EXPOSURE TO CHRONIC PSYCHOSOCIAL STRESS AND CORTICOSTERONE IN THE RAT- EFFECTS ON SPATIAL DISCRIMINATION-LEARNING AND HIPPOCAMPAL PROTEIN-KINASE C-GAMMA IMMUNOREACTIVITY
Hj. Krugers et al., EXPOSURE TO CHRONIC PSYCHOSOCIAL STRESS AND CORTICOSTERONE IN THE RAT- EFFECTS ON SPATIAL DISCRIMINATION-LEARNING AND HIPPOCAMPAL PROTEIN-KINASE C-GAMMA IMMUNOREACTIVITY, Hippocampus, 7(4), 1997, pp. 427-436
Previous reports have demonstrated a striking increase of the immunore
activity of the gamma-isoform of protein kinase C (PKC gamma-ir) in Am
mon's horn and dentate gyrus (DC) of rodent hippocampus after training
in a spatial orientation task. In the present study, we investigated
how 8 days of psychosocial stress affects spatial discrimination learn
ing in a hole board and influences PKC gamma-ir in the hippocampal for
mation. The acquisition of both reference memory and working memory wa
s significantly delayed in the stressed animals during the entire trai
ning period. With respect to cellular plasticity, the training experie
nce in both nonstressed and stressed groups yielded enhanced PKC gamma
-ir in the CA1 and CA3 regions of the posterior hippocampus but not in
subfields of the anterior hippocampus. Stress enhanced PKC gamma-ir i
n the DG and CA3 pyramidal cells of the anterior hippocampus. In stres
sed animals that were subsequently trained, the PKC gamma-ir was incre
ased in the posterior CA1 region to the same level as that found in no
nstressed trained animals. Stress apparently abrogated the PKC gamma-i
r training response in the CA3 region. In a second experiment, the ele
vation of plasma corticosterone levels to values that are found during
stress did not significantly influence reference memory scores but sl
ightly and temporarily affected working memory. The training-induced e
nhancement of PKC gamma-ir in the CA1 region was similar in trained an
d corticosterone-treated trained animals, but the learning-induced PKC
gamma-ir response in the posterior CA3 area was absent after corticos
terone pretreatment. These results reveal that prolonged psychosocial
stress causes spatial learning deficits, whereas artificial elevation
of corticosterone levels to the levels that occur during stress only m
ildly affects spatial memory performance. The spatial learning deficit
s following stress are reflected only in part in the redistribution of
hippocampal PKC gamma-ir following training. (C) 1997 Wiley-Liss, Inc
.