Amygdala β-noradrenergic receptors modulate delayed downregulation of dopamine activity following restraint.

Stress, which involves a heightened arousal and excitability, triggers important adaptive responses to maintain homeostasis and prepare a response. In the current studies, we administered a psychological stressor of 2 h acute restraint on rats, and found that 24 h after the cessation of the restraint session, there was a significant decrease in ventral tegmental area dopaminergic (DA) neuron population activity and a significant attenuation in amphetamine-induced locomotor activity. Systemic or intra-basolateral nuclei of the amygdala administration of the β-noradrenergic receptor antagonist, propranolol, reversed the decrease, suggesting that the delayed attenuation of DA neuron firing following a stressor depends on a noradrenaline-mediated mechanism. This alteration in DA activity may adaptively prepare the individual to avoid the stressor, or in the extreme, may be a factor that contributes to pathological changes in behavior or physiological responses.