Chronic ketamine administration during adolescence in mice produces long-lasting changes in synaptic integration in the dorsal hippocampal dentate gyrus, specifically expanding the temporal window for inputs from the inner molecular layer but not the medial perforant path. Ketamine also reduces inhibitory synaptic efficacy, likely by decreasing the number and function of parvalbumin-positive interneurons, thereby altering the excitatory/inhibitory balance. These findings suggest that adolescent ketamine exposure strongly affects inhibitory synaptic function mediated by parvalbumin neurons, ultimately impacting synaptic integration in adulthood and may help explain the heightened vulnerability of the adolescent brain.
Sleep is a complex neurophysiological process. A new integrative framework proposes that REM sleep is a state where the brain constructs a provisional dummy model of the external world. NREM sleep is a phase of synaptic and network reorganization with glymphatic clearance, updating neural circuits based on waking experience. REM sleep then provides an internal testing ground to simulate reality and refine these updates. The framework distinguishes phasic and tonic REM states and involves subcortical networks like the Papez circuit and claustrum. A central prediction is that prediction errors during REM drive selective synaptic consolidation in subsequent NREM via hippocampal sharp-wave ripple-mediated feedback. Awakening occurs when global prediction error falls below a threshold, and total sleep duration should be proportional to the complexity of novel waking experience.
Using a new rodent model of reversible brain anoxia with continuous electrocorticographic (ECoG) and intracellular recordings, the authors tracked neocortical dynamics from oxygen deprivation through recovery. Oxygen loss caused an early surge of beta-gamma activity with rhythmic membrane depolarizations in pyramidal neurons, followed by low-frequency activity declining to isoelectric levels. During the isoelectric state, a massive depolarizing shift produced a large triphasic ECoG wave known as the "wave-of-death" (WoD). If re-oxygenation occurred within 2–3.5 minutes, this anoxic depolarization reversed. The subsequent slow repolarization generated a second ECoG wave termed "wave-of-resuscitation," marking recovery of pre-anoxic activity. The WoD is not a biomarker of irremediable death; the new wave may predict successful recovery.
The author argues that despite rejecting dualism, neuroscience literature often contains covert dualistic assumptions, particularly in the reluctance to discuss neural mechanisms of consciousness. The prevailing paradigm holds that cognitive functions emerge from networks of simple neurons that only generate electrical potentials and transmit signals. The author contends such networks cannot produce human mental activity or consciousness. Drawing on physiological, morphological, clinical, and genetic studies of cognitive functions (especially linguistic ones), the author proposes that cognitive functions depend on the cooperative activity of "complex" neurons that serve as carriers of "elementary cognition.