Stress impairs prefrontal cortical function in rats and monkeys: role of dopamine D1 and norepinephrine α-1 receptor mechanisms

Evidence from both animals and humans indicates that enhanced long term memory consolidation can be initiated by increased NE β receptor stimulation in the amygdala, which is consistent with the findings of Hockey, who showed that stress narrows the focus of attention onto salient signals.

Abstract

This chapter discusses the evidence suggesting that high levels of dopamine (DA) acting at D1 receptors, and high levels of norepinephrine (NE) acting at α-1 receptors, contribute to stress-induced deficits in working memory function. Evidence from both animals and humans indicates that enhanced long term memory consolidation can be initiated by increased NE β receptor stimulation in the amygdala. Increased catecholamine release in the amygdala also has been shown to enhance the associative memory functions of the hippocampus and the habit memory functions of the slriatum. These mechanisms may enhance the long-term memory of the aversive event, such that one might better avoid it in the future. Increased catecholamine release in the sensory cortices might also alter attentional regulation, allowing attention to be captured by prominent stimuli in the environment by increasing β and/or α-1 receptor enhancement of signal processing in sensory cortices. This hypothesis is consistent with the findings of Hockey, who showed that stress narrows the focus of attention onto salient signals.