Cognitive fatigue: an impaired cortical inhibitory replenishment.

Primary Objective: The present study explores the cause of cognitive fatigue in persons with traumatic brain injury (TBI), as also in persons with Multiple Sclerosis (MS). Since cognitive fatigue shares many symptoms with chronic sleep deprivation (best described as cumulative excess wakefulness), it was hypothesized that cognitive fatigue is caused by cumulative excess wakefulness because of an impaired sleep efficacy. Recent results about the nature of sleep advocate that sleep aims primarily to replenish the efficiency of cortical inhibitory synapses.

Morvan's syndrome and the sustained absence of all sleep rhythms for months or years: An hypothesis.

Despite the predation costs, sleep is ubiquitous in the animal realm. Humans spend a third of their life sleeping, and the quality of sleep has been related to co-morbidity, Alzheimer disease, etc. Excessive wakefulness induces rapid changes in cognitive performances, and it is claimed that one could die of sleep deprivation as quickly as by absence of water.

Sleep: The hebbian reinforcement of the local inhibitory synapses.

Sleep is ubiquitous among the animal realm, and represents about 30% of our lives. Despite numerous efforts, the reason behind our need for sleep is still unknown. The Theory of neuronal Cognition (TnC) proposes that sleep is the period of time during which the local inhibitory synapses (in particular the cortical ones) are replenished.

Neurotrophic signaling molecules associated with cholinergic damage in young and aged rats: environmental enrichment as potential therapeutic agent.

The aim of this study was to determine the neurobiological bases of behavioral deficits associated with cholinergic damage and the potential of long-term environmental enrichment as a therapeutic agent. Rats were submitted to intra-structures injection of 192 IgG-saporin and then behaviorally tested 1 month and 1 year post-lesion in a nonmatching-to-position task. The gene expression changes were assessed by cDNA macroarray technology using the GE array Q series designed to profile the expression of neurotrophic signaling molecules.