6.8: Age Changes in Autonomic Motor Functioning

Aging of the autonomic motor neurons has not been as well studied as aging of other parts of the nervous system because of difficulties in distinguishing such changes from other age‑related changes. Therefore, little can be said with confidence about the effects of aging on autonomic motor neurons. However, some aspects of the aging of these neurons are coming to light. In general, aging seems to have little effect on their ability to regulate body functions under normal conditions. This is due in part to overall slow loss of sympathetic motor neurons in the spinal cord (i.e., 5 percent to 8 percent per decade). Additionally, sympathetic motor neurons compensate for some age changes by modifying their dendrites and axons throughout life. However, when conditions become unfavorable, the autonomic neurons controlling certain structures have difficulty causing adequate adjustments to preserve homeostasis.

Autonomic Motor Neurons

An apparently inadequate autonomic response occurs when older people stand up or remain standing for long periods. Normally, sympathetic neurons prevent a substantial drop in blood pressure by stimulating the heart and causing constriction of many blood vessels. The ability of the sympathetic neurons to cause these adjustments decreases in many people. The resulting low blood pressure when one is in an upright position - orthostatic hypotension, can cause dizziness, light‑headedness, and fainting. This is a major cause of falls and physical injury (e.g., fractures). Orthostatic hypotension does not occur in all older individuals, and some cases result from abnormalities in the circulatory system.

Aging of autonomic neurons can lead to elevated blood pressure as well as low blood pressure. Normally, parasympathetic impulses slow and weaken the heartbeat to keep blood pressure down while a person is at rest, when a person ends vigorous physical activity, and during each inspiration. Aging causes this parasympathetic function to decline and therefore diminishes the ability of these neurons to prevent blood pressure from exceeding the proper levels.

Age changes in autonomic neurons may also contribute to a decrease in the ability to adjust to extremes in temperature. Normally, sympathetic impulses cause blood vessels in the skin to constrict when a person is getting cold; this helps stabilize body temperature by reducing the rate of heat loss. With increasing age, there is a decrease in such constriction. Thus, older individuals are at greater risk of developing hypothermia. This age change may be due largely to age changes in blood vessels.

Another age change that may be due in part to aging of autonomic neurons involves erection of the penis. Normally, erection occurs when parasympathetic neurons cause dilation of blood vessels in the penis during sexual arousal, increasing blood flow into the penis and causing it to enlarge and become stiffer. With advancing age, these processes occur more slowly and to a lesser degree. These age‑related changes may be due to reduced parasympathetic functioning or to age changes or disease in penile vessels. Parasympathetic control of other blood vessels is not changed by aging.

Another age change believed to result from aging of autonomic nerves is a decrease in the responsiveness of the pupil. Normally, sympathetic nerves stimulate muscles in the iris that cause dilation of the pupil and parasympathetic nerves stimulate muscles in the iris that cause constriction of the pupil. Balancing these autonomic influences results in letting enough light enter the eye for vision while preventing the entry of excess light, which can hinder vision and damage the eye. With advancing age, there is a decrease in the amount of pupillary dilation and slower constriction of the pupil, which reduces adaptation by the eye. Both changes may be caused by changes in the autonomic neurons or in the iris.

Finally, there is a decrease in the number of neurons controlling the movements of the esophagus during swallowing. Normally, when solids or liquids enter the esophagus from the throat, these materials are pushed down to the stomach by a wave of muscular contraction in the esophagus. The contraction is initiated by the swallowing reflex and is coordinated by a group of motor neurons (Auerbach's plexus) in the esophagus. With aging, the number of neurons in Auerbach's plexus decreases. Swallowing becomes more difficult because the wave of contraction starts later, is weaker, and is less well coordinated. Sometimes the esophagus fails to empty completely, resulting in considerable discomfort.

Sympathetic Neurotransmitters

Sympathetic functioning is also affected by changes at neuromuscular and neuroglandular junctions. Sympathetic neurons become especially active when conditions become unfavorable and homeostasis is threatened or when such a threat is suspected or anticipated. The effects of sympathetic activity include increases in heart functioning, blood pressure, and perspiration as well as dilation of the airways. At the same time, sympathetic neurons inhibit certain activities, including digestions, urine production, and the functioning of the reproductive organs. Overall, these effects are adaptive and beneficial because they channel more of the body's energies into actions that help the individual overcome or escape danger. The combination of effects caused by the sympathetic neurons is often referred to as the fight‑or‑flight response, which is part of the body's reaction to stress.

Most sympathetic motor neurons use norepinephrine as a neurotransmitter at neuromuscular and neuroglandular junctions. At the direction of sympathetic neurons, norepinephrine is also produced and secreted into the blood by a gland called the adrenal medulla (Chapter 14). Norepinephrine from the adrenal medulla increases the intensity and duration of the effects of sympathetic norepinephrine.

Aging affects blood levels of norepinephrine in three ways:

1. The concentration of norepinephrine in the blood of resting individuals rises.
2. When a stressful situation is encountered, the level of norepinephrine increases faster.
3. Once the stress has passed, the level of circulating norepinephrine returns to its resting concentration more slowly.

There seem to be two reasons for the higher levels of norepinephrine in older individuals. One may be the stiffening of arteries (Chapter 4). The other seems to be a compensatory response for an age‑related decline in the effectiveness of norepinephrine in some organs. This decline may be due to age changes in receptor molecules (e.g., lungs) or in reactions within cells (e.g., heart).

In conclusion, although the effects of age changes in autonomic neurons are not unimportant, such changes are few compared with the number of autonomic functions that seem to be unaffected by aging. Autonomic neurons can provide proper regulatory impulses to most of the structures they control regardless of age or the degree of stress placed on the body.