ABSTRACT
Sleep spindles facilitate memory consolidation in the cortex during mammalian non-rapid eye movement sleep. In rodents, phase-locked firing during spindles may facilitate spike-timing-dependent plasticity by grouping pre-then-post-synaptic cell firing within ~25 ms. Currently, microphysiological evidence in humans for conditions conducive for spike-timing-dependent plasticity during spindles is absent. Here, we analyze field potentials and unit firing from middle/upper layers during spindles from 10 × 10 microelectrode arrays at 400 µm pitch in humans. We report strong tonic and phase-locked increases in firing and co-firing within 25 ms during spindles, especially those co-occurring with down-to-upstate transitions. Co-firing, spindle co-occurrence, and spindle coherence are greatest within ~2 mm, and high co-firing of units on different contacts depends on high spindle coherence between those contacts. Spindles propagate at ~0.28 m/s in distinct patterns, with correlated cell co-firing sequences. Spindles hence organize spatiotemporal patterns of neuronal co-firing in ways that may provide pre-conditions for plasticity during non-rapid eye movement sleep.
Subject(s)
Action Potentials/physiology , Cerebral Cortex/physiology , Memory Consolidation/physiology , Neuronal Plasticity/physiology , Neurons/physiology , Sleep, REM/physiology , Adult , Cerebral Cortex/anatomy & histology , Electrodes, Implanted , Electroencephalography , Epilepsy/pathology , Epilepsy/physiopathology , Female , Humans , Male , Middle Aged , Neurons/cytology , Stereotaxic TechniquesSubject(s)
Dermatitis, Atopic/epidemiology , Seasons , Armenia/epidemiology , Child, Preschool , Dermatitis, Atopic/etiology , Female , Humans , Infant , Male , Parturition , Risk FactorsABSTRACT
Every night, the human brain produces thousands of downstates and spindles during non-REM sleep. Previous studies indicate that spindles originate thalamically and downstates cortically, loosely grouping spindle occurrence. However, the mechanisms whereby the thalamus and cortex interact in generating these sleep phenomena remain poorly understood. Using bipolar depth recordings, we report here a sequence wherein: (1) convergent cortical downstates lead thalamic downstates; (2) thalamic downstates hyperpolarize thalamic cells, thus triggering spindles; and (3) thalamic spindles are focally projected back to cortex, arriving during the down-to-upstate transition when the cortex replays memories. Thalamic intrinsic currents, therefore, may not be continuously available during non-REM sleep, permitting the cortex to control thalamic spindling by inducing downstates. This archetypical cortico-thalamo-cortical sequence could provide the global physiological context for memory consolidation during non-REM sleep.
