Neuroeffector synapses

General characteristics and histological picture

In skeletal muscle, neuroeffector junctions are called neuromuscular junctions. The entire complex consisting of nerve terminals and the underlying part of the muscle is called the motor end plate (or motor plaque). It is important to clearly distinguish these effector structures from neuromuscular spindles, which perform an exclusively receptor (sensory) function.

In histological preparations, the motor end plate is best studied using silver impregnation staining. Against the background of muscle tissue, myelinated nerve fibers stain dark brown. At the contact site, the axon branches repeatedly, forming terminal branches in the form of characteristic tortuous dark structures on the muscle surface.

Synapse formation and ultrastructure

The process of neuromuscular junction formation begins when a motor neuron axon approaches a muscle fiber. In the immediate vicinity of the target, the axon loses its myelin sheath and breaks down into several terminal branches. These branches deeply invaginate into the muscle fiber. The muscle membrane (sarcolemma) is not ruptured, but merely caves inward following the nerve endings.

The plasmalemma of the nerve ending becomes the presynaptic membrane. Inside the cytoplasm of the terminals are a huge number of mitochondria, which provide the energy requirements of the synapse. Synaptic vesicles containing the neurotransmitter acetylcholine are also concentrated there. The enzyme choline acetyltransferase operates in the synapse to constantly replenish its reserves. The mechanism of action of such cholinergic synapses is ionotropic.

Molecular mechanism of exocytosis

The release of the neurotransmitter into the synaptic cleft is a strictly regulated process, in which calcium ions and specialized proteins play the main role:

1. Activation: $Ca^{2+}$ channels are embedded in the presynaptic membrane. Upon depolarization, they open, calcium enters and activates protein kinase, as well as the protein synaptotagmin.
2. Mobilization of the reserve: At rest, vesicles are attached to the cytoskeleton by means of the protein synapsin. Under the action of protein kinase, synapsin detaches from the vesicles, releasing them for transport.
3. Fusion: Synaptotagmin tightly binds the vesicle to the presynaptic membrane. Then, the protein synaptophysin, under the influence of synaptotagmin, forms common pores between the vesicle and the membrane, initiating neurotransmitter exocytosis.

Postsynaptic membrane and contact zone

The postsynaptic membrane is represented by areas of the sarcolemma that have invaginated deep into the fiber and surrounded the axon terminals. Its main feature is the presence of numerous invaginations (folds) that significantly increase the contact area.

Specific nicotinic acetylcholine receptors linked to cation channels are embedded in the postsynaptic membrane. When acetylcholine binds to the receptors, the channels open, triggering muscle excitation. To stop the signal, the enzyme cholinesterase operates in the contact zone, rapidly degrading neurotransmitter molecules.

In the underlying sarcoplasm (directly beneath the nerve terminal), a marked accumulation of mitochondria and muscle nuclei is observed. In histological preparations at the junction area, nuclei of glial cells—Schwann cells (lemmocytes)—which accompany the axon, can also be found.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• The mechanism of action of nicotinic acetylcholine receptors and associated cation channels
• The role and localization of the enzyme cholinesterase in the synaptic cleft
• Ultrastructure and energy metabolism of mitochondria at the presynaptic pole
• Differential diagnosis of glial and muscle nuclei in histological preparations

Other topics in "Nervous tissue: nerve endings and synapses"

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