Kindling stimuli delivered at different times in the sleep-wake cycle.
OBJECTIVE
Clinical and experimental observations argue that sleep disturbances are common and coexist in patients with epilepsy. Our previous observations have suggested that neural-immune interactions between corticotropin-releasing hormone (CRH) and interleukin-1 (IL-1) are involved in the regulation of physiological sleep-wake behavior. In the present study, we determined the involvement of CRH and IL-1 in the alteration of sleep-wake activities in rats when amygdala kindling was given either at the beginning of the light period (light-onset kindling) or at the beginning of the dark period (dark-onset kindling).


METHODS
The analysis of sleep-wake activities was performed before and after full-blown kindling, and the actions of CRH and IL-1 were tested by pharmacological blockade.


METHODS
Neuroscience Laboratory at China Medical University Hospital. PARTICIPANT AND INTERVENTIONS: Male Sprague-Dawley rats were implanted with electroencephalogram (EEG) electrodes and an intracerebroventricular (ICV) guide cannula. Kindling stimuli delivered via a bipolar electrode placing in the right central nucleus of the amygdala.


RESULTS
Amygdala kindling induced diverse effects on sleep. Slow-wave sleep (SWS) and rapid eye movement (REM) sleep decreased during the first 12-hour light period when rats were kindled at light onset. When dark-onset kindling was given, SWS increased but REM sleep was not altered during the first 12-hour dark period. After light-onset kindling, the circulating corticosterone concentrations increased and were blocked by ICV administration of the CRH receptor antagonist, astressin or alpha-hCRH. The ICV administration of the CRH antagonist blocked the light-onset kindling-induced decrease of SWS in a dose-dependent manner. After dark-onset kindling, IL-1 mRNA expression in the hippocampus and cortex increased. The dark-onset kindling-induced SWS was blocked in a dose-dependent manner by ICV administration of IL-1 receptor antagonist (IL-1 ra). The slow-wave activity during SWS was enhanced regardless of when kindling occurred, but both CRH antagonists and IL-1 ra had little effect on the alteration of slow-wave activity.


CONCLUSIONS
These observations argue that amygdala-kindling-induced sleep-wake alterations are modulated by central increases in CRH or IL-1.
Yi
Pei-Lu
PL
Department of Nursing, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan.
Tsai
Chon-Haw
CH
Lin
Jaung-Geng
JG
Lee
Cheng-Chun
CC
Chang
Fang-Chia
FC
D000679:Amygdala / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004567:Electrodes, Implanted; D004569:Electroencephalography; D007375:Interleukin-1 / Q000378:metabolism; D007696:Kindling, Neurologic / Q000187:drug effects / Q000378:metabolism*; D010446:Peptide Fragments; D012333:RNA, Messenger / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D012890:Sleep / Q000187:drug effects; D020178:Sleep Disorders, Circadian Rhythm / Q000378:metabolism* / Q000503:physiopathology*; D012895:Sleep, REM / Q000187:drug effects
D007375:Interleukin-1; D010446:Peptide Fragments; D012333:RNA, Messenger; C104416:astressin; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone