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Chapter 8

Chapter 8: Movement

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Department
Psychology
Course
PSYC 211
Professor
Yogita Chudasama
Semester
Winter

Description
 Monosyaptic stretch reflex: muscle contracts in response to being quickly stretched, involves sensory neuron and motor neuron with one synapse between them – from muscle spindle, afferent impulses conducted to buttons in gray matter of spinal cord; buttons synapse on alpha motor neuron that innervates extrafusal muscle fibers. Spinal cord has some autonomy, particular kinds of somatosensory stimuli can elicit quick responses via neural connections in spinal cord; reflexes are simplest level of motor integration, e.g. patellar reflex takes 50 milliseconds. If weight added, muscle lengthens, increases firing rate of muscle spindle afferent neurons, which increases firing rate of buttons that stimulate alpha motor neurons. Reflex also important for posture.  Gamma motor system: rate of firing determines degree of contraction. When active, they become shorter and more sensitive to changes in muscle length. Adjustable sensitivity simplifies role of brain in controlling movement, since more control in spinal cord means fewer messages sent to/from brain. If muscle spindle contracts faster than muscle as a whole, then there will be afferent activity. By establishing rate of firing in the gamma motor system, brain controls length of muscle spindles and indirectly the length of the entire muscle  Polysynaptic reflexes: afferent axons from Golgi tendon organ are detectors of muscle stretch. Has two populations w/ different sensitivities to streth – more sensitive afferent axons tell brain how hard muscle is pulling, less sensitive ones have buttons that synapse on spinal cord interneurons in gray matter of spinal cord, which synapse on alpha motor neurons for same muscle. Buttons liberate glycine, produce inhibitory postsynaptic potentials on motor neurons. Pathway decreases strength of muscular contraction when danger of damage. Decerebrate: brain stem transected, shows decerebrate rigidity: simultaneous contraction of agonistic and antagonistic muscles, results from excitation from caudal reticular formation which facilitates all stretch reflexes, especially extensor muscles, by increasing activity of gamma motor system. Transection removes inhibitory influence, leaving only excitatory one, causing clasp-knife reflex from activation of Golgi tendon organ reflex. Agonist moves limb in direction being studied, antagonist muscles move limb back in opposite direction. When stretch reflex is elicited in agonist, it contracts, causing antagonist to lengthen, and it relaxes. Afferent axons of muscle spindles synapse on inhibitory interneurons, whose buttons synapose on alpha motor neurons that innervate antagonistic muscle, so stretch reflex excites agonist and inhibits antagonist so limb can move in direction controlled by stimulated muscle.  No single cause of behavior, so we can’t find a single starting point in search for neural mechanisms that control movement. Brain and spinal cord have different motor systems, each can control particular kinds of movements simultaneously.  Organization of motor cortex: primary motor cortex is on precentral gyrus, rostral to central sulcus. Activation of neurons in particular parts of PMC cause movements of particular parts of body; it shows somatotopic organization. PM C is organized in terms of particular movements of particular body parts; each movement may be accomplished by contraction of several muscles. Commands for movement initiated in motor cortex are helped by basal ganglia and cerebellum. Principal cortical input to PMC is frontal association cortex. Supplementary motor area SMA and premotor cortex especially import – both get sensory info from parietal/temporal lobes, send efferent axons to primary motor cortex. PMC also gets projections from primary somatosensory cortex, has specific connection: neurons in primary somatosensory cortex that respond o stimuli applied to particular part of body send axons to neurons in PMC that move muscles in same part of body. Hand movements are controlled by somatosensory feedback received by neurons in postcentral gyrus.  Initiating, imitating, comprehending movements: role of motor association cortex: SMA and premotor cortex involved in planning, execute plans through link with PMC. Motor association cortex also involved in imitating actions of others. SMA and premotor cortex get info from association areas of parietal and temporal cortex. Regions of frontal cortex involved in planning movements get info from temporal and parietal lobes. SMA invoved in learning/performing behaviors that consist of sequences of movements. Premotor cortex is involved in imitating responses of other people and understanding/predicting actions. o SMA: role in behavioral sequences. Damage disrupts ability to execute well learned sequences of responses in which erformance of one response serves as signal that next response must be made. If region inactivated, monkeys could still reach for objects/make particular movements in response to visual cues, but could no longer make sequence of three movements that was learned. In humans, there is more activity in posterior SMA during performance of learned sequence of button press, involved in planning elements yet to come in sequences of movements; execution controlled elsewhere. Pre-SMA involved in control of spontaneous movements don’t understand paragraph 2, p273. Pre-SMA became active just before eople performed spontaneous movements. Neural activity responsible fro decision to move begins before person is aware of making decision. Most important input to SMA comes from parietal lobes; info received from parietal lobes permits pre-SMA to detect that decision to move has been made. People w/ prefrontal lesions will react to events but show deficits in initiating behavior. o Premotor cortex: involved in learning/executing complex moevments guided by sensiory info. Involved in using arbitrary stimuli to indicate what movement should be made. If preomotor cortex inactivated, will respond to nonarbitrary spatila cues but not to arbitrary visual cues. Mirror neurons: located in ventral premotor cortex and inferior arietal lobule, respond when individual makes movement or sees another individual make movement, or even sounds that indicate occurrence of familiar action, part of dorsal stream, which is involved in guiding actions of pointing/grasping. We also tend to copy facial expressions of emotion that other people make, feedback from doing so evokes similar emotional state. Mirror neurons help us understand other people’s itnentions. o Cortical control of movement: descending pathways: lateral group: corticospinal tract (axons of cortical neurons that terminate in gray matter of spinal cord, whose cell bodies are from PMC. Axons leave cortex, travel through subcortical white matter to ventral midbrain, enter cerebral peduncles, leave peduncles in medulla, form pyramidal tracts. At caudal medulla, fibers decussate and descend through contralateral spinal cord, forming lateral corticospinal tract (originate in regions of PMC and SMA that control distal parts of limbs, form synapses w/ motor neurons in gray matter of spinal cord); the rest descend through ipsilateral spinal cord, form ventral corticospinal tract (axons originate in upper leg and trunk regions of PMC)part of ventromedial. Corticospinal pathway necessary for hand/finger movements), corticobulbar tract (projects to medulla, similar pathway as corticospinal but terminates in motor nuclei of cranial nerves that control face, neck, tongue, extraocular eye muscles), rubrospinal tract (originates in red nucleus of midbrain, gets input from motor cortex via corticorubral tract and cerebellum. Axons terminate on motor neruons in spinal cord that control forelimb/hindlimb muscles. If destroyed, affects use of ipsilateral arm; system controls independent movements of forearms and hands, independent of trunk movements involved in control of independent limb movements, esp. hands/fingers. Ventromedial group: vestibulospinal tract, tectospinal tract,
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