DEVELOPMENTAL FACTORS MODIFY STRESS-ULCER INCIDENCE IN A STRESS-SUSCEPTIBLE RAT STRAIN

Citation
Wp. Pare et J. Kluczynski, DEVELOPMENTAL FACTORS MODIFY STRESS-ULCER INCIDENCE IN A STRESS-SUSCEPTIBLE RAT STRAIN, J PHYSL-PAR, 91(3-5), 1997, pp. 105-111
Citations number
17
Journal title
JOURNAL OF PHYSIOLOGY-PARIS
ISSN journal
09284257 → ACNP
Volume
91
Issue
3-5
Year of publication
1997
Pages
105 - 111
Database
ISI
SICI code
0928-4257(1997)91:3-5<105:DFMSII>2.0.ZU;2-D
Abstract
Our multifactor theory of stress ulcer assumes that environmental fact ors that operate during early growth stages influence the elaboration of stress ulcer in adult rats. The theory would predict that rats expo sed to either neonatal handling, or raised in a stimulus enriched envi ronment, would reveal differences in stress ulcer susceptibility. In s tudy 1, some Wistar rats and ulcer-susceptible Wistar Kyoto (WKY) rats were handled daily from birth to day 21, whereas other rats from each strain were not disturbed. In study 2, Wistar and WKY rats were raise d (3 months) in a large stimulus-dense enriched environment, whereas o ther rats from each strain were raised in standard rat cages where Vis ual and auditory stimuli were minimized. At 3 months all rats were obs erved in the open field test (OFT), a test of emotionality, as well as the Porsolt forced swim test (FST), a test of behavioral depression, and subsequently exposed to the ulcerogenic water restraint procedure. Neonatal handling produced results suggesting increased wall climbing activity in the FST, reduced response latency in the OFT, increased b ody weight and reduced ulcer severity, but these differences were not significant. Rearing in an enriched environment produced similar resul ts but these difference were more pronounced and significant in the Wi star rats as compared to the WKY rats. Thus early environmental manipu lations can influence adult behavior and the elaboration of stress ulc er disease, but the impact of these manipulations is less salient in a n organism with an endogenous susceptibility to the disease.