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Journal of Neuroscience, Vol 12, 2313-2320, Copyright © 1992 by Society for Neuroscience
Lesions of the central nucleus of the amygdala, but not the paraventricular nucleus of the hypothalamus, block the excitatory effects of corticotropin-releasing factor on the acoustic startle reflex
KC Liang, KR Melia, S Campeau, WA Falls, MJ Miserendino and M Davis
Ribicoff Research Facilities of the Connecticut Mental Health Center, Department of Psychiatry, Yale University School of Medicine, New Haven 06508.
Intracerebroventricular (icv) infusion of corticotropin-releasing factor
(CRF) was previously found to produce a long-lasting, dose- dependent
(0.1-1.0 microgram) increase in the amplitude of the acoustic startle
reflex. The present study sought to determine where in the CNS CRF acts to
increase startle. Intracisternal infusion of CRF (0.1-1.0 microgram)
increased startle with a time course and magnitude similar to that produced
by icv CRF, unlike intrathecal infusion, which produced a small, more rapid
enhancement of startle. While lesions of the paraventricular nucleus of the
hypothalamus had no effect on icv CRF-enhanced startle, bilateral lesions
of the central nucleus of the amygdala significantly attenuated the
excitatory effect of icv CRF but had no effect on intrathecal CRF-enhanced
startle. Even though lesions of the amygdala blocked icv CRF-enhanced
startle, local infusion of CRF into the amygdala did not significantly
elevate startle. The present data indicate that the amygdala is part of the
neural circuitry required for icv CRF to elevate startle, but does not
appear to be the primary receptor area where CRF acts. The involvement of
the amygdala in icv CRF-enhanced startle is consistent with the hypothesis
that both the amygdala and CRF are critically involved in fear and stress.
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