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Journal of Neuroscience, Vol 11, 3135-3145, Copyright © 1991 by Society for Neuroscience
Effects of locus coeruleus activation on electroencephalographic activity in neocortex and hippocampus
CW Berridge and SL Foote
Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla 92093.
Experiments were conducted to examine the hypothesis that increased
neuronal discharge activity of noradrenergic neurons of the locus coeruleus
(LC) above resting discharge rates can alter forebrain
electroencephalographic (EEG) activity. Small infusions (70-135 nl) of the
cholinergic agonist bethanechol within 500 microns of the LC were used to
activate this nucleus reversibly in halothane-anesthetized rats. A combined
recording-infusion probe allowed verification of this electrophysiological
activation. Simultaneously, EEG activity was recorded from sites in the
frontal cortex and hippocampus and subjected to power-spectrum analyses.
The findings were (1) LC activation was consistently followed, within 5 to
30 sec, by a shift from low- frequency, high-amplitude to high-frequency,
low-amplitude EEG activity in frontal neocortex and by the appearance of
intense theta-rhythm in the hippocampus; (2) forebrain EEG changes followed
LC activation with similar latencies whether infusions were made lateral or
medial to the LC; (3) infusions placed outside the immediate vicinity of
the LC were not followed by these forebrain EEG effects; (4) following
infusion- induced activation, forebrain EEG returned to preinfusion
patterns with about the same time course as the recovery of LC activity
(10-20 min for complete recovery). These infusion-induced effects on EEG
activity were blocked or severely attenuated by pretreatment with the alpha
2- agonist clonidine, which inhibits LC discharge and norepinephrine
release, or the beta-antagonist propranolol. These observations indicate
that enhanced LC discharge activity is the crucial mediating event for the
infusion-induced changes in forebrain EEG activity observed under these
conditions and suggest that LC activation may be sufficient to induce EEG
signs of cortical and hippocampal activation.
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