPS risks and diagnostic challenges due to undetectability in routine drug screenings.
Experimental neurology
April 1, 2020
Jessica Winne, Barbara C Boerner, Thawann Malfatti et al.
34 citations
Salicylate intoxication, which causes tinnitus and anxiety in humans, induces anxiety-like behavior and a specific brain oscillation called type 2 theta (theta2) in the hippocampus of young mice with normal hearing, but not in older mice. A single dose of the hallucinogenic compound 5-MeO-DMT prevents both the anxiety-like behavior and the increase in theta2 and slow gamma oscillations in the ventral hippocampus and medial prefrontal cortex after salicylate injection. These findings suggest that the anxiety triggered by salicylate depends on normal hearing and that hallucinogenic compounds may be effective for treating tinnitus-related anxiety.
Experimental neurology
November 1, 2021
6 citations
Methoxetamine (MXE), a ketamine-like designer drug, alters serotonin levels in the rat medial prefrontal cortex and nucleus accumbens. Blocking serotonin 5-HT2 receptors with selective antagonists attenuated MXE's motor and sensory effects and prevented its reduction of prepulse inhibition, indicating these receptors are key to MXE's sensorimotor actions. In vitro, MXE inhibited NMDA-mediated field potentials and GABA-mediated spontaneous currents in a concentration-dependent manner but did not affect AMPA components or presynaptic glutamate release. The findings suggest MXE acts as an NMDA receptor antagonist, with 5-HT2 receptors crucial for its sensorimotor effects and NMDA and GABA receptors as additional targets.
Experimental neurology
July 1, 2025
Mengqin Shan, Chaoyang Tong, Xin Fu et al.
2 citations
S-ketamine anesthesia in neonatal rats causes a drop in thyroid hormone levels and disrupts myelination, particularly by impairing the differentiation of oligodendrocyte precursor cells into mature oligodendrocytes. This leads to motor coordination deficits. Supplementing with triiodothyronine (T3) reverses these effects by restoring PPARα activity, a key regulator of lipid metabolism. Blocking PPARα with GW6471 eliminates T3's protective effect, while activating PPARα with fenofibrate rescues both coordination and cell maturation. The findings suggest that thyroid hormone supplementation could prevent anesthesia-related white matter damage in infants.
Experimental neurology
September 1, 2026
Javier Calleja-Conde, Víctor Echeverry-Alzate, Marina Sanz-Sancristobal et al.
In a preclinical model of Parkinson's disease, the compound N,N-dimethyltryptamine (DMT), the main psychoactive ingredient in ayahuasca, reduced neuroinflammation and preserved neurons in the nigrostriatal pathway. Treated animals also showed improvements in behavior. These results suggest DMT may have disease-modifying potential for Parkinson's disease, a progressive neurodegenerative disorder marked by loss of dopaminergic neurons and chronic inflammation, for which current treatments only relieve symptoms.