Download neural control of respiration

NEURAL CONTROL OF RESPIRATION
Skeletal muscles provide the motive force for respiration. Unlike cardiac or smooth muscle, they have no
rhythmic "beat" of their own; they depend entirely on the nervous system for a stimulus to contract. Two
separate neural systems control respiration: (1) Voluntary control originates in cerebral cortex neurons, which
send impulses down the corticospinal nerve tracts to motor neurons located in the spinal cord, which relay
excitatory impulses to the muscles of respiration, the intercostal muscles and the diaphragm. This voluntary
system can interrupt or modulate the normal automatic breathing pattern; it is most apparent during speech and
while playing wind instruments, where the lungs serve as air reservoirs to be emptied at controlled rates. (2)
Automatic control originates in lower brain centers, in the pons and the medulla. Impulses arising in this system
also descend in the spinal cord to the motor neurons controlling respiratory muscles, but they travel along nerve
tracts lying in the lateral and ventral parts of the cord, separate from the corticospinal tracts. In general, motor
neurons to expiratory muscles are inhibited during inspiration and vice versa.
The medulla contains a diffuse network of neurons involved in respiration. Although they are collectively
referred to as the respiratory "center" (or "centers"), they are not located in nice discrete packages. There are two
types of these neurons: the I neurons, which fire during inspiration, and the E neurons, which fire during
expiration. During inspiration, E neurons are actively inhibited; during expiration, I neurons are inhibited.
The primitive rhythm for involuntary breathing is apparently generated by the I neurons. They show bursts of
spontaneous activity interspersed with quiet periods about 12 to 15 times/min. In contrast, the E neurons are not
self-excitatory; they are excited only by other neurons (including the I neurons) that send impulses to them.
When the activity of the inspiratory neurons increases, the rate and depth of breathing increase. The primitive
activity of the I neurons, like that of all pacemakers, is modulated by a number of outside influences, including
nerve impulses from centers in the pons and from receptors in the lungs. These influences are dramatically
revealed after injuries and are outlined in the plate.
If the brainstem is transacted below the medulla (at D in the plate), all breathing stops, showing that the brain
drives respiration and that communication between brain and respiratory muscles takes place via the spinal cord.
But if the transaction is made lower in the cord, at E, breathing is not interrupted because the connections
between brain and respiratory neurons remain intact, as do motor nerves (i.e., the phrenic nerve) that carry the
impulses to the muscles of respiration. Regular breathing also continues when all the cranial nerves, including
the vagi, are severed, and the brain is transacted above the pons at A. These results locate the centers for
automatic breathing somewhere between the top of the pons and the lower medulla - clearly, higher brain
centers like those in the cortex are not necessary.
Given this localization, we can dissect the respiratory centers even further. If the vagus nerves are cut and two
transactions are made, one at the top of the pons as before at A and the other in the middle at B, the I cells
discharge continuously, arresting respiration in inspiration. This stopping of respiration in sustained inspiration
is called apneusis, and the neurons in the lower pons, which apparently shower I neurons with excitatory
impulses and keep them firing, are collectively referred to as the apneustic center. Apneusis occurs only when
influences from the upper pons are removed (transaction at B). This suggests that neurons in the upper pons
continually inhibit the apneustic center, holding its inspiratory drive in check. These neurons are members of
another collection called the pneumotaxic center. When xll pons influence is removed by a transaction at C,
respiration continues. Although it may be irregular and punctuated with gasps, it is rhythmic, and it
demonstrates that the neurons of the respiratory centers themselves have a spontaneous rhythmicity. The role of
the pontine centers appears to be to make these rhythmic discharges smooth and regular.
All these responses depend to some extent on whether the vagus nerves are intact. Apneusis, for example,
cannot be demonstrated by transaction of the mid pons (B) unless the vagi are also severed because vagus
nerves carry impulses that originates in stretch receptors located in the lung airways. When the lungs expand
during inspiration, these receptors initiate impulses that reflexively inhibit the inspiratory drive, reinforcing the
actions of the pneumotaxic center and protecting the lungs from overexpansion. This response is called a
Haring-Breuer reflex. In humans, it does not appear to be activated until the tidal volume reaches 1 L, so it plays
no part in regulating ventilation during normal quiet breathing.
Several additional factors influence the respiratory centers so that their activity is commensurate with the body's
metabolic needs. These include reflexes originating in receptors (proprioceptors) located in muscles, tendons,
and joints that are sensitive to movement. They send to the respiratory centers stimulating impulses that
presumably help increase ventilation during exercise. Other important reflexes are initiated by low P02, low pH,
and high PC02 in the plasma; these are taken up in detail in plate 52.