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sleep_physiology [2026/09/15 08:51] – [neurophysiology] gary1sleep_physiology [2026/09/15 08:52] (current) – [neurophysiology] gary1
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     * failure of these appear to be a cause of type 1 narcolepsy     * failure of these appear to be a cause of type 1 narcolepsy
     * inappropriate stimulation of these may cause insomnia     * inappropriate stimulation of these may cause insomnia
-  ***cortical role for falling asleep:** 
-    * an extraordinarily rare population of neurons in the cortex-called Sst-Chodl neurons (0.2% of neurons in the cortex) can synchronize activity across large areas of the brain via  long-range axons and promote sleep and these have been preserved across hundreds of millions of years of evolution, from amphibians and reptiles to humans(([[https://www.nature.com/articles/s41586-026-10876-y|2026: Neocortical long-range inhibition promotes cortical synchrony and sleep]])) 
   ***the locus coeruleus (LC) has a key role in arousal**   ***the locus coeruleus (LC) has a key role in arousal**
     * it is a 2cm long area of a dense group of cells in the in the lateral part of the pontine tegmentum of the brain stem.      * it is a 2cm long area of a dense group of cells in the in the lateral part of the pontine tegmentum of the brain stem. 
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       * analgesic activity is mainly driven by the LC ipsilateral to the site of the pain stimulus, and it appears to be produced by activation of the descending LC pathway to the SC, which enhances the NE release that would in turn contribute to the blockade of nociceptive ascending inputs. NE released from descending pathways in the spinal dorsal horn suppresses pain through the inhibitory influence of α2A adrenoceptors on central terminals of primary afferent nociceptors (presynaptic inhibition), as well as by direct α2-adrenergic action on pain-relay neurons (postsynaptic inhibition) and by α1 adrenoceptor–mediated activation of inhibitory interneurons. Disruption of the normal LC-NE circuit may result in increased pain sensitivity.(([[https://www.biologicalpsychiatryjournal.com/article/S0006-3223(21)01838-2/fulltext]]))       * analgesic activity is mainly driven by the LC ipsilateral to the site of the pain stimulus, and it appears to be produced by activation of the descending LC pathway to the SC, which enhances the NE release that would in turn contribute to the blockade of nociceptive ascending inputs. NE released from descending pathways in the spinal dorsal horn suppresses pain through the inhibitory influence of α2A adrenoceptors on central terminals of primary afferent nociceptors (presynaptic inhibition), as well as by direct α2-adrenergic action on pain-relay neurons (postsynaptic inhibition) and by α1 adrenoceptor–mediated activation of inhibitory interneurons. Disruption of the normal LC-NE circuit may result in increased pain sensitivity.(([[https://www.biologicalpsychiatryjournal.com/article/S0006-3223(21)01838-2/fulltext]]))
     * LC neurons are lost in the course of several neurodegenerative disorders, including Alzheimer's and Parkinson's diseases     * LC neurons are lost in the course of several neurodegenerative disorders, including Alzheimer's and Parkinson's diseases
 +  ***cortical role for falling asleep:** 
 +    * an extraordinarily rare population of neurons in the cortex-called Sst-Chodl neurons (0.2% of neurons in the cortex) can synchronize activity across large areas of the brain via  long-range axons and promote sleep and these have been preserved across hundreds of millions of years of evolution, from amphibians and reptiles to humans(([[https://www.nature.com/articles/s41586-026-10876-y|2026: Neocortical long-range inhibition promotes cortical synchrony and sleep]]))
  
 ====molecular basis==== ====molecular basis====
sleep_physiology.txt · Last modified: 2026/09/15 08:52 by gary1

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