epinephrine acts in the general direction of arousal, and ACh tends toward restorative functions. Norepinephrine dilates the pupil of the eye, strengthens and speeds the heartbeat, and inhibits processes of digestion, all under the heading of what has been called the “fight or flight” response; it also stimulates the adrenal glands to release epinephrine and the liver to release large quantities of glucose, which make more energy available to the muscles for action. Several drugs that work by means of the norepinephrine system are useful in asthma; these are known as the beta-agonists, because they are targeted to a specific group of “beta” receptors in the bronchial muscles, where they relieve constriction.

In some instances, norepinephrine may function not as a transmitter but as a neuromodulator, promoting or blocking the action of some other transmitter at the synapse. Experimental evidence on this point is still coming in; if the hypothesis holds up, it would add a new detail to an already crowded picture and could open up other lines of investigation as well.

The neurons in the brain that contain norepinephrine cluster in a small region of the brainstem; their axons project to the hypothalamus, the cerebellum, and even the forebrain, a good 10 to 15 centimeters away. Norepinephrine is associated not only with alertness and arousal but also with the dreaming phase of sleep and, by way of the hypothalamus and the limbic system, with the regulation of mood. For instance, a number of studies point to depleted levels of norepinephrine at brain synapses, or a reduced ability of receptors to use it, as a factor in depression. Not that this amounts to a scientific formula that a normal brain minus some amount of norepinephrine equals a depressed mind; such formulas are far too coarse—particularly in an area like the basis of mood, where any number of elements may interact. Moreover, some of the factors that are undoubtedly important for mood are unquantifiable, invisible, and perhaps irreproducible for laboratory study. One point of wide consensus, however, is that depression can be helped by two classes of drugs: one class blocks an enzyme that would normally break down norepinephrine in the synaptic cleft, and the other slows the reuptake of norepinephrine into the presynaptic cell.

The neurotransmitter serotonin is a powerful constrictor of

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