The Neuroscientist
January 4, 2005
Olaf Blanke, Shahar Arzy
468 citations
Out-of-body experiences (OBEs), where one's perspective and sense of self seem to leave the body, challenge the everyday assumption that the self resides inside the body. Evidence from neurology, cognitive neuroscience, and neuroimaging indicates that OBEs arise from a failure to integrate multisensory information about one's own body at the temporo-parietal junction (TPJ). This multisensory disintegration disrupts self-processing, producing illusory reduplication, self-location, perspective, and agency that together constitute the OBE.
The Neuroscientist
September 1, 2017
Selen Atasoy, Gustavo Deco, Morten L. Kringelbach et al.
131 citations
Spontaneous brain activity exhibits coherent oscillations across a wide range of frequencies, with temporal patterns highly correlated across distributed cortical areas, forming resting state networks. This work introduces harmonic brain modes as fundamental building blocks of complex spatiotemporal neural activity, defined as harmonic modes of structural connectivity (connectome harmonics) that yield fully synchronous activity patterns with different frequency oscillations constrained by brain structure. This framework links space and time in brain dynamics. The authors show how harmonic brain modes explain neurophysiological, temporal, and network-level changes across mental states (wakefulness, sleep, anesthesia, psychedelic). Spatial and temporal characteristics emerge from the interplay between excitation and inhibition, fitting changes associated with different mental states, offering tools for understanding brain dynamics in various states of consciousness.
The Neuroscientist
May 25, 2022
Georg Northoff, Deniz Vatansever, Andrea Scalabrini et al.
53 citations
Ongoing brain activity, often linked to the default-mode network (DMN) and internally focused thought, is typically contrasted with task-related, externally oriented cognition. This dual model is challenged by a baseline model, which proposes that ongoing activity serves as a neuronal baseline—an internal reference point for both rest and task states. This shared neural code is reflected in the spatiotemporal organization of brain activity, including global signal topography and intrinsic neural timescales. The authors conclude that recent evidence supports the baseline model over the dual model, suggesting that ongoing activity integrates rest and task states, DMN and non-DMN networks, and internally and externally oriented cognition.
The Neuroscientist
December 26, 2025
Kallol Bera, Loren L. Looger, Alex Proekt et al.
5 citations
Ketamine, an anesthetic that produces dissociative anesthesia—characterized by perceptual detachment, analgesia, and altered consciousness—also acts as a rapid antidepressant at low doses and serves as a tool to study consciousness and neuropsychiatric disorders. Its effects stem from actions on cortical circuits: blocking NMDA receptors and HCN1 channels, disinhibiting pyramidal neurons, and altering thalamocortical connectivity. The review synthesizes findings from pharmacology, cell-specific imaging, and systems neuroscience to explain how ketamine alters cortical dynamics to drive dissociation. It also explores the possibility that ketamine enters intracellular compartments, modulating neuronal excitability, signaling, and epigenetic state after a single dose. Understanding these processes may inform new treatments for treatment-resistant depression and the study of consciousness.
The Neuroscientist
August 1, 2000
J. David Jentsch, Jane R. Taylor, Robert H. Roth
Long-term use of drugs like phencyclidine (PCP), which block NMDA glutamate receptors, can produce schizophrenia-like symptoms in people and abnormal behavior in animals. This review evaluates how well PCP-induced animal behaviors model human psychotic disorders and presents a hypothesis about PCP's effects on the prefrontal cortex. The behavioral and neurochemical changes caused by PCP suggest that altered interactions between glutamate and dopamine systems in the prefrontal cortex may contribute to the cognitive problems seen in schizophrenia.