Neuropsychobiology
January 1, 2011
Tomáš Páleníček, M. Fujáková, Martin Brunovský et al.
85 citations
Ketamine at behaviorally active doses induces a robust increase in EEG power spectra and coherence in rats. The drug rapidly penetrates the brain, reaching peak concentrations within 15 minutes after administration. Ketamine also produces marked hyperlocomotion and deficits in prepulse inhibition of the acoustic startle reaction, a measure of sensorimotor gating. The maximum levels of EEG change correlate with the kinetics of ketamine, and the effects are most pronounced at 10-15 minutes after administration of 30 mg/kg.
Schizophrenia Bulletin
December 18, 2015
Filip Španiel, Jaroslav Tintěra, Jan Rydlo et al.
55 citations
Disturbance of the sense of self may be a core marker of schizophrenia. In patients with first-episode schizophrenia-spectrum disorders compared with healthy controls, self-agency experience was associated with reduced cortical activation in the medial frontal gyrus and posterior cingulate gyrus. The ability to judge whether an action is one's own or another's depends on anti-correlated switching between the default mode and central-executive networks, a mechanism substantially impaired in the patient group during the task.
Psychopharmacology
January 1, 2013
Tomáš Páleníček, Michaela Fujáková, Martin Brunovský et al.
51 citations
The synthetic compound 2C-B produces a biphasic effect on movement in rats: initial inhibition followed by excitation, while amphetamine only causes hyperactivity. Both drugs disrupt prepulse inhibition of the acoustic startle reaction, a measure of sensory gating, but have opposite effects on the startle itself. 2C-B increases dopamine and decreases its metabolite DOPAC in the nucleus accumbens, a brain region linked to reward. Low doses of 2C-B reduce electrical brain activity and connectivity; a high dose first decreases then increases brain wave power and connectivity. Increases in theta and alpha brain waves correlate with heightened movement and dopamine levels. These results suggest 2C-B shares properties with hallucinogens, entactogens, and stimulants, and its dopamine effects may indicate psychotomimetic and addictive potential.
Psychological Medicine
December 9, 2009
Jiřı́ Horáček, Martin Brunovský, Tomáš Novák et al.
42 citations
A single dose of ketamine (0.54 mg/kg infused over 30 minutes) rapidly alters brain electrical activity in healthy volunteers, producing a decrease in prefrontal theta cordance—a QEEG measure linked to cerebral blood flow—and an increase in central region theta cordance within 10 to 30 minutes. These changes resemble those seen after one week of treatment with standard antidepressants in people who respond to them, but occur much faster. The prefrontal theta cordance reduction correlated with ketamine and norketamine blood levels at 10 minutes. The findings suggest that theta cordance reduction could serve as a marker and predictor of ketamine's rapid antidepressant effect, a hypothesis warranting testing in depressed patients.
European Psychiatry
March 1, 2015
Filip Španiel, Jaroslav Tintěra, Jan Rydlo et al.
1 citation
The ability to judge whether an action is one's own or another's depends on dynamic switching between two large-scale brain networks: the default mode network (DMN) and the central-executive network (CEN), which normally work in opposition. In people with first-episode schizophrenia spectrum disorders, this antagonistic switching mechanism is substantially impaired, and the degree of impairment correlates with poorer performance on self-agency judgment tasks. The findings suggest that a core pathology in schizophrenia may lie in the higher-order regulatory mechanisms that coordinate these networks.
Neuroscience and biobehavioral reviews
July 1, 2008
Věra Bubeníková-valešová, Jiří Horáček, Monika Vrajová et al.
Research using non-competitive NMDA receptor antagonists—phencyclidine, ketamine, and dizocilpine—produces behavioral changes in humans and rats that resemble schizophrenia symptoms. Acute and chronic administration models show phenomenological validity and help test potential antipsychotic drugs. However, schizophrenia's pathophysiology remains unexplained. The neurodevelopmental model suggests that early-life NMDA receptor antagonism increases apoptosis or alters glutamatergic receptor function during central nervous system development, leading to psychosis that often emerges only in adulthood. Chronic antagonist administration triggers adaptation mechanisms that match findings in schizophrenia patients, making this model useful for studying the disease's pathophysiology.