Thankachan S, Kaur S, Blanco-Centurion C, Sakurai T, Yanagisawa M, Shiromani PJ (2008) Ventrolateral periaquaductal gray (vlPAG): Key area for REM sleep propensity. Neuroscience 2008 Abstracts 586.3/SS36. Society for Neuroscience, Washington, DC.
Summary: In an effort to determine how loss of hypocretin/orexin (HOX) increases REM sleep we have used the neurotoxin, hypocretin-2-saporin (HCRT2-SAP), to lesion HOX receptor bearing neurons. Our efforts have focused on the pons (Blanco-Centurion et al., EJN 19:2741, 2004) since REM sleep is generated from there. Here, we investigate the vlPAG, a region where muscimol robustly increases REM sleep in cats (Sastre et al., Neuroscience, 74:415, 1996), and where HOX might activate GABA neurons that inhibit REM sleep. Lesion of vlPAG neurons with HCRT2-SAP should increase REM sleep. HCRT2-SAP (16.5ng/23nl) or saline (23nl; 0.9%) was injected (glass pipette; isofluorane anesthesia) to the vlPAG area in hypocretin/orexin null mice (HOX null) and in GAD-GFP mice [TgN(GadGFP)45704Swn; to visualize the GABA neurons]. Sleep was recorded 15th and 16th days after the lesion (12:12LD cycle). vlPAG lesion (n=5) significantly (+48.19%) increased REM sleep at night in HOX null mice compared to saline treated HOX null mice (n=7); REM sleep during the day was not changed. Over the 24h period REM sleep was significantly increased (+18.78%). However, cataplexy did not increase. In the GAD-GFP mice vlPAG lesions (n=8) also significantly increased REM sleep at night (+79.4%) compared to saline controls (n=8). The vlPAG lesions caused a significant increase in the number of short bouts (<40sec) of wake, NREM and REM sleep during both day and night. HOX null mice already have highly fragmented sleep, and increased REM sleep at night. Since vlPAG lesions produced a greater sleep fragmentation and increased REM sleep even further suggests that the vlPAG represents a key area, downstream of HOX neurons, in gating REM sleep propensity.
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