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The Journal of Neuroscience, September 1, 2002, 22(17):7695-7711
Anatomical, Physiological, and Pharmacological Characteristics of
Histidine Decarboxylase Knock-Out Mice: Evidence for the Role of Brain
Histamine in Behavioral and Sleep-Wake Control
Régis
Parmentier1,
Hiroshi
Ohtsu2,
Zahia
Djebbara-Hannas1,
Jean-Louis
Valatx1,
Takehiko
Watanabe2, and
Jian-Sheng
Lin1
1 Institut National de la Santé et de la
Recherche Médicale U480, Department of Experimental Medicine,
Faculty of Medicine, Claude Bernard University, 69373 Lyon, France, and
2 Department of Cellular Pharmacology, Tohoku University,
School of Medicine, Aoba-ku, Sendai 980-8575, Japan
The hypothesis that histaminergic neurons are involved in brain
arousal is supported by many studies. However, the effects of the
selective long-term abolition of histaminergic neurons on the
sleep-wake cycle, indispensable in determining their functions, remain
unknown. We have compared brain histamine(HA)-immunoreactivity and
the cortical-EEG and sleep-wake cycle under baseline conditions or
after behavioral or pharmacological stimuli in wild-type (WT) and
knock-out mice lacking the histidine decarboxylase gene (HDC /). HDC/mice showed an increase in paradoxical sleep, a decrease in cortical EEG power in  -rhythm during waking (W), and a decreased EEG slow wave sleep/W power ratio. Although no major difference was
noted in the daily amount of spontaneous W, HDC/mice showed a
deficit of W at lights-off and signs of somnolence, as demonstrated by
a decreased sleep latencies after various behavioral stimuli, e.g.,
WT-mice placed in a new environment remained highly awake for 2-3 hr,
whereas HDC/mice fell asleep after a few minutes. These
effects are likely to be attributable to lack of HDC and thus of HA. In WT mice, indeed, intraperitoneal injection of
 -fluoromethylhistidine (HDC-inhibitor) caused a decrease in W,
whereas injection of ciproxifan (HA-H3 receptor antagonist) elicited W. Both injections had no effect in HDC/mice. Moreover,
PCR and immunohistochemistry confirmed the absence of the HDC gene and
brain HA-immunoreactive neurons in the HDC/mice. These data
indicate that disruption of HA-synthesis causes permanent changes in
the cortical-EEG and sleep-wake cycle and that, at moments when high
vigilance is required (lights off, environmental change... ), mice
lacking brain HA are unable to remain awake, a prerequisite condition
for responding to behavioral and cognitive challenges. We suggest that
histaminergic neurons also play a key role in maintaining the brain in
an awake state faced with behavioral challenges.
Key words:
wakefulness; sleep-wake cycle; cortical activation; arousal; histaminergic neurons; histamine; histidine decarboxylase
knock-out mice; cortical EEG; behavioral challenge
Copyright © 2002 Society for Neuroscience 0270-6474/02/22177695-17$05.00/0
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