The Role of β1,2-Adrenoceptors in the Amygdala in the Behavior of Rats with Different Levels of Freezing in Conditioned Reflex Fear

Abstract

Individual sensitivity to blockade of β1,2-adrenoceptors was studied by dividing rats into groups depending on the manifestation of conditioned reflex fear in a classical defensive conditioned reflex (low- and high-freezing animals) and on the level of anxiety in the elevated plus maze and dark-light box tests (highand low-anxiety animals). The effects due to local administration of the β1,2-adrenoceptor antagonist propranolol (1.25 μg/0.5 μl) and physiological saline (controls, 0.5 μl) into the basolateral amygdala were compared in the different groups of rats. Administration of propranolol into the amygdala before testing of previously acquired conditioned reflex fear led to a decrease in freezing time in response to the conditioned signal only in low-freezing animals, but not in high-freezing animals. Administration of propranolol into the amygdala accelerated extinction and degraded the productivity of retraining in high-freezing rats, having virtually no effect on low-freezing animals. In addition, administration of propranolol into the amygdala did not induce any significant changes in measures of anxiety in these tests in either high- or low-anxiety rats. A difference in the sensitivity of high- and low-freezing rats to injections of propranolol into the amygdala was seen. Amygdalar β1,2-adrenoceptors play a significant role in the acquisition and extinction of conditioned reflex fear in high-freezing rats, facilitating the appearance of prolonged freezing and resistance to extinction of the reflex.