The Neuromuscular Junction
Muscles must be stimulated to contract. In the case of skeletal muscle (the muscle making up the form of the body), the stimulation is in the form of a neurotransmitter released by nerve endings. The microscopic site of "contact" between muscle and nerve is called a neuromuscular or myoneural junction. Although the discussion here is limited to skeletal muscle, it should be understood that smooth muscle (of the the walls of internal organs) also has a neuromuscular junctions of lesser complexity than described here. The neuromuscular junctions of cardiac muscle are less well known, but in certain cases they are similar to those of smooth muscle.
Skeletal muscle of the arm and its source of stimulation, a motor nerve. The branch giving off the axon ensheathed in myelin and a schwann cell. The axon divides into branches each of which terminates in a number of neuromuscular junctions with muscle cells. The number of muscle fibers supplied by one axon in and its branches varies from four (in the muscles of the orbit, which track the eyeball) to several hundred (as in the gluteus maximus muscle of the buttock.) A motor neuron and the muscle fibers it supplies constitute a motor unit.
Each axon branch terminates on a muscle fiber by forming an expanded ending called an axon terminal. The circled illustration depicts the appearance, as seen in an electron micrograph, of an axon terminal adjacent to the specialized region of a muscle cell membrane called the motor end plate. Before the axon branch reaches the motor end plate, it loses its myelin sheath but retains its Schwann cell covering, which flows over and covers the myoneural junction. At this level of magnification it can be seen that the axon terminal does not enter the muscle fiber but appears to lie in a trough of the fiber, flush agains its cell membrane or sarcolemma.
The presynaptic membrane of the axon terminal an extension of the cell membrane is separated from the sarcolemma by a space 20 to 60 nanometers wide. This space is the synaptic cleft. The sarcolemma adjacent to the cleft exhibits convolutions, called junctional folds which project into the sarcoplasm. Neurotransmitter receptor sites are found on the sarcolemma between junctional folds.
Neurotransmitter, released from synaptic vesicles in the axon terminal, is cast by the presynaptic membrane into the synaptic cleft, from which it can stimulate the receptor sites. At these sites it induces an increased permeability to sodium ions, resulting in depolarization of the muscle fiber and subsequent contraction. The acetylcholine remaining in the synaptic cleft is rapidly inactivated by an enzyme (acetylcholinesterase). the choline is taken back up by the axon terminal for re-synthesis of the transmitter. the energy for this transfer of stimulus and related events is developed within the mitochondria.
Diseases involving profound muscle weakness are often related to disturbances in neurotransmitter release, uptake, or clearance. In the case of myasthenia gravis (myo, "muscle"; asthenia, "weakness"), fewer receptor sites between the junctional folds are found. As a result, only feeble muscle contractions can take place.
FINAL COMMON PATHWAY
The somatic, or skeletal, muscles that perform the work of moving parts of the body are all under direct control of lower motor neurons and contract only in response to activation by these neurons. Each muscle performs a particular movement, but each muscle may be involved in several different motor activities organized by the lower motor neurons and their pools of interneurons. Alpha motor neurons and their surrounding interneuronal pool integrate activity from central and peripheral sources and transmit action potentials to the muscles to produce the appropriate level of contraction. Disease processes that impair the function of a motor unit prevent the normal activation of muscle fiber s in that motor unit. This is manifested as an inability of the muscle to contract fully (weakness or paralysis).
The final common pathway is the effector mechanism by which all motor activity is mediated. It includes the motor neurons in the ventral horn of the spinal cord and brainstem and their axons that extend peripherally via nerves to innervate muscles. These motor neurons are called alpha motor neurons. The axons from the motor neurons innervate the muscle fibers that are responsible for skeletal muscle contraction. This combination of alpha motor neuron, peripheral axon, and all the muscle fibers innervated by them is the motor unit, the basic functional component of the final common pathway.
The nerve terminals of a single motor axon innervate muscle fibers that may be distributed widely throughout the muscle, intermingling with muscle fibers innervated by other neurons. A muscle may contain from 50 to 2,000 motor units. The size of a motor unit is determined by the number of fibers innervated by a single motor neuron, expressed as the innervation ratio, the number of muscle fibers per axon. The motor units of the powerful limb muscles each contain from 500 to 2,000 muscle fibers. In contrast, motor units in intrinsic hand muscles have innervation ratios of only 50-400.
Diseases may affect the final common pathway at the level of the ventral horn cell, the axon, or the muscle fiber. Damage to any of these sites produces weakness, atrophy, loss of reflexes and loss of tone.
The alpha motoneuron and spinal interneurons. Alpha motoneurons are the final common pathway since all upper motoneuron influence can reach muscle only through them; these influences integrated by the motoneuron include.
