Stress, Central Neurotransmitters, and the Mechanism of Action of α2-Adrenoceptor Agonists

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Abstract
Summary: In the past, treatment of hypertension frequently involved bed rest, a procedure known to reduce the activity of the sympathetic nervous system (SNS), generally implied in the defense reaction of the organism that is elicited by salient, environmental stimuli. Evidence is presented that brain noradrenaline (NA) neurons in the locus coeruleus (LC) and major parts of the SNS respond by burst activation in concert to stressful stimuli implying novelty or fear. α-Adrenoceptor agonists such as clonidine exert a powerful inhibitory action on both LC neurons and the SNS, thereby reducing the impact of salient environmental events on the organism. Our most recent data suggest that clonidine can reduce burst firing of catecholamine neurons and cause a more regular firing pattern. This may explain reduced release of coexisting neuropeptides such as neuropeptide Y (NPY) in sympathetic nerves, which we have observed following clonidine treatment, since such neuropeptides are particularly effectively released in burst sequences. Coexisting neuropeptides have been thought to be involved in learning processes and the encoding of short-term memory. Consequently, treatment with α2-adrenoceptor agonists may imply reduced engraving of stressful events, conveyed by central and peripheral catecholamine neurons.

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