motor neuron

n.
A neuron that conveys impulses from the central nervous system to a muscle, gland, or other effector tissue.

Two way communication between individuals, or, stated differently, between their nervous systems, is entirely dependent on muscular contraction. This is so because although information concerning the external world is received and processed through our senses, the resulting percepts and mental (cognitive) activities remain entirely private within one's own consciousness. They remain so unless communicated to others by movement, whether through an infant's cry, a Gallic shrug, or an aggressive or submissive posture; whether through writing a poem, a philosophical work, or just graffiti; but above all through vocalization, whether simply as an approving grunt, or linguistically refined by articulation into speech or song; and for the deaf by hand signing. Even when disease has resulted in a major loss of muscle, as in motoneuron disease, communication remains possible providing that a single tiny muscle remains under conscious control, so that either its contractile force or associated electrical activity can be used in a prosthesis to control a typewriter, or to generate artificial speech. This is no better instanced than by the remarkable feat of communication by the mathematician Professor Stephen Hawking in explaining his reasoning about the origin and nature of the universe to the rest of us who dwell within it.

Skeletal (voluntary) muscles normally contract only in response to commands from the central nervous system (CNS). With its cell body within the spinal cord or brain stem, and its emergent process, the axon, innervating a group of muscle fibres known as the motor unit, the motor neuron forms the interface between the sentient, perceiving, and thinking human nervous system and the external world; it is, therefore, of paramount importance as the key structure mediating communication between individuals. Its importance was clearly recognized by Sir Charles Sherrington who, at the beginning of the twentieth century, designated the motor neuron as ‘the final common path’ from the CNS to the muscles. (These are now also called alpha motor neurons, because since Sherrington's time another type has been described, the gamma or fusimotor neurons; the specialized muscle fibres which these innervate do not directly contribute to force production and external work. Instead they control the discharge properties of the muscle spindles, receptors in the muscle that signal information about length and about the velocity of changes in length.

The spinal and cranial alpha motor neurons are among the largest neurons in the CNS, many having cell bodies in excess of 50 μm in diameter. From the cell body extend 5-7 long processes, the dendrites, and the axon, an extra-long process, which arises from a conical bulge known as the axon hillock. The axon innervates muscle that can be more than a metre away in the case of muscles moving the toes. The surface membrane of both the cell body and the dendrites is covered with microscopic structures of button-like shape, the ‘synaptic boutons’. These are formed by the axon terminals of other neurons, and indicate the sites at which information is transferred to this one neuron from many others. Such transfer is not achieved by cellular continuity — a matter of fierce debate in the late nineteenth century; instead, it is mediated by a process which Sherrington, by deduction from the properties he disclosed through studies of spinal reflexes, conceived as a functional though flowing discontinuity between neurons. That time discontinuity at the junction was attributed to a ‘synapse’, which he named from the Greek word for ‘clasp’. The delay is now understood to be due to the process of chemical transmission, following the release of a transmitter substance ‘presynaptically’ when a nerve impulse invades an axon terminal at a synapse with another neuron. The transmitter diffuses across the narrow gap, some 0.1 μm wide, between the terminal and the motor neuron dendrite or cell body, where it acts ‘postsynaptically’ by briefly altering the membrane potential of the motor neuron. It may either decrease it (depolarization) or increase it (hyperpolarization), thereby enhancing or depressing the motor neuron excitability. These brief unitary events, the excitatory and inhibitory synaptic potentials, respectively, have a triangular shape, taking about 1-2 milliseconds (0.001 sec) to rise or fall to their peak value and declining over 10-15 milliseconds. They have the property of summation when they overlap in time; thus the motor neuron (and most other neurons) can be described as integrating the information it receives moment by moment via its presynaptic inputs. Here a sense of scale has to be introduced. There is an estimated total of 30 000-50 000 boutons of different types across the entire surface. On average perhaps five of them are formed by the branching of each presynaptic axon, (analogous to the branching of the motor neuron axon that forms the motor unit within a muscle). In order for a motor neuron to discharge repetitively, say at rates typically between 5-20 impulses/sec, the motor neuron surface has to be exposed to a barrage of synaptic inputs (excitatory) with a net rate of approximately 12 000-20 000 inputs/sec. Then the summed activity lowers the membrane potential sufficiently to trigger a sustained discharge of the motor neuron in the region of the axon hillock. If each presynaptic input itself fired at 100/sec then it would require the co-operative but random activity of 150-200 individual neurons to provide the necessary excitation; and such steady state firing underlies the maintenance of posture. For rhythmic or strongly phasic movements, the presynaptic inputs themselves become progressively more synchronized, to generate the time course of the intended movement. The fastest, such as those that move the eyes rapidly from one target to another, are called ballistic movements. But willed movements rarely achieve the speed of pathological ones, for example the jerks typical of ‘myoclonic’ epilepsy or, for that matter, the speed of normal ones as in the knee-jerk reflex.

When the patellar tendon at the knee is tapped, the motor neurons that innervate the quadriceps muscles (many thousands of neurons in the grey matter of the spinal cord) are subjected suddenly to a highly synchronized synaptic input from the several hundred nerve fibres from muscle receptors which were briefly stretched by the tap. The synaptic potentials all occur at much the same time, because the receptors project directly to the motor neurons to form a ‘monosynaptic’ pathway. Temporal and spatial summation therefore is great indeed. This causes the depolarization to reach the firing threshold for a substantial fraction of the quadriceps motor neurons, and their combined axonal discharge leads to the rapid muscle twitch that extends the leg at the knee joint. At the other extreme of quadriceps activation is the steady discharge of motor neurons that underlies the holding of a posture. Between these extremes is a whole range of movements at different velocities and with varying time course in relation to their force, as required for example for the diverse finger movements in playing a musical instrument, a ‘stop volley’ in tennis, or for increasing one's walking pace. Each participating motor neuron receives a time-varying pattern of excitation and inhibition such that its output pattern of discharge acts in concert with others to produce the desired movement. It is not surprising therefore that when the capacity to perform movements is impaired by one of the motor neuron diseases, such as amyotrophic lateral sclerosis, which specifically destroy motor neurons, or others that affect them, such as poliomyelitis, without impairing intellect, the effects are so catastrophic for the patient.

— Tom Sears

See also central nervous system; neurotransmitters; reflexes; synapse; skeletal muscle.

n

One of the various efferent nerve cells that transmit nerve impulses from the brain or from the spinal cord to muscular or glandular tissue.

A neuron having a motor function; an efferent neuron conveying motor impulses.

• m. n. disease — see abiotrophy.
• equine m.n. disease — (EMND) a syndrome of mature horses of uncertain etiology, but possibly an oxidative disorder associated with insufficient green forage in the diet and a deficiency of vitamin E. Characterized by generalized weakness, muscle fasciculations and weight loss, despite a normal appetite, that is caused by neurogenic muscle atrophy. There is also a distinctive retinopathy.
• lower m. n's — peripheral neurons whose cell bodies lie in the ventral gray columns of the spinal cord and whose terminations are in skeletal muscles. Called also LMN. See also lower motor neuron.
• peripheral m. n's — neurons in a peripheral reflex arc that receive impulses from interneurons and transmit them to voluntary muscles.
• upper m. n's — neurons in the cerebral cortex that conduct impulses from the motor cortex to the motor nuclei of the cerebral nerves or to the ventral gray columns of the spinal cord. Lesions of the upper motor neuron interrupt the inhibitory effect that upper motor neurons have on lower motor neurons, resulting in exaggerated or hyperactive reflexes. This is called also extensor rigidity. See also upper motor neuron. Called also UMN.

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