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Wojtowicz lecture summary 1-4.pdf

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Hae- Young Kee

Kim Spinal Reflexes 1. Aside: NOTE for all Wojtowicz’s lectures  loosely refers to FLEXION and EXTENSION a lot  flexion: general term referring to the muscle actions involved in bending of a joint (e.g., curling your biceps)  extension: refers to straightening out of a joint (e.g., your leg in the stance phase) 2. Overview: Nervous system anatomy  PNS o basically all neurons/neuron parts residing outside of the brain, spinal cord  CNS o brain, spinal cord o Spinal Cord ‒ white matter = myelinated axonal tracts (on the periphery of spinal cord, and called “COLUMNS”)  dorsal column – ascending tracts that send sensory info to brain  lateral & ventral columns – contain both ascending & descending tracts ‒ grey matter = unmyelinated cell bodies (on the inside of spinal cord, and called “HORNS”)  dorsal horn – receives sensory input  intermediate zone – integrates sensory input  ventral horn – motor output3 3. Clinical Implications  neuronal stem cells in central canal of spinal cord  can we repair spinal cord damage?  back pain: result of abnormal synaptic plasticity o pain signals keep firing even when the stimulus is removed, b/c wired so strongly when the stimulus was there 4. Overview: Spinal Reflexes  simplest circuits in nervous system (very few synapses) o often a feedback loop for regulating position, force, etc. o ***stimulus  receptor  sensory neuron  to spinal cord (dorsal horn)  then to interneuron OR directly to  efferent (motor) neuron (ventral horn, α motoneurons)  effectors (= glands, organs)  response  sensory info entering spinal cord  output by spinal cord o action is taken w/o consultation of brain o but info gets sent up to brain anyway, and then brain may have modulating influences on outputs  begins when receptor detects change which needs to be acted upon o e.g., proprioceptors (tell something about position) ‒ (1) muscle spindle detects changes in muscle length  a stretch receptor which lies w/i EXTRAFUSAL FIBERS (responsible for contraction of muscles), and contain INTRAFUSAL FIBERS together  gamma motor neurons from CNS innervate intrafusal, and regulate sensitivity of muscle spindle; not necessary for movement, but used as ‘fine-tuning’ ‒ (2) Golgi tendon organ detects ACTIVE muscle contraction  initiates inhibition of the homonymous muscle (the same muscle which initiated the stimulus, i.e., contraction)  links muscle and tendon 5. Stretch Reflex  stretching of a muscle  reflexive contraction of that same muscle  monosynaptic o simplest, FASTEST reflex o 35 ms  muscle spindles activated by any motion of the joint (passive/active, doesn’t matter) o afferent  efferent  homonymous muscle  f’n: to stabilize limb postures (important for sitting and standing)  example: patellar (knee jerk) reflex o stimulus: tap to tendon stretches muscle  muscle spindle activation  afferent  efferent paths (1) contraction of quadriceps, (2) relaxation of hamstring, allowing extension of leg (reciprocal inhibition) 6. Golgi Tendon Reflex  contraction of a muscle  reflexive relaxation of the same muscle  multisynaptic (disynaptic?) o GTO afferent (type Ib)  inhibitory Ib interneuron  efferent, α motoneurons ‒ inhibitory NT = glycine Page 1 of 7 Kim  f’n: if excessive load is placed, muscle contraction is inhibited as to prevent injury o load is dropped o acts in concert w/ stretch reflex to stabilize posture 7. Flexor Withdrawal Reflex  adverse stimulus  reflexive flexion in direction away from the stimulus o i.e., flexion of joints proximal to stimulus & extension distal to stimulus  Aδ, C nociceptors afferents  interneurons (in superficial dorsal horn)  motoneurons  multisynaptic o fast, but not as fast as stretch reflex o fast enough s.t. we are unaware of what happened until moments later  require divergent signal transmission: (1) excitatory interneurons (flexor muscles), (2) inhibitory neurons (antagonistic muscles)  reciprocal inhibition: basic property of intermediate zone o w/o it, arm would snap back into the adverse stimulus o activation of flexor motoneurons causes inhibitions of antagonist extensors o for co-contraction of antagonists, this circuit is suppressed (e.g., for joint stiffness; what happens perpetually in tetanus) 8. Crossed Extensor Reflex  for balancing when switching from bipedal stance to putting all weight on one foot o can be in concert w/ FWR ‒ when flexor withdrawn, need postural support for vestibular perturbation  opposite pattern of activation in contralateral limbs o signal by commissural interneurons  # of synapses not specified  divergence required for o (1) simultaneous flexor activation & extensor inhibition on ipsilateral side (for FWR) o (2) transmission of sensory info to CONTRALATERAL side: flexor inhibition & extensor activation (i.e., opposite pattern to that produced on ipsilateral side to adverse stimulus)  nociceptor  1° sensory neuron diverges in spinal cord  postural adjustment (CER) + ascending for sensation of pain + FWR 9. Extensor Thrust Reflex  pressure on sole of foot  reflexive activation of extensor motor nuclei o i.e., non-painful pressure on foot sole  POSITIVE FEEDBACK to put more pressure and plant foot down firmly o operates only during stance  Aβ mechanoreceptors  sensory neuron  excitatory interneuron  extensor motoneurons (extensor motor n.)  F’n: for maintaining stance  Babinski sign = indicator of working ETR o normal (antigravity) pattern: point toes forward upon pressure on foot o Babinski (flexion withdrawal) pattern: point toes up upon pressure on foot ‒ babies do this normally b/c reflex circuit not fully wired ‒ also occurs in adults w/ corticospinal tract damage 10. Vestibulospinal Reflex  perturbation in balance  reflexive compensation to maintain balance  receptor = vestibular system of inner ear o recall: SEMICIRCULAR CANALS – rotational, OTOLITH ORGAN – translational, head tilt  falling  activation of OOs  afferent  (interneuron?)  