The name is absent

The assertion that REM sleep replenishes depleted ATP reserves in the
hippocampus and associated brain structures rest on four primary assumptions. First, the
hippocampus becomes especially active during REM sleep (Lerma-Garcia-Austt, 1985;
Rimbaud, Passouant, & Cadilhac, 1955). Second, the hippocampus requires ATP to
function (e.g., Inoue, 1998; Inoue et al., 1999). Third, ATP in the brain comes almost
exclusively from the metabolism of glucose (Peters et al., 2004). Fourth, glucose in the
brain comes from two primary sources: cerebral glycogen and blood glucose (Benington
& Heller, 1995).

A preliminary interpretation of the physiological features associated with REM
sleep may now be offered. Preparations for replenishing depleted ATP reserves in the
hippocampus appear to begin prior to the onset of REM sleep. It seems that a sequence of
events ensures that an adequate amount of glucose will be available for significant ATP
generation during REM sleep. Hormonal changes rhythmically increase blood glucose
levels in the hours before nocturnal sleep in healthy young adults, and blood glucose
levels remain elevated throughout sleep (Van Cauter, 2005). During NREM sleep,
cerebral glycogen levels become elevated (Anchors & Burrows, 1983; Benington &
Heller, 1995). “Glycogen represents the largest store of glucose equivalents in the brain”
(Gruetter, 2003).

Tonic REM sleep begins with the complete immobilization of the body (Rama,
Cho, & Kushida, 2006). Glycogen is metabolized, increasing the amount of glucose
available in the brain (Rechtschaffen, 1998). Increased cerebral glycogen metabolism has
also been observed in organisms exerting effort (Gruetter, 2003). However, this is “an
unlikely end point of sleep’s functional role in brain energy homeostasis” (Franken, Gip,

preliminary draft (9/24/2006)

<<   4   5   6   7   8   9   10   >>

More intriguing information