Sleep-promoting functions of the hypothalamic median preoptic nucleus: inhibition of arousal systems.
Recent work supports the hypotheses developed by von Economo and Nauta and elaborated by Sallanon et al. that the POA contains a sleep-promoting output that opposes wake-promoting neuronal groups in the PH. The POA gives rise to descending pathways that terminate within wake-promoting populations in pLH, PH and midbrain. Current evidence suggests that this output originates in POA sleep-active GABAergic neurons. This output also seems to convey the signals of homeostatic drive. Disynaptic projections from the SCN to both MnPN and VLPO were recently identified. These may regulate the circadian control of sleep propensity. The hypothesis that the descending projections from POA sleep-active neurons to sites of arousal-related neurons originates in GABAergic neurons must be confirmed. Also to be further clarified is the anatomical distribution of putative sleep-active GABAergic neurons within the POA. Segregated groups have been found in the MnPN and VLPO, but unit recording studies of sleep-active neurons, lesion studies and local neurochemical application studies all indicate that sleep-active neurons may be found diffusely in the POA and adjacent areas. The MnPN has been shown previously to be involved in water balance and blood pressure regulation and to be responsive to hyperthermia. Our studies suggest that this nucleus also contains sleep-active, putative sleep-promoting neurons. However, interactions between sleep control and physiological variables must be considered. In particular, the details of neuronal basis of the coupling of warm-sensitive neurons in MnPN to the POA hypnogenic output has not been explored. It is also worth noting that both the VLPO and MnPN lie close to the ventricular and subarachnoid surface and are punctuated by radial arterioles. The possibility that the sleep-regulatory functions of these sites is coupled to physiological signals conveyed through epithelial cells has been suggested for the actions of PGD2 but has yet to be explored in detail for other putative hypnogens.
McGinty
D
D
Veterans Administration, Sepulveda, Greater Los Angeles Health System and Departments of Psychology and Medicine, UCLA, USA. dmcginty@ucla.edu
Gong
H
H
Suntsova
N
N
Alam
Md N
MN
Methippara
M
M
Guzman-Marin
R
R
Szymusiak
R
R
D000200:Action Potentials / Q000502:physiology; D001143:Arousal / Q000502:physiology*; D008959:Models, Neurological; D009433:Neural Inhibition / Q000502:physiology; D009434:Neural Pathways / Q000033:anatomy & histology / Q000502:physiology*; D011301:Preoptic Area / Q000033:anatomy & histology / Q000502:physiology*; D012890:Sleep / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D005680:gamma-Aminobutyric Acid