The team further characterized GABAergic neurons in the VLPO
that make direct synaptic contact with hypothalamic arousal-related neurons.
Prostaglandins and proinflammatory cytokines (and bacterial fragments) also promote VLPO activation.
Once activated, the VLPO triggers the release of gamma aminobutyric acid (GABA) in the brainstem.
VLPO is also regulated by the SCN, which is the body's internal clock, generating a circadian rhythm that dictates we sleep at night and are wakeful during the day.
In the first two hours after glucose was injected directly into the VLPO, mice fell into a deep sleep called slow-wave sleep faster and stayed there longer than mice injected with a nonsugar solution.
VLPO neurons can directly sense the glucose in their neighborhood, other experiments revealed.
continent in VLPO
area increases; tuberomammillary nucleus [TMN] and LC decrease) .
The contemporary theory for the mechanism of NREM sleep thus suggests a reciprocal interaction between two antagonistic neurons in the VLPO
of the anterior hypothalamus and wake-promoting neurons in the tuberomammillary nuclei of the posterior hypothalamus, as well as locus coeruleus, dorsal raphe, basal forebrain and mesopontine tagmentum (6,20).
(9,14,20) There are also mutual projections between the VLPO
neurons and the hypocretin neurons.
Further experiments revealed that isoflurane works by changing how these VLPO
neurons respond to potassium atoms, though exactly how that happens isn't clear.
The anesthetized rodents exhibited increased brain-cell activity in the VLPO and decreased activity in the TMN, the same pattern seen during deep, dreamless sleep.
The VLPO region doesn't contain GABA receptors, however.