Jm. Aubry et al., CORTICOTROPIN-RELEASING FACTOR AND VASOPRESSIN MESSENGER-RNA LEVELS IN ROMAN HIGH-AVOIDANCE AND LOW-AVOIDANCE RATS - RESPONSE TO OPEN-FIELDEXPOSURE, Neuroendocrinology, 61(2), 1995, pp. 89-97
Roman high-(RHA) and low-(RLA) avoidance rats are selected acid bred f
or rapid versus non-acquisition of two-way, active avoidance behavior
in a shuttle box. They also show a number of other behavioral differen
ces which appear to be essentially related to emotional factors, the R
LA rats being emotionally more sensitive. The ACTH secretory response
to stressors is also augmented in RLA rats. We thus raised the questio
n whether the expression of corticotropin-releasing factor (CRF) and v
asopressin (VP), two neurohormones exerting a synergistic action on AC
TH release from corticotropic cells, is different in the two strains.
Steady-state mRNA levels were examined in the parvicellular neurons of
the paraventricular nucleus under basal conditions and 4 h after a si
ngle 8-min exposure to an open-field stressor. In situ hybridization h
istochemistry with S-35-labeled oligonucleotide probes was followed by
quantitative cell by cell autoradiography. When basal CRF and VP mRNA
levels were compared in the two lines, we found that the RLA rats had
a significantly higher VP-labeling density than the RHA rats. No diff
erence was found for CRF mRNA. During open-field exposure, we observed
behavioral differences paralleled by elevated corticosterone compatib
le with an increased emotional response in RLA rats. Open-field exposu
re produced a significant increase in CRF but not VP mRNA in both RHA
and RLA rats (by 43 and 57%, respectively). These results suggest that
differences in basal VP expression in CRF neurons may participate in
the mechanisms underlying the hyperactivity of the hypothalamo-pituita
ry-adrenal (HPA) axis in the emotionally more sensitive RLA rats. Thus
, these Swiss sublines of RHA-RLA rats might provide a useful model to
study the role of genetic predisposition and superimposed environment
al factors on the regulation or dysregulation of the HPA axis.