Neuroreport
November 7, 2005
Sara W. Lazar, Catherine E. Kerr, Rachel H. Wasserman et al.
1,707 citations
Long-term meditation practice is linked to structural changes in the brain. Magnetic resonance imaging of 20 experienced Insight meditation practitioners showed greater cortical thickness in regions involved in attention, interoception, and sensory processing, including the prefrontal cortex and right anterior insula, compared to matched controls. The difference in prefrontal thickness was most pronounced in older participants, suggesting meditation may counteract age-related cortical thinning. Thickness in two regions also correlated with meditation experience. These findings provide the first structural evidence that meditation practice can induce experience-dependent cortical plasticity.
Neuroreport
December 1, 1998
Franz X. Vollenweider, M. F. I. Vollenweider-Scherpenhuyzen, Andreas Bäbler et al.
1,023 citations
The hallucinogen psilocybin induces a psychosis-like state in healthy people that resembles early schizophrenia. In human volunteers, these effects were blocked in a dose-dependent manner by the serotonin-2A antagonist ketanserin or the atypical antipsychotic risperidone, but were increased by the dopamine antagonist and typical antipsychotic haloperidol. This provides the first human evidence that psilocybin-induced psychosis results from serotonin-2A receptor activation, independent of dopamine stimulation. The findings suggest that serotonin-2A overactivity may play a role in schizophrenia and that blocking this receptor may contribute to antipsychotic benefits.
Neuroreport
April 1, 1995
440 citations
A subanesthetic dose of the NMDA antagonist ketamine temporarily activated psychotic symptoms in people with schizophrenia, closely resembling their usual episodes. In a PET study using radioactive water, ketamine increased blood flow in the anterior cingulate cortex and decreased flow in the hippocampus and primary visual cortex. These findings support the idea that altered glutamate transmission may contribute to schizophrenia and PCP-induced psychosis.
Neuroreport
May 28, 2008
229 citations
The default mode network, a set of brain regions active during rest, can be identified by both region of interest-based correlation analyses and independent component analysis. In a study of 40 participants, both methods successfully identified the network. Age and sex differences in the network were small, and the two analytic techniques agreed less on these differences than on the network's structure.
Neuroreport
November 1, 1999
Norberto Aguirre, Meritxell Barrionuevo, Marı́a J. Ramı́rez et al.
89 citations
A single dose of MDMA (20 mg/kg) given to rats caused significant hyperthermia and reduced serotonin content and serotonin transporter density by 40–60% in the frontal cortex, striatum, and hippocampus one week later. MDMA also increased glial fibrillary acidic protein (GFAP) immunoreactivity in the hippocampus. Repeated administration of the metabolic antioxidant α-lipoic acid before MDMA did not prevent the acute hyperthermia but fully prevented the serotonergic deficits and glial changes. These results support the hypothesis that free radical formation is responsible for MDMA-induced neurotoxicity.
Neuroreport
August 1, 2004
Olivia Carter, John D. Pettigrew, David C. Burr et al.
83 citations
The hallucinogenic drug psilocybin, which activates serotonin receptors, selectively impairs the ability to perceive coherent motion in random dot patterns, a task that relies on high-level global motion detectors, while leaving contrast sensitivity for drifting gratings, mediated by low-level detectors, unaffected. This pattern of visual processing deficits mirrors those seen in schizophrenia, suggesting psilocybin may serve as a pharmacological model for studying psychosis and the neural basis of visual perception.
Neuroreport
September 1, 1990
L G Sharpe, J H Jaffe
79 citations
Ibogaine, despite anecdotal reports of eliminating opioid withdrawal symptoms in humans, did not alleviate opioid withdrawal in a rat model. Morphine-dependent rats received ibogaine at doses of 5, 10, 20, or 40 mg/kg before naloxone-precipitated withdrawal. Of twelve withdrawal signs scored, only two significant changes occurred: decreased grooming at 10 mg/kg and increased teeth chatter at 5 mg/kg. These results indicate that ibogaine does not reduce opioid withdrawal in this animal model at either non-tremorigenic or tremorigenic doses.
