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Vol. 281, Issue 1, 163-172, 1997
Department of Psychiatry, Allegheny University, Philadelphia,
Pennsylvania
Corticotropin-releasing factor (CRF) administered
intracerebroventricularly (i.c.v.) activates noradrenergic locus
coeruleus (LC) neurons of halothane-anesthetized and unanesthetized
rats. This study used a technique for microinfusing CRF into the LC from calibrated micropipettes to characterize and quantify the effects
of locally administered CRF on LC discharge in halothane-anesthetized rats. CRF (3-100 ng) microinfusion into the LC increased discharge rate in a dose-dependent manner from 28 ± 8 to 105 ± 26%
above preinfusion discharge rates. The CRF dose-response curve
generated by local microinfusion was parallel to, and shifted
approximately 200-fold to the left, of that generated by i.c.v.
administration. Intracoerulear microinfusion of the CRF antagonist,
[DPhe12,Nle21,38,C
MeLeu37]r/hCRF(12-41),
greatly attenuated LC activation produced by a maximally effective dose
of i.c.v. administered CRF, suggesting that these effects are primarily
due to actions within the LC. In rats in which both LC discharge rate
and norepinephrine levels in prefrontal cortex were measured by
in vivo microdialysis, CRF microinfused into the LC
increased both endpoints. Finally, LC activation produced by CRF (60 ng) microinfusion into the LC was associated with cortical
electroencephalographic activation. Taken together with previous
anatomical and electrophysiological evidence for endogenous CRF
interactions in the LC, our results support the hypothesis that CRF
serves as an excitatory neurotransmitter in the LC, and suggest that
its actions on LC neurons are translated to enhanced norepinephrine
release and an impact on cortical targets.
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