Lecture 10 - Control of Movement - 10 5 16 PDF

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Lecture 10 - Control of Movement - 10/5/16 ● Peripheral Nervous System: everything outside of brain/spinal cord ○ Autonomic N.S ○ Somatic N.S ● Autonomic N.S: visceral functions ○ Involuntary functions (below level of consciousness) ○ Controls heart rate, respiratory rate, salivation, etc ○ Sympathetic, Parasympathetic, Enteric (gut) divisions ● Somatic N.S: voluntary control ○ Skeletal muscle innervation (sensory input; motor output) ○ Cranial nerves, spinal nerves ● Control of Movement ○ All motor neurons that innervate skeletal muscle have: ■ A cell body in CNS ■ An axon that is initially in CNS and leaves to enter PNS ■ An axon terminal that synapses onto a muscle fiber ○ Somatic motor neurons innervate skeletal muscles ■ Attached to the bone; move bones around their joints ■ “Voluntary” muscles ○ CNS motor neurons ■ → Brainstem: Medulla; cranial nerve nuclei ○

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■ → Spinal cord: Ventral horn Motor neurons that control skeletal muscles in face/head are located in the Medulla ■ Run through cranial nerves Motor neurons that control skeletal muscles in body are in Ventral Horn ■ Runs through spinal nerve All skeletal muscle motor neurons (SMMN) make/release acetylcholine (ACh) ■ Neurotransmitter released by axon terminals at the muscle fiber Neuromuscular junctions: synapses of M.N axon terminals ←→ skeletal muscle

fibers ■ M.N send messages directly to muscle; ACh = neurotransmitter ● Signaling at the Neuromuscular Junction ○ ACh released from axon terminal of M.N ■ Binds to specific transmitter-gated ion channels in postsynaptic membrane ■ Causes depolarization → produces EPSPs in skeletal muscle ■ EPSPs cause enough depolarization → muscle contraction ○ Termination of synaptic transmission → get rid of neurotransmitter so ion

channels can close ○ Excess ACh is removed from synaptic cleft through enzyme destruction ■ Enzyme → Acetylcholinesterase (AChE) ■ AChE produced along with ACh and released along at into synapse ■ ACh → only neurotransmitter whose action is terminated by enzymatic destruction within the synaptic cleft ○ Drugs/natural chemicals can affect motor control of skeletal muscle ■ Agonists: enhance/mimic the effects of a neurotransmitter ● Promote release, prevent inactivation, stimulate ACh receptors ● Snake venom ■ Antagonists: block/reduce the effects of neurotransmitter ● Block release; block receptor binding ACh Antagonists ○ Curare: used by South American Native Americans to paralyze their prey ■ Enters the bloodstream, blocks ACh receptors throughout body ■ ACh cannot bind to receptors and cannot cause depolarization ■ Muscles become relaxed; cannot contract ○ Botulin toxin: (bacteria, clostridium botulinum) blocks ACh release; prevents muscles from contracting (Antagonist) ○ Black widow spider venom: enhances ACh release; causes heart muscle cells to over-contract (Agonist) ○ If ACh is not broken down → released into the synapse → would keep ion channels open ■ NA+ would continue to flow inside; depolarized for too long ■ Muscles continue contracting → stop breathing (death) ● Simple Motor Reflexes: involve control of M.N activity directly by synaptic inputs from sensory neurons ○ No involvement of cerebellum, cortex, higher brain areas ○ Skeletal muscles move mainly when we consciously want them to (voluntary) ○ Example: stretch reflex (knee-jerk reflex) and pain reflex (withdrawal reflex) ● Stretch Reflex → knee tap, patellar tendon is stretched, leads to contraction of quads ○ Based on sensory stimulus caused by stretching a muscle ○ Monosynaptic: Sensory neuron → Motor neuron ● Pain Withdrawal Reflex→ nociceptor stimulation, move body part away from damage before you realized the danger ○ No conscious pain perception needed ○ Polysynaptic: sensory neuron → excitatory/inhibitory interneuron → motor neuron

○ One set of muscles contracts; opposite set of muscle relax → inhibitory interneuron ○ Inhibitory interneuron: releases inhibitory neurotransmitters at synapses, producing IPSPs in postsynaptic M.N ■ Motor neurons unlikely to depolarize to fire action potential; muscles do not contract ● Neural Control of Movement ○ Neurons come from high levels to affect only a small number of motor neurons at low levels ○ Motor Pathways: convergent, descending circuits ○ Motor commands originate in frontal lobe’s association cortex (planning) ○ Conveyed to command centers in primary motor cortex (precentral gyrus) ○ Delivered to the brainstem/spinal cord → to a M.N that innervate skeletal muscles ● Prefrontal cortex plans → premotor cortex sequences → motor cortex executes actions ● M.N in the medulla/spinal cord controlled by 3 brain regions: ○ Primary Motor Cortex ■ Pyramidal neurons: form synapses with M.N in the medulla (cranial nerve nuclei) or spinal cord (ventral horn) ■ Motor homunculus: topographic body map organization of pyramidal neurons in cortex that controls different body muscle groups (precentral gyrus) ● Mild stimulation causes muscles to contract ○ Cerebellum ■ Muscle pathway: cortex → M.N → muscle ● More complex signaling done by cerebellum ● Motor commands sent to cerebellum are sent to pyramidal neurons aswell → primary motor cortex → M.N ■ ■ ■

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brainstem/spinal cord Informed about limb position, posture, balance, eye position Frontal lobe (association/motor cortex) informs cerebellum what motor movements are being planned/executed Field Sobriety Test: hold arm out straight in front of you; touch each finger to nose in turn ● Task is initiated voluntarily; accuracy of movement controlled by cerebellum Critical for rapid, simultaneous movements ● Motor programs ● Typing: carefully planned and executed by frontal lobe and motor

cortex ○ Movements become smooth and rapid when cortex isn’t fully involved ○ Finger movement becomes automatic ■ Frontal lobe can plan/initiate movements but not contain the neural circuitry needed to calculate the complex, closely timed sequences of muscle contractions ● Needed for rapid, skilled movements ● Job of the cerebellum ■ Damage to cerebellum → decomposition of movement syndrome ● Movements become jerky, erratic, uncoordinated ■ Prism glasses: simulation of how cerebellum adjusts movements ○ Basal Ganglia...