Motor neuron

Motor neuron
Micrograph of the hypoglossal nucleus showing motor neurons with their characteristic coarse Nissl substance ("tigroid" cytoplasm). H&E-LFB stain.
Details
Location	Ventral horn of the spinal cord, some cranial nerve nuclei
Morphology	Projection neuron
Function	Excitatory projection (to NMJ)
Neurotransmitter	UMN to LMN: glutamate; LMN to NMJ: ACh
Presynaptic connections	Primary motor cortex via the Corticospinal tract
Postsynaptic connections	Muscle fibers and other neurons
Identifiers
NeuroLex ID	Motor Neuron
TA	A14.2.00.021
FMA	5867
Anatomical terminology

A motor neuron (or motoneuron) is a nerve cell (neuron) whose cell body is located in the spinal cord and whose fiber (axon) projects outside the spinal cord to directly or indirectly control muscles.^[1] Motor neurons are efferent nerves (also called effector neurons), that carry signals from the spinal cord to the muscles to produce (effect) movement.^[2] Types of motor neurons are alpha motor neurons, beta motor neurons and gamma motor neurons.

Clinical neuroscientists refer to upper and lower motoneurons, with the cell type described above being a lower motoneuron. Upper motoneurons are cortico-spinal interneurons that arise from the motor cortex and descend to the spinal cord where they activate the lower motoneurons through synapses. Non-clinical neuroscientists tend to restrict the use of the term 'motoneuron' to the efferent neurons that actually innervate muscles (the lower motoneurons).

A single motor neuron may innervate many muscle fibres (muscle cells), and a muscle fibre can undergo many action potentials in the time taken for a single muscle twitch. As a result, if an action potential arrives before a twitch has completed, the twitches can superimpose on one another, either through summation or tetanus. In summation, the muscle is stimulated repetitively such that additional action potentials coming from the somatic nervous system arrive before the end of the twitch. The twitches thus superimpose on one another, leading to a force greater than that of a single twitch. On the other hand, tetanus is caused by constant, very high frequency stimulation - the action potentials come at such a rapid rate that individual twitches are indistinguishable, and tension rises smoothly eventually reaching a plateau.^[3]

Anatomy and physiology

According to their targets, motor neurons are classified into three broad categories:

Somatic motor neurons, which originate in the central nervous system, project their axons to skeletal muscles ^[4] (such as the muscles of the limbs, abdominal, and intercostal muscles), which are involved in locomotion .

Special visceral motor neurons, also called branchial motor neurons, which directly innervate branchial muscles (that motorize the gills in fish and the face and neck in land vertebrates).

General visceral motor neurons (visceral motor neurons for short) which indirectly innervate cardiac muscle and smooth muscles of the viscera ( the muscles of the arteries): they synapse onto neurons located in ganglia of the autonomic nervous system (sympathetic and parasympathetic), located in the peripheral nervous system (PNS), which themselves directly innervate visceral muscles (and also some gland cells).

In consequence:

• the motor command of skeletal and branchial muscles is monosynaptic (involving only one motor neuron, respectively, somatic and branchial, which synapses onto the muscle).
• the command of visceral muscles is disynaptic (involving two neurons: the general visceral motor neuron located in the CNS, which synapses onto a ganglionic neuron, located in the PNS, which synapses onto the muscle).

It could be argued that, in the command of visceral muscles, the ganglionic neuron, parasympathetic or sympathetic, is the real motor neuron, being the one that directly innervates the muscle (whereas the general visceral motor neuron is, strictly speaking, a preganglionic neuron). But, for historical reasons, the term motor neuron is reserved for the CNS neuron.

All vertebrate motor neurons are cholinergic, that is, they release the neurotransmitter acetylcholine. Parasympathetic ganglionic neurons are also cholinergic, whereas most sympathetic ganglionic neurons are noradrenergic, that is, they release the neurotransmitter noradrenaline. (see Table)

Function

The interface between a motor neuron and muscle fiber is a specialized synapse called the neuromuscular junction. Upon adequate stimulation, the motor neuron releases a flood of neurotransmitters that bind to postsynaptic receptors and triggers a response in the muscle fiber which leads to muscle movement.

• In invertebrates, depending on the neurotransmitter released and the type of receptor it binds, the response in the muscle fiber could be either excitatory or inhibitory.
• For vertebrates, however, the response of a muscle fiber to a neurotransmitter can only be excitatory, in other words, contractile. Muscle relaxation and inhibition of muscle contraction in vertebrates is obtained only by inhibition of the motor neuron itself. Muscle innervation may eventually play a role in the maturation of motor activity. This is how muscle relaxants work by acting on the motoneurons that innervate muscles (by decreasing their electrophysiological activity) or on cholinergic neuromuscular junctions, rather than on the muscles themselves.

Somatic motor neurons

Somatic motor neurons are the alpha efferent neurons, beta efferent neurons, and gamma efferent neurons. They are called efferent to indicate the flow of information from the central nervous system (CNS) to the periphery.

• Alpha motor neurons innervate extrafusal muscle fibers (a type of slow switch fiber) located throughout the muscle. Their cell bodies are in the ventral horn of the spinal cord and they are sometimes called ventral horn cells.

In addition to voluntary skeletal muscle contraction, alpha motor neurons also contribute to muscle tone, the continuous force generated by noncontracting muscle to oppose stretching. When a muscle is stretched, sensory neurons within the muscle spindle detect the degree of stretch and send a signal to the CNS. The CNS activates alpha motoneurons in the spinal cord, which cause extrafusal muscle fibers to contract and thereby resist further stretching. This process is also called the stretch reflex.

• Beta motor neurons innervate intrafusal muscle fibers of muscle spindles, with collaterals to extrafusal fibres.
• Gamma motor neurons innervate intrafusal muscle fibers found within the muscle spindle. They regulate the sensitivity of the spindle to muscle stretching. With activation of gamma neurons, intrafusal muscle fibers contract so that only a small stretch is required to activate spindle sensory neurons and the stretch reflex.

Motor units

A single motor neuron may synapse with one or more muscle fibers.^[5] The motor neuron and all of the muscle fibers to which it connects is a motor unit. Motor units are split up into 3 categories:^[5]

• Slow (S) motor units stimulate small muscle fibers, which contract very slowly and provide small amounts of energy but are very resistant to fatigue, so they are used to sustain muscular contraction, such as keeping the body upright. They gain their energy via oxidative means and hence require oxygen. They are also called red fibers.^[5]
• Fast fatiguing (FF) motor units stimulate larger muscle groups, which apply large amounts of force but fatigue very quickly. They are used for tasks that require large brief bursts on energy, such as jumping or running. They gain their energy via glycolytic means and hence don't require oxygen. They are called white fibers.^[5]
• Fast fatigue-resistant motor units stimulate moderate-sized muscles groups that don't react as fast as the FF motor units, but can be sustained much longer (as implied by the name) and provide more force than S motor units. These use both oxidative and glycolytic means to gain energy. ^[5]

See also

References

Sources

• Sherwood, L. (2001). Human Physiology: From Cells to Systems (4th ed.). Pacific Grove, CA: Brooks-Cole. ISBN 0-534-37254-6. 
• Marieb, E. N.; Mallatt, J. (1997). Human Anatomy (2nd ed.). Menlo Park, CA: Benjamin/Cummings. ISBN 0-8053-4068-8.