Neurons in the primary motor cortex have specific functional roles related to particular muscles, not movements and upstream premotor areas are responsible for motor planning, it has a crucial role in the proximal arm movements in seeking targets. The prefrontal cortex and frontal lobes are the ultimate upper motoneurons and even their output depends on the integrity of converging sensory-motor input from remote cortical areas.
Skeletal muscle of the arm and its source of stimulation, a motor nerve. The branch giving off the axon ensheathed in myelin and a schwann cell. The axon divides into branches each of which terminates in a number of neuromuscular junctions with muscle cells. The number of muscle fibers supplied by one axon in and its branches varies from four (in the muscles of the orbit, which track the eyeball) to several hundred (as in the gluteus maximus muscle of the buttock.) A motor neuron and the muscle fibers it supplies constitute a motor unit.
Each axon branch terminates on a muscle fiber by forming an expanded ending called an axon terminal. The circled illustration depicts the appearance, as seen in an electron micrograph, of an axon terminal adjacent to the specialized region of a muscle cell membrane called the motor end plate. Before the axon branch reaches the motor end plate, it loses its myelin sheath but retains its Schwann cell covering, which flows over and covers the myoneural junction. At this level of magnification it can be seen that the axon terminal does not enter the muscle fiber but appears to lie in a trough of the fiber, flush agains its cell membrane or sarcolemma.
The presynaptic membrane of the axon terminal an extension of the cell membrane is separated from the sarcolemma by a space 20 to 60 nanometers wide. This space is the synaptic cleft. The sarcolemma adjacent to the cleft exhibits convolutions, called junctional folds which project into the sarcoplasm. Neurotransmitter receptor sites are found on the sarcolemma between junctional folds.
Neurotransmitter, released from synaptic vesicles in the axon terminal, is cast by the presynaptic membrane into the synaptic cleft, from which it can stimulate the receptor sites. At these sites it induces an increased permeability to sodium ions, resulting in depolarization of the muscle fiber and subsequent contraction. The acetylcholine remaining in the synaptic cleft is rapidly inactivated by an enzyme (acetylcholinesterase). the choline is taken back up by the axon terminal for re-synthesis of the transmitter. the energy for this transfer of stimulus and related events is developed within the mitochondria.
Diseases involving profound muscle weakness are often related to disturbances in neurotransmitter release, uptake, or clearance. In the case of myasthenia gravis (myo, "muscle"; asthenia, "weakness"), fewer receptor sites between the junctional folds are found. As a result, only feeble muscle contractions can take place.
FINAL COMMON PATHWAY
The somatic, or skeletal, muscles that perform the work of moving parts of the body are all under direct control of lower motor neurons and contract only in response to activation by these neurons. Each muscle performs a particular movement, but each muscle may be involved in several different motor activities organized by the lower motor neurons and their pools of interneurons. Alpha motor neurons and their surrounding interneuronal pool integrate activity from central and peripheral sources and transmit action potentials to the muscles to produce the appropriate level of contraction. Disease processes that impair the function of a motor unit prevent the normal activation of muscle fiber s in that motor unit. This is manifested as an inability of the muscle to contract fully (weakness or paralysis).
The final common pathway is the effector mechanism by which all motor activity is mediated. It includes the motor neurons in the ventral horn of the spinal cord and brainstem and their axons that extend peripherally via nerves to innervate muscles. These motor neurons are called alpha motor neurons. The axons from the motor neurons innervate the muscle fibers that are responsible for skeletal muscle contraction. This combination of alpha motor neuron, peripheral axon, and all the muscle fibers innervated by them is the motor unit, the basic functional component of the final common pathway.
The nerve terminals of a single motor axon innervate muscle fibers that may be distributed widely throughout the muscle, intermingling with muscle fibers innervated by other neurons. A muscle may contain from 50 to 2,000 motor units. The size of a motor unit is determined by the number of fibers innervated by a single motor neuron, expressed as the innervation ratio, the number of muscle fibers per axon. The motor units of the powerful limb muscles each contain from 500 to 2,000 muscle fibers. In contrast, motor units in intrinsic hand muscles have innervation ratios of only 50-400.
Diseases may affect the final common pathway at the level of the ventral horn cell, the axon, or the muscle fiber. Damage to any of these sites produces weakness, atrophy, loss of reflexes and loss of tone.
The alpha motoneuron and spinal interneurons. Alpha motoneurons are the final common pathway since all upper motoneuron influence can reach muscle only through them; these influences integrated by the motoneuron include.
Neurons in the primary motor cortex have specific functional roles related to particular muscles, not movements and upstream premotor areas are responsible for motor planning, it has a crucial role in the proximal arm movements in seeking targets. The prefrontal cortex and frontal lobes are the ultimate upper motoneurons and even their output depends on the integrity of converging sensory-motor input from remote cortical areas.