Volume 17, Number 15,
Issue of August 1, 1997
pp. 5979-5992
Copyright ©1997 Society for Neuroscience
Lesions of the Medial Geniculate Nuclei Specifically Block
Corticosterone Release and Induction of c-fos mRNA in the
Forebrain Associated with Audiogenic Stress in Rats
Received March 17, 1997; revised May 14, 1997; accepted May 15, 1997.
Serge Campeau,
Huda Akil, and
Stanley J. Watson
Mental Health Research Institute, The University of Michigan, Ann
Arbor, Michigan 48109
Audiogenic stress is known to activate the
hypothalamo-pituitary-adrenocortical (HPA) axis in rats. The goal of
the present study was to determine whether the medial geniculate nuclei
(including all auditory nuclei of the thalamus), which are obligatory
relays in the transmission of auditory information to the forebrain, are critically involved in HPA activation by audiogenic stress. To this
end, corticosterone levels and regional brain activity indexed by
c-fos mRNA induction, elicited by 30 min of 105 dB white
noise, were measured. Compared with unoperated and sham-operated rats,
complete medial geniculate nuclei lesions blocked corticosterone release normally induced by loud noise. The effects of the lesions were
specific to loud noise insofar as corticosterone release in response to
restraint or ether stress was not reduced in lesioned rats.
We have determined previously that audiogenic stress is associated with
a specific regional pattern of c-fos mRNA induction. Rats sustaining complete medial geniculate lesions demonstrated a
blockade of c-fos mRNA induction in several audiogenic
stress responsive regions, also known to directly innervate medial
parvocellular neurons of the paraventricular hypothalamic nucleus.
Thus, in addition to blockade in the paraventricular hypothalamic
nucleus, c-fos mRNA induction in the lesioned animals
was abolished in the bed nucleus of the stria terminalis, especially
its anterior medial and ventral aspects, the septohypothalamic nucleus,
and the anteroventral preoptic area, compared with unoperated and sham-operated rats. Several additional regions in the lesioned rats
failed to show reliable c-fos mRNA induction compared
with naive rat controls. Nearly all other regions that showed reliable c-fos mRNA induction in the unoperated and sham-operated
rats displayed either similar or slightly reduced levels in complete medial geniculate-lesioned rats, suggesting that these regions are not
part of a critical HPA activational circuit in response to audiogenic
stress. On the basis of these results, putative circuits from the
medial geniculate nuclei to the paraventricular nucleus of the
hypothalamus involved in activation of the HPA axis by audiogenic
stress are discussed.
Key words:
corticosterone;
loud noise;
auditory;
restraint;
ether;
rat