Prenatal stress alters Fos protein expression in hippocampus and locus coeruleus stress-related brain structures
Psychoneuroendocrinology. 2006-07-01; 31(6): 769-780
DOI: 10.1016/j.psyneuen.2006.02.007
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Prenatal stress (PS) durably influences responses of rats from birth throughout
life by inducing deficits of the hypothalamo-pituitary-adrenal (HPA) axis
feedback. The neuronal mechanisms sustaining such alterations are still unknown.
The purpose of the present study was to determine whether in PS and control rats,
the exposure to a mild stressor differentially induces Fos protein in hippocampus
and locus coeruleus, brain areas involved in the feedback control of the HPA
axis. Moreover, Fos protein expression was also evaluated in the hypothalamic
paraventricular nucleus (PVN) that reflect the magnitude of the hormonal response
to stress. Basal plasma corticosterone levels were not different between the
groups, while, PS rats exhibited higher number of Fos-immunoreactive neurons than
controls, in the hippocampus and locus coeruleus in basal condition. A higher
basal expression of a marker of GABAergic synapses, the vGAT, was also observed
in the hypothalamus of PS rats. Fifteen minutes after the end of the exposure to
the open arm of the elevated plus-maze (mild stress) a similar increased plasma
corticosterone levels was observed in both groups in parallel with an increased
number of Fos-immunoreactive neurons in the PVN. Return to basal plasma
corticosterone values was delayed only in the PS rats. On the contrary, after
stress, no changes in Fos-immunoreactivity were observed in the hippocampus and
locus coeruleus of PS rats compared to basal condition. After stress, only PS
rats presented an elevation of the number of activated catecholaminergic neurons
in the locus coeruleus. In conclusion, these results suggest for the first time
that PS alters the neuronal activation of hippocampus and locus coeruleus
implicated in the feedback mechanism of the HPA axis. These data give anatomical
substrates to sustain the HPA axis hyperactivity classically described in PS rats
after stress exposure.
DOI: 10.1016/j.psyneuen.2006.02.007
PMID: 16624492 [Indexed for MEDLINE]