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Chapter 8

Chapter 8. Control of Movement. Muscles. 3 types of muscles: Skeletal muscles – move us (and our bones) around; attached to bones, fastened via tendons, which are sting bands of connective tissue Flexion – contraction of a flexor muscle, bending the joints

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Chapter 8

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  1. Chapter 8 Control of Movement

  2. Muscles • 3 types of muscles: • Skeletal muscles – move us (and our bones) around; attached to bones, fastened via tendons, which are sting bands of connective tissue • Flexion – contraction of a flexor muscle, bending the joints • Extension – contraction of an extensor muscle, straitening the joints • Anatomy of skeletal muscle • Extrafusal muscle fibers – responsible for force exerted by contraction of skeletal muscle; served by axons of alpha motor neurons • Intrafusal muscle fibers (a.k.a. muscle spindles) – contain sensory endings sensitive to stretch; served by axons of gamma motor neurons • An alpha motor neuron, its axon, and the several extrafusal muscles fibers it innervates constitute a motor unit • A single muscle fiber consist of bundle of myofibrils, each containing the proteins actin and myosin, which serve to contract the muscle; where these protein filaments overlap, the muscle appears to be striated, or striped, thus referred to as striated muscle

  3. Muscles • Skeletal muscles (con’t) • The physical basis of muscular contraction • The synapse b/t the axon of an efferent neuron and the muscle fiber it innervates is called the neuromuscular junction • The terminal buttons synapse onto motor endplates, which are located in grooves on the muscle fibers • ACh is released into the neuromuscular junction to depolarize the postsynaptic membrane – this is called an endplate potential (much larger than EPSPs; always causes muscle fiber to fire, causing a “twitch”) • Depolarization causes the actin and myosin filaments to work together (see “rowing movement” figure in book, Fig 8.2) to contract or shorten the muscle fiber • A single impulse from motor neuron produces a single twitch of muscle fiber, with the strength of the contraction determined by rate of firing of motor units

  4. Muscles • Skeletal muscles (con’t) • Sensory feedback from muscles • The afferent stretch receptors of the intrafusal muscle fibers serve to detect muscle length • Located within the tendon, in the Golgi tendon organ, and encode the degree of stretch by rate of firing • The Golgi tendon organs detect the strength of the muscle contraction, and thus fire in proportion to the stress on the muscle • Smooth muscle • Nonstriated muscle innervated by the ANS • Found in blood vessel walls, reproductive tracts, in sphincters, within eye, in gut, around hair follicles • Multiunit smooth muscles contract in response to neural stimulation or hormones; Single-unit smooth muscles normally contract in a rhythmic pattern

  5. Muscles • Cardiac muscle • Found in the heart, responsible for contractions • Looks striated, but acts like single-unit smooth muscle • Neural activity and certain hormones serve to modulate heart contraction rate

  6. Reflex control of movement • The spinal cord can work autonomously from the brain in certain situations • Monosynaptic stretch reflex • A reflex in which a muscle contracts in response to being quickly stretched • e.g. knee tap, leg kick reflex • Too short for brain involvement (i.e. sensory info travel up, motor command travel back down) • Involves one sensory and one motor neuron, with one synapse in between • Begins at muscle spindle, synapsing on an alpha motor neuron, and innervating the extrafusal muscle fibers of that same muscle

  7. Reflex control of movement • Polysynaptic reflexes • All other spinal reflexes besides the previously mentioned monosynaptic reflex are polysynaptic • The Golgi tendon organs have two types of afferent axons that detect muscle stretch: highly sensitive axon that sends info to brain about the degree of the stretch; less sensitive axon that synapse on interneurons in the gray matter of the SC, which then inhibit the alpha motor neurons of that same muscle • This functions to decrease the strength of the muscle contraction to prevent damage to tendons or bones attached

  8. Reflex control of movement • Polysynaptic reflexes (con’t) • This inhibitory reflex provided early evidence for neural inhibition, even before most was known about synaptic mechanisms • In a decerebrate (where brain stem is transected from the rest of the brain) animal, we see an extension of the muscles caused by excitation of neurons located in brain stem, which is normally inhibited by neurons rostral to the transection (decerebrate rigidity) • Stretch reflexes excite the agonist (produces movement) muscle and inhibiting the antagonist (resists movement) muscle

