Wakefulness affecting

Matching the flow between the impeller and the diffuser is complex because the flow path changes from a rotating system into a stationary one. This complex, unsteady flow is strongly affected by the jet-wake of the flow leaving the impeller, as seen in Figure 6-29. The three-dimensional boundary layers, the secondary flows in the vaneless region, and the flow separation at the blades also affects the overall flow in the diffuser. 

The basal forebrain is an important way station in the activation of the cerebral cortex from the reticular activating system. AMPA and NMDA injections into the basal forebrain increase wakefulness and reduce sleep (Cape Jones, 2000 Manfridi et al, 1999), effects that are blocked by AMPA and NMDA receptor antagonists (Manfridi et al, 1999). The excitatory cortical projections of the basal forebrain have long been considered purely cholinergic, but many basal forebrain neurons that project to the cortex are now known to contain Glu, which may function as a co-transmitter or even as the primary excitatory neurotransmitter (Manns et al, 2001). The basal forebrain also affects vigilance via synapses to HCT cells in the lateral hypothalamus some of these synapses are glutamatergic (Henny Jones, 2006). 

A role for A2 Rs in sleep-wake regulation was also supported by studies in mice with constitutional knockout of A2ARs (Urade et al., 2003). Infusion into the lateral ventricle of CGS 21680 increased NREM and REM sleep in wild-type mice, but not in the knockouts. In contrast, the AiR agonist CPA did not affect sleep in either genotype, which indicated that AiRs could not compensate for the absence of A2aRs under these conditions. 

The importance of adenosine deaminase in the duration and intensity of sleep in humans has been noted recently (Retey et al. 2005). Animal studies suggest that sleep needs are genetically controlled, and this also seems to apply in humans. Probably, a genetic variant of adenosine deaminase, which is associated with the reduced metabolism of adenosine to inosine, specifically enhances deep sleep and slow wave activity during sleep. Thus low activity of the catabolic enzyme for adenosine results in elevated adenosine, and deep sleep. In contrast, insomnia patients could have a distinct polymorphism of more active adenosine deaminase resulting in less adenosine accumulation, insomnia, and a low threshold for anxiety. This could also explain interindividual differences in anxiety symptoms after caffeine intake in healthy volunteers. This could affect the EEG during sleep and wakefulness in a non-state-specific manner. 

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