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2015 ; 3
(5
): 648-650
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Hypocretin/orexin prevents recovery from sickness
#MMPMID26405539
Tanaka S
; Toyoda H
; Honda Y
; Seki Y
; Sakurai T
; Honda K
; Kodama T
Biomed Rep
2015[Sep]; 3
(5
): 648-650
PMID26405539
show ga
Sickness behavior is defined as states of lethargy, depression, anxiety, loss of
appetite, hypersomnia, hyperalgesia, reduction of grooming and failure to
concentrate that can be induced by inflammatory diseases, such as infections and
cancer. Recent findings revealed that the lipopolysaccharide (LPS) injection
causes lethargy as a consequence of the inhibition of hypocretin signaling. The
hypocretin system maintains the vigilance state in various physiological
processes. In order to investigate the sleep arousal system against sickness
behavior, LPS-induced sickness behavior was examined in hypocretin-ataxin-3
transgenic mice, whose hypocretin neurons were postnatally ablated. Sleep-wake
activity was determined following the administration of LPS at Zeitgeber time
(ZT) 8.0 in ataxin-3 transgenic mice, and the age-, gender-matched wild-type
littermates. LPS injection induced increases in non-rapid eye movement (REM)
sleep in the matched wild-type littermates. In addition, a further increase in
periods of sleep according to the loss of hypocretin neurons was identified in
the ataxin-3 transgenic mice. A marked reduction of awakening during ZT12-ZT18
was observed as expected following LPS injection in the mouse lines. The increase
in the period of non-REM sleep was not observed on the next day following LPS
administration in either of the mouse lines. Complete recovery of physical
activity was not observed in the matched wild-type littermates. Ataxin-3
transgenic mice recovered their physical activity to the same level as that on
the first day before LPS administration. These results suggest the possibility
that a faster recovery is the result of deeper resting according to the absence
of hypocretin neurons, as ataxin-3 transgenic mice demonstrated more non-REM
sleep.
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