REM sleep promotes bidirectional plasticity in developing visual cortex .

Sleep is required for the full expression of plasticity during the visual critical period (CP). However, the precise role of rapid-eye-movement (REM) sleep in this process is undetermined. Previous studies in rodents indicate that REM sleep weakens cortical circuits following MD, but this has been explored in only one class of cortical neuron (layer 5 apical dendrites).

Anatomical correlates of rapid eye movement sleep-dependent plasticity in the developing cortex.

Rapid eye movement (REM) sleep is expressed at its highest levels during early life when the brain is rapidly developing. This suggests that REM sleep may play important roles in brain maturation and developmental plasticity. We investigated this possibility by examining the role of REM sleep in the regulation of plasticity-related proteins known to govern synaptic plasticity in vitro and in vivo.

Differential origin of the activation of dorsal and ventral dentate gyrus granule cells during paradoxical (REM) sleep in the rat.

We recently demonstrated that granule cells located in the dorsal dentate gyrus (dDG) are activated by neurons located in the lateral supramammillary nucleus (SumL) during paradoxical sleep (PS) hypersomnia. To determine whether these neurons are glutamatergic and/or GABAergic, we combined FOS immunostaining with in situ hybridization of vesicular glutamate transporter 2 (vGLUT2, a marker of glutamatergic neurons) or that of the vesicular GABA transporter (vGAT, a marker of GABAergic neurons) mRNA in rats displaying PS hypersomnia (PSR). We found that 84 and 76 % of the FOS+ SumL neurons in PSR rats expressed vGLUT2 and vGAT mRNA, respectively.

Rapid eye movement sleep promotes cortical plasticity in the developing brain.

Rapid eye movement sleep is maximal during early life, but its function in the developing brain is unknown. We investigated the role of rapid eye movement sleep in a canonical model of developmental plasticity in vivo (ocular dominance plasticity in the cat) induced by monocular deprivation. Preventing rapid eye movement sleep after monocular deprivation reduced ocular dominance plasticity and inhibited activation of a kinase critical for this plasticity (extracellular signal-regulated kinase).

The supramammillary nucleus and the claustrum activate the cortex during REM sleep.

Evidence in humans suggests that limbic cortices are more active during rapid eye movement (REM or paradoxical) sleep than during waking, a phenomenon fitting with the presence of vivid dreaming during this state. In that context, it seemed essential to determine which populations of cortical neurons are activated during REM sleep. Our aim in the present study is to fill this gap by combining gene expression analysis, functional neuroanatomy, and neurochemical lesions in rats.

Extracellular signal-regulated kinase (ERK) activity during sleep consolidates cortical plasticity in vivo.

Ocular dominance plasticity (ODP) in the cat primary visual cortex (V1) is induced during waking by monocular deprivation (MD) and consolidated during subsequent sleep. The mechanisms underlying this process are incompletely understood. Extracellular signal-regulated kinase (ERK) is activated in V1 during sleep after MD, but it is unknown whether ERK activation during sleep is necessary for ODP consolidation.

Tuberal hypothalamic neurons secreting the satiety molecule Nesfatin-1 are critically involved in paradoxical (REM) sleep homeostasis.

The recently discovered Nesfatin-1 plays a role in appetite regulation as a satiety factor through hypothalamic leptin-independent mechanisms. Nesfatin-1 is co-expressed with Melanin-Concentrating Hormone (MCH) in neurons from the tuberal hypothalamic area (THA) which are recruited during sleep states, especially paradoxical sleep (PS). To help decipher the contribution of this contingent of THA neurons to sleep regulatory mechanisms, we thus investigated in rats whether the co-factor Nesfatin-1 is also endowed with sleep-modulating properties.