Ja. Salinas et al., POSTTRAINING INTRAAMYGDALA INFUSIONS OF OXOTREMORINE AND PROPRANOLOL MODULATE STORAGE OF MEMORY FOR REDUCTIONS IN REWARD MAGNITUDE, Neurobiology of learning and memory, 68(1), 1997, pp. 51-59
These experiments examined the effects of posttraining intraamygdala a
dministration of the muscarinic agonist, oxotremorine, and the beta-no
radrenergic antagonist, propranolol, on memory for reduction in reward
magnitude. Male Sprague-Dawley rats (175-200 g) implanted with bilate
ral intraamygdala cannulae were food deprived (maintained at 80% of bo
dy weight) and trained to run a straight alley (six trials/day) for ei
ther ten 45-mg food pellets (high reward) or one 45-mg food pellet (lo
w reward) for 10 days. In Experiment One, the animals in the high-rewa
rd group were then shifted to a one-pellet reward and immediately give
n intraamygdala infusions (0.5 mu l/side) of either oxotremorine (10 n
g) or phosphate buffer. Shifted training continued for 4 more days and
no further injections were given. Shifted animals given the buffer so
lution displayed an increase in runway latencies but returned to presh
ift latencies by the fifth day of shifted training. In contrast, anima
ls given oxotremorine exhibited increased latencies through the fifth
day. In Experiment Two, rats were trained as in Experiment One but imm
ediately following the shift received intraamygdala infusions of oxotr
emorine (10 ng), propranolol (0.3 mu g), both, or phosphate buffer. Sh
ifted vehicle-injected rats returned to preshift performance by the fi
fth day of shifted training. Shifted propranolol rats returned to pres
hift latencies by the third day of shifted training. In contrast, the
shifted oxotremorine and the shifted oxotremorine/propranolol rats dis
played longer latencies than unshifted controls through 5 days of shif
ted training. The findings indicate that the muscarinic cholinergic an
d beta-noradrenergic systems within the amygdala interact in regulatin
g memory and support the view that noradrenergic influences are mediat
ed through cholinergic activation. (C) 1997 Academic Press.