Alpha motor neurons

Following the development of the motor program, neurons originating in the multimodal motor association areas transmit impulses by way of association tracts to neurons of the primary motor cortex. The primary motor cortex is located in the precentral gyrus, which is the most posterior region of the frontal lobe adjacent to the multimodal motor association areas (see Figure 6.3) this area initiates voluntary contractions of specific skeletal muscles. Neurons whose cell bodies reside here transmit impulses by way of descending projection tracts to the spinal cord, where they innervate the alpha motor neurons (which innervate skeletal muscles). 

Alpha motor neurons innervate skeletal muscle fibers to cause contraction. 

Alpha motor neuron that transmits impulses to skeletal muscles... 

Synapses between first-order sensory neurons and alpha motor neurons, either directly or by way of intemeurons, result in spinal cord reflexes. Reflexes are discussed in more detail in a subsequent section in this chapter. 

Descending tracts. Voluntary movement of skeletal muscles is controlled by two types of descending tracts. Neurons in these tracts terminate on and influence activity of alpha motor neurons in the ventral horn. The two types of tracts include ... 

The corticospinal tracts originate in the cerebral cortex. Neurons of the primary motor cortex are referred to as pyramidal cells. Most of these neurons axons descend directly to the alpha motor neurons in the spinal cord. In... 

As with the ascending tracts, descending tracts cross from one side of the CNS to the other. Most of the tracts cross over in the medulla of the brainstem. Therefore, the right side of the brain influences the activity of the alpha motor neurons and thus the skeletal muscles on the left side of the body. The locations of specific descending tracts are illustrated in Figure 7.2 and a summary of their functions is found in Table 7.1. 

The excitatory intemeuron then synapses with the alpha motor neuron that innervates Hie flexor muscles of the right leg. Consequently, stimulation of the excitatory intemeuron leads to stimulation of the alpha motor neuron, which then stimulates the flexor muscles to contract and pick up or withdraw the foot from the painful stimulus. The inhibitory intemeuron synapses with the alpha motor neuron that innervates the extensor muscles of the right leg. Therefore, stimulation of the inhibitory intemeuron leads to inhibition of the alpha motor neuron. As a result, the extensor muscles relax. 

Release autonomic nervous system all postganglionic neurons of parasympathetic system some sympatheticpostganglionicneurons innervating sweat glands (alpha motor neurons innervating skeletal muscle)b adrenal medulla (20% of secretion) secretion)... 

Muscle fibers are incapable of mitosis. In fact, the number of muscle fibers per muscle is likely determined by the second trimester of fetal development. Therefore, enlargement of a whole muscle is not due to an increase in the number of fibers in the muscle, but rather to the hypertrophy of existing fibers. Because muscle fibers have no gap junctions between them, electrical activity cannot spread from one cell to the next. Therefore, each muscle fiber is innervated by a branch of an alpha motor neuron. A motor unit is defined as an alpha motor neuron and all of the muscle fibers that it innervates. 

Each muscle fiber is innervated by a branch of an alpha motor neuron. The synapse between the somatic motor neuron and the muscle fiber is referred to as the neuromuscular junction. Action potentials in the motor neuron cause release of the neurotransmitter acetylcholine. Binding of acetylcholine to its receptors on the muscle fiber causes an increase in the permeability to Na+ and K+ ions. The ensuing depolarization generates an action potential that travels along the surface of the muscle fiber in either direction that is referred to as a propagated action potential. This action potential elicits the intracellular events that lead to muscle contraction. 

When the action potentials in the alpha motor neuron cease, stimulation of muscle fiber is ended. Ca++ ions are pumped back into the sarcoplasmic reticulum and troponin and tropomyosin return to their original positions. As a result, the myosin-binding sites on the actin are covered once again. The thin filaments return passively to their original positions, resulting in muscle relaxation. 

A motor unit is defined as an alpha motor neuron and all of the skeletal muscle fibers it innervates. The number of muscle fibers innervated by an alpha motor neuron varies considerably, depending upon the function of the muscle. For example, the muscles of the eyes and hands have very small motor units. In other words, each alpha motor neuron associated with these muscles synapses with only a few muscle fibers. As a result, each of these muscles is innervated by a comparatively large number of alpha motor neurons. Densely innervated muscles are capable of carrying out more precise, complex motor activities. On the other hand, antigravity muscles have very large motor units. For example, the gastrocnemius muscle of the calf has about 2000 muscle fibers in each motor unit. Muscles with large motor units tend to be more powerful and more coarsely controlled. 

Skeletal muscle is neurogenic and requires stimulation from the somatic nervous system to initiate contraction. Because no electrical communication takes place between these cells, each muscle fiber is innervated by a branch of an alpha motor neuron. Cardiac muscle, however, is myogenic, or self-excitatory this muscle spontaneously depolarizes to threshold and generates action potentials without external stimulation. The region of the heart with the fastest rate of inherent depolarization initiates the heart beat and determines the heart rhythm. In normal hearts, this "pacemaker region is the sinoatrial node. 

Slow component a (SCa) comprises largely the cyto-skeletal proteins that form NFs and MTs. Rates of transport for SCa proteins in mammalian nerve range from 0.2-0.5 mm/day in optic axons tol mm/day in motor neurons of the sciatic nerve, and can be even slower in poikilotherms such as goldfish. Although the polypeptide composition of SCa is relatively simple, the relative contribution of SCa to slow transport varies considerably. For large axons (e.g. alpha motor neurons in the sciatic nerve), SCa is a large fraction of the total protein in slow transport, while the amount of material in SCa is relatively reduced for smaller axons (i.e. optic axons) [32]. The amount and phosphorylation state of SCa protein in axons is the major determinant of axonal diameter. 

