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10.3389/fneur.2015.00123 http://scihub22266oqcxt.onion/10.3389/fneur.2015.00123 C4448509!4448509!26074874     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Neurol 2015 ; 6 (ä): ä Nephropedia Template TP {{tp|p=26074874|t=2015. REM Sleep at its Core ? Circuits, Neurotransmitters, and Pathophysiology |pdf=|usr=}}{{26074874}} gab.com Text REM Sleep at its Core Circuits, Neurotransmitters, and Pathophysiology JO: Front Neurol http://www.kidney.de/pget.php?&tw=1&pmid=26074874 #FOAvip Rapid eye movement (REM) sleep is generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. Within these circuits lies a core region that is active during REM sleep, known as the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus. It is hypothesized that glutamatergic SubC neurons regulate REM sleep and its defining features such as muscle paralysis and cortical activation. REM sleep paralysis is initiated when glutamatergic SubC cells activate neurons in the ventral medial medulla, which causes release of GABA and glycine onto skeletal motoneurons. REM sleep timing is controlled by activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal paragigantocellular reticular nucleus as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the laterodorsal and pedunculo-pontine tegmentum in the brainstem. Determining how these circuits interact with the SubC is important because breakdown in their communication is hypothesized to underlie narcolepsy/cataplexy and REM sleep behavior disorder (RBD). This review synthesizes our current understanding of mechanisms generating healthy REM sleep and how dysfunction of these circuits contributes to common REM sleep disorders such as cataplexy/narcolepsy and RBD. Twit Text FOAVip REM Sleep at its Core Circuits, Neurotransmitters, and Pathophysiology ????Front Neurol http://www.kidney.de/pget.php?&tw=1&pmid=26074874 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26074874 #FOAvip English Wikipedia <ref>{{Cite pmid|26074874}}</ref> REM Sleep at its Core ? Circuits, Neurotransmitters, and Pathophysiology #MMPMID26074874 Fraigne JJ; Torontali ZA; Snow MB; Peever JH Front Neurol 2015[]; 6 (ä): ä PMID26074874show ga Rapid eye movement (REM) sleep is generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. Within these circuits lies a core region that is active during REM sleep, known as the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus. It is hypothesized that glutamatergic SubC neurons regulate REM sleep and its defining features such as muscle paralysis and cortical activation. REM sleep paralysis is initiated when glutamatergic SubC cells activate neurons in the ventral medial medulla, which causes release of GABA and glycine onto skeletal motoneurons. REM sleep timing is controlled by activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal paragigantocellular reticular nucleus as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the laterodorsal and pedunculo-pontine tegmentum in the brainstem. Determining how these circuits interact with the SubC is important because breakdown in their communication is hypothesized to underlie narcolepsy/cataplexy and REM sleep behavior disorder (RBD). This review synthesizes our current understanding of mechanisms generating healthy REM sleep and how dysfunction of these circuits contributes to common REM sleep disorders such as cataplexy/narcolepsy and RBD. äREM Sleep at its Core ? Circuits, Neurotransmitters, and Pathophysiolo(epmc).pdf DeepDyve Pubget Overpricing