Transmission Across Synapses

Transmission across synapses in the ANS is mediated by chemicals known as neurotransmitters. These chemicals are synthesized within the nerves and in most instances are stored in synaptic vesicles in the nerve endings. Upon activation of the nerve, nerve action potentials invade the nerve ending, causing the release of a portion of the stored neurotransmitter. Once released, the neurotransmitter binds to specific receptors located on postsynaptic structures. Only those cells that possess specific receptors for that neurotransmitter will be affected. Shortly after its release, the neurotransmitter is then inactivated.

As is the case in the brain, a multitude of neurotrans-mitters act within the ANS. The two about which most is known are acetylcholine and norepinephrine; thus, this chapter will deal mainly with them. Acetylcholine (ACh) acts as the neurotransmitter at synapses between somatic motor nerves and skeletal muscle. ACh also acts at the synapses between preganglionic and postganglionic neurons in both the sympathetic

FIGURE 1 Organization of the sympathetic and parasympathetic divisions of the autonomic nervous system. Parasympathetic pathways are denoted by dark blue lines, whereas sympathetic pathways are illustrated by light blue lines.

FIGURE 2 Autonomic control centers located in the brain stem.

Respiratory centeK

FIGURE 2 Autonomic control centers located in the brain stem.

and parasympathetic divisions. Finally, ACh is the transmitter acting between many postganglionic parasympathetic nerves and effector organs. Norepinephrine acts as the neurotransmitter between many postganglio-nic sympathetic nerves and the effector organs they innervate.

Receptors are identified according to the specific chemicals with which they interact (Table 1). Cholinergic receptors are those that bind acetylcholine; adrenergic receptors are those that bind norepinephrine and epinephrine. In addition to binding and reacting to the naturally occurring neurotransmitters, these receptors also bind a number of other structurally related chemicals. Many of these chemicals mimic the naturally occurring neurotransmitters and initiate cellular reactions; these chemicals are referred to as agonists. On the other hand, some chemicals bind with receptors but do not induce a cellular reaction. Furthermore, their binding to a receptor inhibits the ability of an agonist, when present, to bind with and/or activate the receptor; such chemicals are referred to as antagonists.

The cholinergic receptors present on skeletal muscles and in autonomic ganglia are activated by nicotine and are blocked by the antagonists tubocurarine and hexamethonium. On the other hand, cholinergic receptors on many end organs are activated by muscarine and are blocked by the antagonist atropine. Thus, these receptors are referred to as nicotinic-cholinergic and muscarinic-cholinergic receptors, respectively.

Central nervous system

Peripheral nervous system

Effector organ

Alpha or beta receptors

Central nervous system

Peripheral nervous system

Effector organ

Alpha or beta receptors

Smooth muscle, cardiac muscle,

Muscarinic receptors

Postganglionic fiber

Smooth muscle, cardiac muscle, gland

FIGURE 3 Overview of synaptic pathways and mediators of the somatic, sympathetic, and parasympathetic neural subsystems.

Nicotinic receptors

Postganglionic fiber

Smooth muscle, cardiac muscle,

Muscarinic receptors

Smooth muscle, cardiac muscle, gland

FIGURE 3 Overview of synaptic pathways and mediators of the somatic, sympathetic, and parasympathetic neural subsystems.

TABLE 1 Agonists and Antagonists at Specific Receptors

Receptor

Agonist

Antagonist

Nicotinic-cholinergic ACh, nicotine

Muscarinic-cholinergic ACh, muscarine Alpha-adrenergic Epinephrine, norepinephrine, isoproterenola Beta-adrenergic Isoproterenol, epinephrine, norepinephrinea

Tubocurarine, hexamethonium Atropine Phentolamine, phenoxybenzamine

Propranolol aIn order of potency, the most potent first.

On the adrenergic side, two major classes of receptors have been defined based on the potency of epinephrine, norepinephrine, and the synthetic compound isoproter-enol to act as agonists. Receptors for which the order of potency is epinephrine > norepinephrine ^ isoproterenol are known as a-adrenergic receptors, and two antagonists selective for these receptors are phentola-mine and phenoxybenzamine. Receptors for which the order of potency is isoproterenol > epinephrine ^ norepinephrine are known as ft-adrenergic receptors. Propranolol is an example of a ft-adrenergic antagonist. One should note that the pharmacology of cholinergic and adrenergic receptor-agonist/antagonist interactions is considerably more varied than just described. For example, ft-adrenergic receptors have been subdivided into ft1 and ft2 receptors. However, the general concepts presented here form much of the basic foundation upon which traditional autonomic physiology and pharmacology are based.

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