Skeletal muscle spasms are used to describe the increased tension often seen in skeletal muscle after certain musculoskeletal injuries and inflammation (muscle strains, nerve root impingements, etc.) occur.20,96 This tension is involuntary, so the patient is unable to relax the muscle. Spasms differ from spasticity because spasms typically arise from an orthopedic injury to a musculoskeletal structure or peripheral nerve root rather than an injury to the CNS. Likewise, muscle spasms are often a continuous, tonic contraction of specific muscles rather than the velocity-dependent increase in stretch reflex activity commonly associated with spasticity. The exact reasons for muscle spasms are poorly understood. According to some authorities, muscle spasms occur because a vicious cycle is created when the initial injury causes muscular pain and spasm, which increases afferent nociceptive input to the spinal cord, further exciting the alpha motor neuron to cause more spasms, and so on.61,96 Other experts believe that muscle spasms occur because of a complex protective mechanism, whereby muscular contractions are intended to support an injured vertebral structure or peripheral joint.96 Regardless of the exact reason, tonic contraction of the affected muscle is often quite painful because of the buildup of pain-mediating metabolites (e.g., lactate). 

It is not clear, however, exactly how these drugs inhibit neurons involved in the polysynaptic pathways. There is preliminary evidence that one of these compounds (cyclobenzaprine) might block serotonin receptors on spinal interneurons, thereby decreasing the excitatory influence of serotonin on alpha motor neuron activity.50,55 Although this effect has been attributed to cyclobenzaprine in animals (rats), the effect of this drug and other muscle relaxants in humans remains to be determined. 

Tizanidine (Zanaflex) is classified as an alpha-2 adrenergic agonist, meaning that this drug binds selectively to the alpha-2 receptors in the CNS and stimulates them. Alpha-2 receptors are found at various locations in the brain and spinal cord, including the presynaptic and postsynaptic membranes of spinal interneurons that control alpha motor neuron excitability. Stimulation of these alpha-2 receptors inhibits the firing of interneurons that relay information to the alpha motor neuron that is, interneurons that comprise polysynaptic reflex arcs within the spinal cord.27 Tizanidine appears to bind to receptors on spinal interneurons, decrease the release of excitatory neurotransmitters from their presynaptic terminals (presynaptic inhibition), and decrease the excitability of the postsynaptic neuron (postsynaptic inhibition).40 Inhibition of spinal interneurons results in decreased excitatory input onto the alpha motor neuron, with a subsequent decrease in spasticity of the skeletal muscle supplied by that neuron. 

The tendency for MAO inhibitors to produce symptoms related to neuromuscular excitability, the serotonin syndrome, has been recognized in cases of overdose (SEDA-10, 18) and in interactions with other antidepressants or tryptophan (SEDA-10, 16, 17) (20). The authors of a thorough review of the preclinical and clinical literature have drawn attention to these phenomena, which occur at therapeutic doses with a MAO inhibitor alone, and have speculated that the mechanism is related to a combination of increased serotonergic tone and central disin-hibition of alpha motor neuron-mediated spinal activity (21). They discussed ten previous reports of myoclonus, hyper-reflexia, muscle twitching, and increased muscle tone in patients taking MAO inhibitors. These neuromuscular effects appear to occur in up to 15% or more of patients, and are more likely when tryptophan is given in combination. They usually appear after 10-14 days. Tolerance does not occur, but the effects may abate or... 

The somatic nervous system controls skeletal muscle movement through motor neurons. Alpha motor neurons extend from the spinal cord and terminate on indi-... 

Voluntary skeletal muscle movements are initiated by the motor cortex in the brain. Then signals travel down the spinal cord to the alpha motor neuron to result in contraction. However, not all movement of skeletal muscles is voluntary. Certain reflexes occur in response to dangerous stimuli, such as extreme heat. Reflexive skeletal muscular movement is controlled at the level of the spinal cord and does not require higher brain initiation. Reflexive movements are processed at this level to minimize the amount of time necessary to implement a response. 

I. Mechanism of toxicity. The growth of C tetani in a wound under anaerobic conditions produces the toxin tetanospasmin. The toxin enters the myoneural junction of alpha motor neurons and travels via retrograde axonal transport to the synapse. There it biocks the release of the presynaptic inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and glycine, causing intense muscular spasms. 

FIG. 6-4 (A) Neutral position. (B) Stretch of extrafusal and intrafusal alpha motor neuron stimulated to reflexively initiate extrafusal muscle contraction. (C) Gamma motor neuron innervation of muscle spindle. Contraction of ends stretches spindle, activating lb fibers, lb sensory fiber activates alpha motor neuron to cause extrafusal muscle contraction. (D) Compression of whole muscle or contraction of extrafusal muscle results in shortening of muscle spindle and deactivation of sensory fiber firing. 

Increased tension in a skeletal muscle distorts the Golgi tendon organ, producing a generator potential that initiates an action potential. The action potential travels over the Ib neurons to the spinal cord. Afferent action potentials activate the intemeurons, which inhibit the alpha motor neurons back to the skeletal muscle. The increased muscle tension that initiates the reflex can result from contraction of the skeletal muscle or from marked passive stretch of the muscle. 

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