Acoustic startle response (ASR) and open-field activity was examined in the
46th generation of mice that have been selectively bred for high analgesia
(HA) and for low analgesia (LA) induced by 3-min swimming in 20 degreesC w
ater. These lines were earlier found to differ in brain opioid receptor den
sity and in the expression of opioid-mediated phenomena, as analgesic sensi
tivity to opiates and reversibility of swim stress-induced analgesia (SSIA)
by naloxone. For comparison, a randomly bred control (C) line was used. To
measure the amplitude of ASR, the mice were exposed to IIO-dB acoustic sti
muli in a Coulboum apparatus. In saline-injected mice, the ASR force was fo
und significantly lower in the LA than in the HA, as well in the C line, bu
t did not differ between the two last lines. Naltrexone hydrochloride (10 m
g/kg IP 30 min before ASR testing) augmented the startle in the opioid rece
ptor-dense HA line, but had no effect in the opioid receptor-deficient LA l
ine, as well in the C line; therefore, the ASR magnitude in naltrexone-inje
cted HA mice was significantly higher compared to the C line. HA mice displ
ayed less activity in an open-field test; that is, they remained immobile l
onger in the center of the field, and thereafter performed less ambulation
and less rearing against the wall compared to the LA line. Naltrexone faile
d to modify the open-field activity in any line. The results confirm that t
he pattern of ASR depends on the genetic makeup of the animals. The higher
amplitude of ASR, taken together with the lower open-field activity of HA m
ice, can be interpreted in terms of higher anxiety level, compared to the L
A line. It is suggested that the higher ASR in HA mice relies on a nonopioi
d mechanism, which is tonically inhibited by the opioid system. (C) 2000 El
sevier Science Inc. All rights reserved.