Evidence that Neurons of the Sublaterodorsal Tegmental Nucleus Triggering Paradoxical (REM) Sleep Are Glutamatergic

Olivier, C; Sapin, Emilie; Bérod, Anne; Fort, Patrice; Luppi, Pierre‐Hervé

doi:10.1093/sleep/34.4.419

Cited by 146 publications

(105 citation statements)

References 16 publications

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“…Then, Lu et al [63] reported for the first time the presence of vGlut2-containing neurons in the SLD. We recently further demonstrated that most of the Fos-labeled neurons localized in the SLD after PS recovery express vGlut2 [21]. Altogether, these results indicate that the PS-on SLD neurons triggering PS are glutamatergic.…”

Section: Sld Neurons Triggering Ps Are Glutamatergicmentioning

confidence: 63%

Brainstem mechanisms of paradoxical (REM) sleep generation

Luppi

Olivier

Sapin

et al. 2011

Pflugers Arch - Eur J Physiol

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118

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Paradoxical sleep (PS) is characterized by EEG activation with a disappearance of muscle tone and the occurrence of rapid eye movements (REM) in contrast to slow-wave sleep (SWS, also known as non-REM sleep) identified by the presence of delta waves. Soon after the discovery of PS, it was demonstrated that the structures necessary and sufficient for its genesis are restricted to the brainstem. We review here recent results indicating that brainstem glutamatergic and GABAergic, rather than cholinergic and monoaminergic, neurons play a key role in the genesis of PS. We hypothesize that the entrance to PS from SWS is due to the activation of PS-on glutamatergic neurons localized in the pontine sublaterodorsal tegmental nucleus. The activation of these neurons would be due to a permanent glutamatergic input arising from the lateral and ventrolateral periaqueductal gray (vlPAG) and the removal at the onset of PS of a GABAergic inhibition present during W and SWS. Such inhibition would be coming from PS-off GABAergic neurons localized in the vlPAG and the adjacent deep mesencephalic reticular nucleus. The cessation of activity of these PS-off GABAergic neurons at the onset and during PS would be due to direct projections from intermingled GABAergic PS-on neurons. Activation of PS would depend on the reciprocal interactions between the GABAergic PS-on and PS-off neurons, intrinsic cellular and molecular events, and integration of multiple physiological parameters.

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Section: Sld Neurons Triggering Ps Are Glutamatergicmentioning

confidence: 63%

Brainstem mechanisms of paradoxical (REM) sleep generation

Luppi

Olivier

Sapin

et al. 2011

Pflugers Arch - Eur J Physiol

Self Cite

118

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show abstract

“…In contrast, functional mapping studies using the c-fos method in animals with a compensatory hyper-expression of REMS after sustained periods of REMS deprivation did not report any significant activation of the medial parabrachial nucleus (Verret et al, 2005;Clément et al, 2011). These studies identified clusters of activated neurons in the central subnucleus of the lateral parabrachial complex (Verret et al, 2005;Clément et al, 2011).…”

Section: The Role Of the Parabrachial Complex In Remsmentioning

confidence: 68%

“…These studies identified clusters of activated neurons in the central subnucleus of the lateral parabrachial complex (Verret et al, 2005;Clément et al, 2011).…”

Section: The Role Of the Parabrachial Complex In Remsmentioning

confidence: 99%

The emerging role of the parabrachial complex in the generation of wakefulness drive and its implication for respiratory control

Martelli

Stanić

Dutschmann

2013

Respiratory Physiology & Neurobiology

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“…The VLPO sends inhibitory projections to the areas of the pontine tegmentum (as well as the ventrolateral periaqueductal gray area) not active during REM, thus "REM-off" neurons. These neurons then project to other "REM-on" areas of the brain, including glutamatergic neurons that send inhibitory messages to the spine, contributing to the muscle atonia associated with REM sleep (Clement, Sapin, Berod, Fort, & Luppi, 2011;Fuller & Lu, 2009;. In fact, recent evidence suggests that damage to the glutamatergic regions projecting to the spine may have some involvement in REM behavior disorder, a sleep dysfunction that exhibits signs of REM sleep without muscle atonia, as well as the cataplexy associated with the most well-known REM disorder, narcolepsy Luppi et al, 2011).…”

Section: Rem Sleepmentioning

confidence: 99%