Gamma motor neurons

Gamma motor neurons innervate intrafusal fibers of the muscle spindle, which monitors muscle length. 

As an alpha-2 agonist, tizanidine decreases presynaptic excitatory neurotransmitter release and postsyn-aptic neurotransmitter effectiveness. Alpha-2 receptor agonists attenuate monosynaptic and polysynaptic reflexes in the spinal cord [25]. Tizanidine decreases excitatory neurotransmitter release and Substance P release from small sensory afferents [28]. Tizanidine decreases locus coeruleus activity, thereby modulating descending motor regulatory pathways [28]. Tizanidine decreases activity of both alpha and gamma motor neurons [28]. 

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. 

Altered release. Tetanus is an infectious disease caused by the bacterium Clostridium tetani. This bacterium produces a neurotoxin active on inhibitory synapses in the spinal cord. Motor neurons, which supply skeletal muscle and cause contraction, have cell bodies that lie in the spinal cord. Under normal circumstances, these motor neurons receive excitatory and inhibitory inputs from various sources. The balance of these inputs results in the appropriate degree of muscle tone or muscle contraction. Tetanus toxin prevents the release of gamma amino butyric acid (GABA), an important neurotransmitter active at these inhibitory synapses. Eliminating inhibitory inputs results in unchecked or unmodulated excitatory input to the motor neurons. The resulting uncontrolled muscle spasms initially occur in the muscles of the jaw, giving rise to the expression lockjaw. The muscle spasms eventually... 

Le,W. D., Appel, S. H. (2002). Immunoglobulin Fc gamma receptor promotes immunoglobulin uptake, immunoglobulin-mediated calcium increase, and neurotransmitter release in motor neurons. J. Neurosci. Res. 69, 110-116. 

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. 

Park, S. W., Yi, J. H., Miranpuri, G., Satriotomo, I., Bowen, K., Resnick, D. K., and Vemuganti, R. (2007). Thiazolidinedione class of peroxisome proliferator-activated receptor gamma agonists prevents neuronal damage, motor dysfunction, myelin loss, neuropathic pain, and inflammation after spinal cord injury in adult rats. J. Pharmacol. Exp. Ther. 320, 1002—1012. 

Skeletal muscles are controlled by large nerves in the spinal cord. The nerve cell or neuron is part of the spinal cord, but its projections, the axon and the many dendrites course outward to connect to muscle cells. The nerve axon is a sensory device that senses the muscle cells current condition. The dendrites are motor fibers that deliver the instructions to change its state to the muscle fiber. The area at which the muscle and nerve connect is called the neuromuscular junction. It is here that the end releases a chemical called a neurotransmit-ter that crosses the microscopic space between the nerve and muscle and causes the desired response. Five such neurotransmitters have been described acetylcholine, serotonin, norepinephrine, glycine, and gamma-ammi-nobutyric acid or GABA. Of these, the functions of three are known. Acetylcholine excites muscle activity and glycine and GABA inhibit it. 

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