motoneurons  extensor muscles in arms & legs  head tilt  asymmetric activation of OOs    downhill limbs EXTEND, uphill limbs FLEX  note: visual postural reflexes readjusts body stance to maintain alignment w/ vertical axes in visual env’t, regardless of vestibular or proprioceptive inputs Central Pattern Generation 11. Central pattern generators (CPGs)  REFLEXES = insufficient to generate complex, rhythmic motor patterns (e.g., breathing, locomotion) o e.g., stretch reflexes cannot restore postural stability after a perturbation: a CENTRALLY COORDINATED response required o done by central pattern generators (CPGs) Page 2 of 7 Kim ‒ neural networks that make up these CPGs are distributed across many regions of nervous system (i.e., functional networks = complex integration) ‒ the ARRANGEMENT of neural networks determines: (i) nature of outputs, (ii) temporal sequence and (iii) periodicity of sequence repetition  Locomotion: Leg Step Cycle o programmed by network of neurons in intermediate zone of lumbar cord o 2 major characteristics that enable rhythmic activation: ‒ (1) pacemaker neurons: express specific ion channels  repetitive BURSTS of activity  feed-forwardexcitation – PMNs excite other PMNs ‒ (2) reciprocal inhibition (RI): inhibition of INTERNEURONS by other interneurons  (* distinct from RI of antagonistic motoneurons in spinal reflexes)  e.g., arm movement: when BICEPS (= flexor) active  TRICEPS (= extensor) inactive (& vice versa)  observable in muscle EMGs, but actually happening b/w the interneurons of spinal cord o Step cycle has 2 stages: (1) SWING phase (= flexion), (2) STANCE phase (= extension) ‒ similarly, the neural activity underpinning these stages are also in 2 distinct phases  (1) flexor burst generator (FBG)  flexor motor nuclei (swing)  (2) extensor burst generator (EBG)  extensor motor nuclei (stance) ‒ these CPGs mutually inhibit one another (i.e., RI)  both exhibit spontaneous activation when not inhibited  thus, inhibition is what produces a change  also an important feature of all neural systems  also input from proprioception (spinal cord), reticular formation (Raphé 5-HT  tonic excitation)  the only inhibition is from RI b/w FBG and EBG  once in STANCE  get reafference from receptors in limbs  input to intermediate zone o (1) Flexor Burst Generator – lifting leg against gravity ‒ has fixed duration (independent of speed of locomotion) ‒ FBG inhibits itself  build-up of inhibition  ↓ RI on EBG  ↑ activity of EBG  EBG further inhibits FBG (RI)  STANCE phase o (2) Extensor Burst Generator ‒ has variable duration (dependent on speed) ‒ regulated by sensory feedback: “no two steps are ever the same”  sensory input used to adapt motor output  reflexes  automatic adjustment of extensor contraction to suit load experienced  inform CPG when it’s safe to begin next swing phase  i.e., CPG produces predictable patterns, but also must be flexible enough to respond to demands of a constantly changing env’t ‒ phase dependency of the involved SPINAL REFLEXES (i.e., responses diff at diff phase of step cycle for a given stimulus)  i.e., the spinal reflexes don’t always act the same in CPGs as they do during isolated reflexes ‒ spinal reflexes: used to tune extensor muscle activity according to loads being experienced  (i) STRETCH  buildup of gain (i.e., size of output) ↑ throughout stance phase (makes sense b/c muscles stretching to fullest when whole foot planted)  lowering the gain to zero as foot peels off  leg lifts = swings  (ii) GOLGI TENDON  positive feedback: activation of GTO  activation of extensor n. (vs. inhibition normally = example of phase dependency)  (iii) EXTENSOR THRUST  also positive feedback (recall from Spinal Reflexes): pressure on foot sole  reflexive extension (i.e., plant foot down completely)  BUT, in the SWING phase, output = flexion, not extension (phase dependency? I think it’s just that there’s no pressure on sole during swing phase that extensor thrust is not activated…) ‒ all spinal reflexes modulated by the CPGs thru pre-synaptic inhibition (GABA) o Transition from stance to swing ‒ E3 phase (last phase of stance) stops  removes inhibition of FBG, but only if:  (i) leg is not bearing weight, (ii) hip is extended (i.e., 180°), (iii) opposite leg is in stance (i.e., bearing weight)  if you go into swing when the other leg is in the air, you’re gonna have a bad time ‒ crossed extensor reflex important  achieved by DIVERGENT signaling in spinal cord (ensures when EBG active on one leg, it’s inhibited on the other) Page 3 of 7 Kim  also goes for ARM SWINGS (CPGs in cervical cord, not lumbar) – arms go in opposite direction  also, diagonal pattern b/w arms + legs to cancel torque on trunk (try walking w/ arm swinging on the same side as leg swinging  makes you twist body = torque)  i.e., multiple CPGs are diff levels of spinal cord must be IN PHASE w/ one another for effective locomotion – achieved by propriospinal tracts o Upper Body Balance ‒ postural CPGs in reticular formation (of PONS + MEDULLA) coordinate postural correction w/ spinal step cycles  to spinal cord via reticulospinal tracts  relies on 3 sensory sources: (i) somatosensory (esp. proprioceptive), (ii) vestibular, (iii) visual o Speed of locomotion ‒ mesencephalic locomotary region (midbrain)  (1) acts as a ‘switch’ initiates activation of reticulospinal CPGs  in turn activate spinal CPGs  does not produce rhythmic motor commands (i.e., is not a CPG)  but (2) governs the speed of locomotion (faster firing here = faster locomot
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