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Control of Movement It’s purpose: Self-propagation, self-protection Species propagation, species-protection Biodiversity-propagation, biodiversity-protection Types: Involuntary Rhythmic movements Voluntary Need for more complex movements -> more complex nervous tissue (induces development of sensory organs, memory formation and planning) More complex nervous tissue -> more complex movement Learning -> more complex structures and functions -> planning movements -> more efficient movement Speed, force, dimension, complexity determined by: State of development of nervous system Biomechanical properties State of development More advance nervous system -> more complex movement Simple – 2 neuronal system of sea angel Complex – mammals (some species can walk right after birth) Humans – 1 year for walking (Toddlers can’t walk, because there isn’t a strong enough skeleton-muscular and neuronal system.) Biomechanical properties 206 bones, 200-300 muscles Different joints for different movement Muscle binds to bones via collagen, surrounded by protective tissue Muscle cell membrane – Sarcolemma Myofibrils – Thin filaments (actin), Thick filaments (myozin) -> create stipes Functional structure: sarcomere Troponin (attached to tropomyosin), tropomyosin, torponin C (binds Ca2+ ions) Excitation -> contraction One motor unit can innervate hundreds of muscle fibers Different motor units are intermingled Ca2+ is stored and then released from the sarcoplasmatic reticulum -> troponin C Motor unit types Slow (red muscle) – slower contraction, low force, fatigue resistant Fast, fatigue resistant – fast contraction, medium force Fast, fatigable – fast contraction, high force AP -> muscle response More AP -> more response and the amplitude will increase until reaching the plateau At first: summation -> incomplete tetanus -> tetanus (the responses melt together) It takes time to remove the Ca2+ and by rapidly stimulating the muscle, there is no time to remove it entirely thus increasing the response Tetanus can be caused by bacteria We can suddenly change the contraction by missing or adding an impulse Modulation Golgi – protects the muscle, inhibits the neurons Muscle spindle – parallel to the extrafusal muscles Human gait Phasic component: without central regulation, rhythmic alternating contractions, functional at birth Tonic component: postural muscles, immature at birth Lesions Spinal cord injury, Decerebration, Decortication Spinal cord - reflexes Brainstem – breathing, eye movements walking -> rigidity Diencephalon – eating, drinking Basal ganglia – initiation of movement Cerebral cortex – speech, hand/finger movements Central (motor) pattern generator (CPG/MPG): rhythmic output Generated by: endogen oscillating neurons, network activity of non-oscillating neurons Clione – 2 neuron system Half-center oscillator: 2 neuron reciprocal innervation -> rhythms (contraction and relaxation) Partially inactivated voltage-dependent Na and Ca channels -> hyperpolarisation -> activation -> it’s easier to depolarise it -> AP -> inhibit the other cell -> hyperpolarisation etc. Lobster Different inputs cause different outputs -> reaction depends on the neurotransmitter Leech Sensory information -> trigger neurons -> rhythmic activity Gating neurons: determines the duration ode the activity Short activation of trigger neurons -> long-lasting activation of gating neurons -> long lasting activation of CPGs and motoneurons Lamprey – command system of vertebrates In CPG - excitatory and inhibitory interneurons, reciprocal inhibition with the other half Stretch receptors will feed-back to CPG Excitatory reticulospinalis neurons -> induce plateau potentials in pattern-generating neurons NMDA -> Ca2+ level increases Stimulating the dorsal root -> rhythmic burst activity of CPGs Skin -> interneuron of ipsilater side -> modify the motor program (neuron firing) Movement initiation – basal ganglia Pallidum inhibits other motor centers -> if we want to do something we need disinhibition Substantia nigra (dopaminergic) – activation of the neurons -> if it’s not working properly (Parkinson) it’s difficult to start and stop the movement Too much dopamine -> can’t control the movement Posture and balance Sensory, vestibular and visual input -> muscle compensation Proprioception – sense of position and movement Compensatory reflexes – stretch reflex Phasic and tonic components, reciprocal innervation Adjustable sensitivity – fuzimotor fiber Modified by presynaptic inhibition Nociceptive reflex – pain induced reflexes Multisensor convergence Contralateral inhibition Moving platform Triggers the ankle strategy – feed-back mechanism If the movement is small, we can analyze it Forward movement – backward sway -> activation of quadriceps, abdominal muscles Tilted platform Triggers hip strategy – feed-back mechanism Forward tilting – forward sway -> paraspinal, ham string, triceps surae muscle activation, Feed-back if unexpected postural disturbance occurs, feed forward if expected -> preventing mechanisms Vestibulocervical an vestibulospinal reflexes stabilize head and body posture Romberg test No visual input -> proprioceptive and vestibular sensors only Won’t be able to maintain balance Can be use to test proprioceptive and vestibular damage Medial posture system Proprioceptive, vestibular and visual information -> motor response Innervates axial muscles and proximal part of limbs Vestibular nuclei – connection with cerebellum, receives sensory information from the body Medial longitudinal fascicle > superior vestibular nucleus -> motor nuclei of the eye Lateral vestibular nucleus -> spinal cord -> ipsilater extensor muscle of the limbs Lateral voluntary system Corticospinal pathway Rubrospinal pathway Cortical areas involved in motor control Stimulation induce or alters movements Area 4, 6 (Brodman) (and 1,2,3,5,7,24) Communicate with other motor structures and receive subcortical and cortical afferents Somatotopic representation – the size of the area shows how fine the movement of that body part is in the cortex Primary motor cortex Agranular – layer 4 is small or absent, no internal granular layer Pyramid cells are dominant Plasticity of motor cortex Occurs: Denervation, stroke, intensive use of muscles After denervation, many function can be regained, but need training Planning, voluntary movements Complex hand movements bilateral activation: sensorimotory, supplementar motor, ventrolateral premotor areas Contralateral: Dorsolateral premotor, medial cortical areas M1 neurons regulate the dynamics of movement – discharged neuron number correlate with the force exerted Discharged neuron number is correlated with the direction Processing the visual input More visual input -> delay time increases Children can’t respond that fast -> not able to process the speed of the cars If we have to think about the movement, it activates the same areas as during actual movement Lesion of supplementer area Can’t coordinate bimanual movements If supplement is active -> inhibits the other side If it’s injured, it can’t -> it will be the same movement Premotor neuron encodes the goal of the movement Sources: http://www.proprofs.com/flashcards/upload/a7091936.jpg http://faculty.etsu.edu/forsman/Histology%20of%20musclefor%20web_files/image014.jpg https://acewebcontent.azureedge.net/blogs/blog-examprep-031615-2.png https://image.slidesharecdn.com/lec201072010-100119060010-phpapp02/95/cogs-107b-winter2010-lecture-2-proprioception-and-the-vestibular-system-4-728.jpg?cb=1264356704 http://humanphysiology.academy/Neurosciences%202015/Images/2/flexor%20withdrawal%20reflex %20docstoc.JPG L4_MotCont_SpinalCord_KallóI_2017-03-07.pdf