  9. Control of movement by the brain • Organization of motor cortex • Somatotopic organization – topographically organized map of the different parts of the body represented in a certain area of the brain

  10. Control of movement by the brain • Organization of motor cortex (con’t) • Main input to primary motor cortex is frontal association cortex: • Supplementary motor cortex – located medial and rostral to primary motor cortex • Premotor cortex – located laterally and rostral to primary motor cortex • Both involved in planning movements, and receive info from association areas in parietal and temporal cortices • Also receives info from primary somatosensory cortex about sensory stimuli

  11. Control of movement by the brain • Cortical control of movement: Descending pathways • Neurons in primary motor cortex control movements by 2 groups of descending tracts: • Lateral group – control independent limb movements (i.e. not coordinated) • Corticospinal tract • Corticobulbar tract • Rubrospinal tract • Ventromedial group – controls automatic movements such as gross movements of trunk, posture and locomotion • Vestibulospinal tract • Tectospinal tract • Reticulospinal tract • Ventral corticospinal tract

  12. Lateral group (L) & Ventromedial group (R)

  13. Control of movement by the brain • Deficits of verbally controlled movements: The Apraxias • Difficulty in carrying out purposeful movements, in the absence of paralysis or muscular weakness • Limb Apraxia • characterized by movement of the wrong part of the limb, incorrect movement of the correct part, or correct movements but the wrong sequence in response to a verbal command • Can be caused by: • Callosal apraxia – apraxia of the left hand from by damage to anterior corpus callosum • Sympathetic apraxia – disorder of left hand by damage to left frontal lobe • Left parietal apraxia – caused by damage to left parietal lobe; produces difficulty in performing movement sequences by verbal command or imitating others’ movements • Constructional apraxia • Caused by damage to right parietal lobe; produces difficulty in drawing pictures or diagrams

  14. Control of movement by the brain • The basal ganglia • Anatomy and function • Caudate nucleus, putamen & globus pallidus – motor nuclei • Receive input from cortex (esp. primary motor and somatosensory) and substantia nigra • 2 primary outputs: • To primary motor, supplementary and premotor cortices via the thalamus • To motor nuclei in brain stem as part of the ventromedial pathway • 2 thalamic nuclei associated with BG: • Ventral anterior nucleus & ventrolateral nucleus

  15. Control of movement by the brain • The basal ganglia (con’t) • Direct pathway – includes caudate and putamen, internal globus pallidus and thalamic nuclei; excitatory effect on movement • Indirect pathway – includes caudate and putamen, external and internal globus pallidus, subthalamic nucleus & thalamic nuclei; inhibitory effect on movement

  16. Parkinson’s disease • Primary symptoms: muscular rigidity, movement slowness, resting tremor, postural instability • Caused by lack of inhibitory control (lack of DA in indirect pathway of BG) to balance out excitatory (direct pathway) • Standard treatment: admin of L-DOPA, precursor for DA; allows more DA to be created in BG • Side effects: dyskinesias ( involuntary movements) and dystonias (involuntary postural movements) caused by too much DA in BG • Deep brain stimulation • Permanent electrode in the subthalamic nucleus; allows patient to induce electrical stimulation

  17. Huntington’s disease • Caused by degeneration of caudate and putamen, specifically of GABA and ACh neurons • Symptoms: uncontrollable movements especially jerky limb movements • Hereditary disorder, usually appears after age 30-40 • Progressive and eventually fatal

  18. The cerebellum • Outputs project to every major motor structure in brain • Consists of 2 hemispheres that contain deep cerebellar nuclei surrounded by the cortex • Flocculonodular lobe – caudal region; control of postural reflexes • Vermis – midline; receives auditory, somatosensory & visual info • Deep cerebellar nuclei – control of descending motor tracts • Fastigial nucleus • Interposed nuclei • Dentate nucleus

  19. Reticular formation • Consists of large number of nuclei located in core of medulla, pons, and midbrain • Controls activity of gamma motor system and thus regulates muscle tonus • Mesencephalic locomotor region – region of RF of midbrain; stimulation of this region causes alternating movements of limbs normally seen during locomotion

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