Noradrenergic Modulation of Sleep-Related Seizures.
Abstract number :
1.047
Submission category :
Year :
2001
Submission ID :
199
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
M.N. Shouse, Ph.D., Sleep Disturbance Research & Dept of Neurobiology, VAGLAHS & UCLA, Los Angeles, CA; C. Thammasitit, B.S., Sleep Disturbance Research & Dept of Neurobiology, VAGLAHS & UCLA, Sepulveda, CA; P.R. Farber, Sleep Disturbance Research, VAGLAH
RATIONALE: The objective was to determine whether [arrowdown] norepinephrine (NE) release contributes to [arrowup] seizure discharge in seizure-prone sleep states, specifically slow-wave-sleep (SWS) and transitions into REM (RTs).
METHODS: 5-min microdialysis samples were obtained from amygdala and locus ceruleus (LC) in 8 kittens prior to amygdala kindling and one month later (n=[gte] 8 samples per state/per site pre & post kindling). Post-kindling data (n=2 records per subject) were divided based on [arrowup] vs. [arrowdown] density of spontaneous ictal and interictal disharge (IID) (n=1 record per kitten).
RESULTS: Subjects had spontaneous ictal and IID discharge mostly during SWS and RTs. NE concentrations were [arrowdown] in seizure-prone sleep states vs. waking states at both collection sites before and after kindling. After kindling [arrowdown] NE preceded [arrowup] seizure activity; this pattern alternated with [arrowup] NE release during seizure discharge. See Table 1.
CONCLUSIONS: Peak chronic NE depletion may reflect a rebound reduction following [arrowup] spontaneous IID and seizures.[table]
Support: Department of Veterans Affairs