Parasympathetic Nervous System

Cell bodies giving rise to preganglionic parasympathetic nerves exit the CNS at cranial and sacral levels (see Fig. 9-2). The cranial portion of the parasympathetic outflow (cranial nerves III, VII, IX, and X) innervates structures in the head, neck, thorax, and abdomen. The sacral division of the parasympathetic nervous system forms the pelvic nerve and innervates the remainder of the GI tract and the pelvic viscera, including the bladder and reproductive organs.

The preganglionic neurons of the parasympathetic nervous system are myelinated and very long, such that parasympathetic ganglia are located in or near the effector organs. Consequently, postganglionic parasympathetic neurons, which are generally unmyelinated, are short.

Sympathetic Nervous System

Cell bodies for preganglionic sympathetic neurons originate in the intermediolateral cell column of the spinal cord at the thoracic and lumbar levels from T1 to L2 (see Fig. 9-2). Relatively short preganglionic, usually myelinated, neurons project to the sympathetic ganglia outside the spinal vertebrae. Most of these neurons synapse in the 22 segmentally arranged ganglia that form two chains located bilaterally adjacent to the spinal cord, and are often called the paravertebral chain. Postganglionic sympathetic neurons are generally unmyelinated and send long postganglionic fibers to their effector organs. Although most preganglionic sympathetic neurons synapse in the paravertebral sympathetic ganglia, several are prevertebral and lie near the bony vertebral column in the abdomen and pelvis (celiac, superior and inferior mesenteric, and aorticorenal), while a few (cervical ganglia and ganglia connected to urinary bladder and rectum) lie near the organs innervated.

The adrenal medulla is also a part of the sympathetic nervous system. It contains chromaffin cells that are embryologically and anatomically similar to sympathetic ganglia. Chromaffin cells are innervated by typical preganglionic sympathetic nerves and synthesize and secrete epinephrine (Epi, also called adrenaline) into the blood, analogous to postganglionic sympathetic neurons, which release NE.

Autonomic Regulation of Peripheral Organs

Both parasympathetic and sympathetic nerves innervate most organs of the body. Generally, these two branches of the ANS produce opposing responses in effector organs. There is generally a balance between sympathetic and parasympathetic effects on most organs, such that inhibition of one often leads to an increase in the response mediated by the other. However, there are some exceptions where the two systems cause similar responses. Some organs, such as the vasculature and spleen, receive only one type of innervation, which, in these cases, is sympathetic.

The importance of the dual innervation of most organs is evidenced by hypertension, which may involve an increase in sympathetic relative to parasympathetic control of the heart. Increased sympathetic effects can be produced by changes in neural firing rate, catecholamine concentrations at the neuroeffector junction or postjunctional receptors, or signal transduction pathways. Although there is support for each of these mechanisms, the first two are likely most important. Thus drugs that inhibit sympathetically mediated cardiovascular effects are useful for treating hypertension (see Chapters 11 and 12).

One sympathetic preganglionic neuron may ramify and ultimately synapse with many postganglionic sympathetic neurons, leading to diffuse responses. By contrast, parasympathetic preganglionic neurons generally form only single synapses with postganglionic neurons, resulting in more discrete and localized responses. This anatomical distinction has profound physiological significance. Activation of sympathetic outflow, triggered by anger, fear, or stress, causes a state of activation characteristic of the “fight, flight, or fright” response. Heart rate is accelerated, blood pressure is increased, perfusion to skeletal muscle is augmented as blood flow is redirected from the skin and splanchnic region, the blood glucose concentration is elevated, bronchioles and pupils are dilated, and piloerection occurs.

In contrast, activation of parasympathetic outflow is associated with conservation of energy and maintenance of function during periods of lesser activity. Activation of parasympathetic outflow reduces heart rate and blood pressure, activates GI movements, and results in emptying of the urinary bladder and rectum. Furthermore, lacrimal, salivary, and mucous cells are activated, and the smooth muscle of the bronchial tree is contracted. Although the parasympathetic nervous system is essential for life, the sympathetic nervous system is not. Animals completely deprived of their sympathetic nervous system can survive in a controlled environment but have difficulty responding to stressful conditions.

Neurotransmission

Neurotransmission is the process of effective transfer and integration of information in the nervous system. Neurotransmitters are endogenous substances released from nerve terminals, which act on receptors present on the membrane of postsynaptic cells. It is the interaction of the released neurotransmitter with the receptor that produces a functional change in the cell (Fig. 9-3).

FIGURE 9–3 The process of chemical neurotransmission. Neurotransmitter molecules are released from synaptic vesicles within the nerve terminal into the synaptic cleft, where they diffuse to the postjunctional side and interact with their receptors.

Depolarization of a presynaptic nerve terminal leads to release of a neurotransmitter into the extracellular fluid between the presynaptic and postsynaptic cells (the synaptic cleft). Calcium (Ca⁺⁺) provides the essential link between depolarization and transmitter release. When a nerve terminal is depolarized, there is a large influx of Ca⁺⁺ caused by opening of voltage-dependent Ca⁺⁺ channels in the membrane. This influx promotes fusion of transmitter-containing synaptic vesicles with the plasma membrane resulting in exocytosis, which releases neurotransmitter into the synapse. After exocytosis, the voltage-dependent Ca⁺⁺ channels inactivate rapidly, and the intracellular Ca⁺⁺ concentration returns to normal by sequestration into intracellular compartments and active extrusion from the cell. The steps linking the arrival of an action potential to neurotransmitter release are summarized in Figure 9-4.

FIGURE 9–4 Sequence of events linking nerve terminal depolarization to release of neurotransmitter. A, The action potential arrives at the nerve terminal and depolarizes the membrane. B, Voltage-gated Ca⁺⁺ channels open, allowing the influx of Ca⁺⁺ down its concentration gradient. C, The increased intracellular Ca⁺⁺ concentration promotes the fusion of transmitter-containing synaptic vesicles with the plasma membrane, resulting in exocytosis of the vesicular contents. D, The Ca⁺⁺ channels rapidly inactivate, and the intracellular Ca⁺⁺ concentration is returned to normal by both sequestration into mitochondria and active extrusion from the cell.

It is important to understand that voltage-dependent Ca⁺⁺ channels in nerve terminals differ from those in other tissues. The Ca⁺⁺ channel antagonists are an important class of drugs that block voltage-dependent Ca⁺⁺ channels in cardiac and smooth muscle (see Chapter 20). However, there are distinct subtypes of these channels that can be distinguished by their electrical and pharmacological properties. The Ca⁺⁺ channel antagonists block the channels most often found in cardiac and smooth muscle (L type) and have no effect on most of the voltage-dependent Ca⁺⁺ channels found in nerve terminals (N type). This is fortunate, because if Ca⁺⁺ channel antagonists also blocked neurotransmitter release, their toxicity would undoubtedly prevent them from being useful therapeutically.

After release, the neurotransmitter diffuses across the synaptic cleft to interact with specific receptors on the dendrites and cell body of the postganglionic neuron or on cells of the effector organ. The postsynaptic cell responds in an appropriate fashion to the received message. Thus the nerve terminal has mechanisms for storing and releasing neurotransmitters in response to depolarization, and the postsynaptic cell has receptors for detecting the presence and identity of different neurotransmitters and initiating appropriate changes in physiology or metabolism. Nerve terminals also have efficient mechanisms for the degradation and reutilization (reuptake

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