Neuroreport
August 21, 1995
E O'Hearn, P Zhang, M E Molliver
77 citations
Ibogaine triggers degeneration of Purkinje cells in the brain, likely by activating inferior olive neurons that release glutamate at climbing fiber terminals. After ibogaine administration, some Purkinje cells begin expressing NADPH-diaphorase and neuronal NOS, enzymes not normally present in these cells. This NOS induction is delayed, dose-related, and occurs in neurons next to degenerated Purkinje cells. The findings show that nNOS induction can follow excitotoxic injury, but nitric oxide is unlikely to be involved in the initial damage. The late induction and spatial pattern suggest NO may play a role in neuronal recovery or delayed cell death after excitotoxic injury.
Neuroreport
March 1, 1993
E O'Hearn, D B Long, M E Molliver
72 citations
Ibogaine, a drug proposed for treating addiction, activates glial cells in the cerebellum of rats, indicating possible neurotoxicity. After one to three doses of ibogaine (100 mg per kg of body weight), markers for microglia and astrocytes increased, and these cells changed shape. The activated glial cells appeared in striped patterns within the cerebellar vermis, suggesting degeneration of Purkinje neurons.
Neuroreport
October 1, 2003
Jörg Daumann, Ralph Schnitker, Jürgen Weidemann et al.
46 citations
Working memory performance and brain activation were examined in eight abstinent people who used only MDMA (ecstasy), a group who used MDMA plus other drugs, and non-users. Pure MDMA users showed lower brain activation than controls and polyvalent users, particularly in the inferior temporal regions, angular gyrus, and striate cortex. Polyvalent users did not differ from controls. The findings suggest that altered brain activation during cognitive tasks may be primarily linked to prior MDMA use, and that concomitant use of other drugs may modify this effect.
Neuroreport
May 11, 1998
B Rho, S D Glick
35 citations
Ibogaine, a natural alkaloid from the African shrub Tabernanthe iboga, can interrupt opioid dependence in humans and reduce morphine self-administration and withdrawal signs in animals, but it has neurotoxicity. A safer synthetic congener, 18-Methoxycoronaridine (18-MC), mimics ibogaine's effects on morphine self-administration in animals without neurotoxicity. In this study, 18-MC attenuated five of seven signs of morphine withdrawal in rats. The data suggest that 18-MC will ameliorate symptoms of opioid dependence in humans.
Neuroreport
January 5, 1998
J P Pablo, D C Mash
27 citations
Noribogaine, a metabolite produced in the body from the natural compound ibogaine, acts as a full agonist at the mu-opioid receptor. In rat thalamic membranes, noribogaine stimulated a 170% increase above basal G-protein activation at sub-micromolar concentrations, an effect blocked by naloxone, confirming opioid receptor involvement. Its intrinsic activity matched that of the full agonists DAMGO and morphine. Ibogaine itself had no significant effect. This full mu-opioid agonist efficacy may explain ibogaine's ability to block acute opiate withdrawal and reduce morphine self-administration.
Neuroreport
October 4, 2023
William D S Killgore, Samantha Jankowski, Kymberly Henderson-Arredondo et al.
19 citations
Among 20 young adults with insomnia symptoms, resting-state functional connectivity between the default mode network (DMN) and certain cortical regions before bedtime predicted objectively measured sleep quality. Greater connectivity between the DMN and cortical areas involved in executive function and complex cognition was associated with more total sleep time, more REM sleep, and higher sleep efficiency, while connectivity with the pons was linked to lower sleep efficiency. The findings suggest that pre-sleep DMN activation may contribute to insomnia by supporting ruminative thinking, and that interventions to suppress such activation could improve sleep.
Neuroreport
February 12, 2001
M B Leal, T Emanuelli, L D Porciúncula et al.
14 citations
Ibogaine, a compound proposed as a potential treatment for addiction, affects glutamate handling in brain cells. In mouse cortical synaptosomes, high concentrations of ibogaine (500–1000 µM) inhibited glutamate uptake and stimulated its release, while having no effect on rat synaptosomes or cerebellar synaptosomes. Additionally, ibogaine (1000 µM) nearly abolished glutamate uptake by cortical astrocyte cultures from both rats and mice. These results provide direct evidence that ibogaine alters glutamate handling in specific brain regions and support cells, linking its mechanism to neurotoxicity rather than therapeutic effects.