ABSTRACT
While sleeping, many vertebrate groups alternate between at least two sleep stages: rapid eye movement and slow wave sleep1-4, in part characterized by wake-like and synchronous brain activity, respectively. Here we delineate neural and behavioural correlates of two stages of sleep in octopuses, marine invertebrates that evolutionarily diverged from vertebrates roughly 550 million years ago (ref. 5) and have independently evolved large brains and behavioural sophistication. 'Quiet' sleep in octopuses is rhythmically interrupted by approximately 60-s bouts of pronounced body movements and rapid changes in skin patterning and texture6. We show that these bouts are homeostatically regulated, rapidly reversible and come with increased arousal threshold, representing a distinct 'active' sleep stage. Computational analysis of active sleep skin patterning reveals diverse dynamics through a set of patterns conserved across octopuses and strongly resembling those seen while awake. High-density electrophysiological recordings from the central brain reveal that the local field potential (LFP) activity during active sleep resembles that of waking. LFP activity differs across brain regions, with the strongest activity during active sleep seen in the superior frontal and vertical lobes, anatomically connected regions associated with learning and memory function7-10. During quiet sleep, these regions are relatively silent but generate LFP oscillations resembling mammalian sleep spindles11,12 in frequency and duration. The range of similarities with vertebrates indicates that aspects of two-stage sleep in octopuses may represent convergent features of complex cognition.
Subject(s)
Central Nervous System , Integumentary System , Octopodiformes , Sleep , Wakefulness , Animals , Mammals/physiology , Octopodiformes/physiology , Sleep/physiology , Sleep, REM/physiology , Wakefulness/physiology , Integumentary System/innervation , Integumentary System/physiology , Movement/physiology , Time Factors , Local Field Potential Measurement , Learning/physiology , Central Nervous System/anatomy & histology , Central Nervous System/physiology , Arousal/physiologyABSTRACT
We develop a phenomenological coarse-graining procedure for activity in a large network of neurons, and apply this to recordings from a population of 1000+ cells in the hippocampus. Distributions of coarse-grained variables seem to approach a fixed non-Gaussian form, and we see evidence of scaling in both static and dynamic quantities. These results suggest that the collective behavior of the network is described by a nontrivial fixed point.
Subject(s)
Hippocampus/physiology , Models, Neurological , Neurons/physiology , Animals , Hippocampus/cytology , Humans , Mice , Nerve Net/cytology , Nerve Net/physiology , Neurons/cytologyABSTRACT
Discussions of the hippocampus often focus on place cells, but many neurons are not place cells in any given environment. Here we describe the collective activity in such mixed populations, treating place and non-place cells on the same footing. We start with optical imaging experiments on CA1 in mice as they run along a virtual linear track and use maximum entropy methods to approximate the distribution of patterns of activity in the population, matching the correlations between pairs of cells but otherwise assuming as little structure as possible. We find that these simple models accurately predict the activity of each neuron from the state of all the other neurons in the network, regardless of how well that neuron codes for position. Our results suggest that understanding the neural activity may require not only knowledge of the external variables modulating it but also of the internal network state.
Subject(s)
Hippocampus/cytology , Hippocampus/physiology , Nerve Net/cytology , Nerve Net/physiology , Neurons/physiology , Space Perception/physiology , Action Potentials , Algorithms , Animals , CA1 Region, Hippocampal/cytology , CA1 Region, Hippocampal/physiology , Entropy , Male , Mice , Mice, Inbred C57BL , Mice, Transgenic , Models, Neurological , Photic Stimulation , User-Computer InterfaceABSTRACT
The growing recognition that brain pathologies do not affect neurons only but rather are, to a large extent, pathologies of glial cells as well as of the vasculature opens to new perspectives in our understanding of genetic disorders of the CNS. To validate the role of the neuron-glial-vascular unit in the etiology of genome instability disorders, we report about cell death and morphological aspects of neuroglia networks and the associated vasculature in a mouse model of Ataxia Telangiectasia (A-T), a human genetic disorder that induces severe motor impairment. We found that A-T-mutated protein deficiency was consistent with aberrant astrocytic morphology and alterations of the vasculature, often accompanied by reactive gliosis. Interestingly similar findings could also be reported in the case of other genetic disorders. These observations bolster the notion that astrocyte-specific pathologies, hampered vascularization and astrocyte-endothelium interactions in the CNS could play a crucial role in the etiology of genome instability brain disorders and could underlie neurodegeneration.
