Class Notes (811,659)
Canada (494,847)
Physiology (634)
PSL201Y1 (124)
Lecture 16

Lecture 16 - Central Pattern Generators

4 Pages
Unlock Document

Michelle French

PSY300H1F L16; Oct. 19, 2011 • flexor neurons network has a build-up of inhibition that Central pattern generator (CPG) eventually stops the burst of action potentials after a • Reflexes can perform simple elements of movements, few ms end of activation of flexor motoneurons but not complex patterns by selves – need central • reciprocal inhibition of extensor burst network ceases organizing generator to plan&structure a functional  extensor network active movement • e.g. stretch reflexes cannot restore postural stability after a perturbation: a centrally coordinated response is required • posture and movement are ‘programmed’ by CPGs (central pattern generators), functional networks of neurons Locomotion: leg step cycle • The step cycle of each leg during walking is programmed by a network of neurons within the intermediate zone of the lumbar cord • properties of network: - vaguely known in most animals • 1) pacemaker neurons, diffuse excitation – automatically produce depolarization&hyperpolarization in endless seq aqs long as given background excitation (membrane in right ballpark) – due to ion channel pops • Generators – reciprocal inhibition, ossicilation – 1 present interacting w each other, constantly alternating active at a time; extend all way thru lumbar cord to • 2) reciprocal inhibition – built right in; flexors then lower thoracic segments – long column, medial extensors… location near central canal • 3) phase-dependent reflexes – used when positive ○ Drive corresponding motor neurons on swing & influence on movement; turning off when working stance against movement ○ Reflex loops operating on them – especially • 2 phases subdivided into 2 Extensor Burst gen phases • Swing when in air, not ○ Stretch flexes, cutaneous reflexes (extensive thrust – reinform activity in extensor burst gen supporting weight: F starts w while leg bearing weight) toe coming off ground (pure  Regulated by network: flexion, leg suspended in air) • Propriospinal (in spinal) – regulate reflex strength of  E1 when foot brought back swing & stance to ground (extension, mostly passive – gravity doing work • Spinoreticulothalamic neurons have pain-related neurons near central canal – so when very painful so minimal muscle activity) stimulus, tends to turn on some of these locomotor • Stance when on ground, networks supporting weight: E2 heel Stance Phase strike, flat foot at end, weight• Variable duration depending on speed duration right over ball of foot, totally supporting weight; E3 starts • regulated by sensory feedback, important to when heel lifted off ground, determine duration, stays in stance as long as supporting weight so not internally determined by CPG power stroke pushing against • phase-dependent reflexes: substrate w big toe, then toe • stretch reflex; gain increases to peak in E3 – loading comes off  swing phase extensor muscles w body weight, stretching postural ‘Half-center’ structure • CPG organized into 2 half-centers: muscles • 1) flexor burst generator drives flexor motor nuclei (1t • Golgi tendon reflex: mild positive feedback (instead of normal neg) – action contraction activating golgi tendon part of swing) afferents • 2) extensor burst generator drives extensors (down • extensor thrust: extension only during stance, ventral part of brain matter, active for longer than flexor (reversed to flexion during swing phase); from burst generator so CPG asymmetrical – very typical) cutaneous mechanoreceptors in sole of foot, reinforce • mutually inhibit one another • both spontaneously active when not inhibited  so extensor activity when pressure built from body weight • During swing, no extensor thrust function, reflex inhibition determines where activity is, infinitely more reverses fine important than excitation in NS ○ So is foot stimulated, get increased flexion than normal, functional since means hit obstacle and Flexor burst generator • Flexion phase of swing has a fixed duration, regardless increase flexion to get over it instead of stepping of speed of locomotion – ex. Always lift leg up at same on hid ○ So dif connections in spinal cord, presynaptic pace in initial swing, extensors cause changes afters inhibition, easy for NS to change signal effect when right leg lifted in flexion phase generate counterclockwise torque, left arm is lifted and makes opposite torque, torques cancel out across backbone • phase-linking via propriospinal tracts (from one segment of cord to another) - interconnections Upper body balance • Bipedal humans must produce postural compensations in trunk and head to maintain stability on top of moving legs • Gain = output of reflex for given stimulus, always • takes a long time to learn how to walk on 2 legs; learn giving same stimulus/stretch to muscle; fluctuates how in 1 year, low better in next 15 yrs (inertia changes dramatically as you grow) ○ Strong during stance face, esp power stroke • requires postural CPGs in reticular formation in ○ Dramatically falls as get into swing  no reflex • Strong during stance since loading extensor muscles brainstem to coordinate upper body motion with spinal step cycles w body weight, so stretched; reflex helps adjust • spinally-injured patients cannot walk without trunk muscle activity exactly to weight experiencing, so support, lose these connections from spinal cord to CPG of spinal cord doesn’t have to exactly compute brainstem, CPGS still there so if on treadmill and support how much activity required in muscle (impossible) upper body in harness then can walk using lumbar ○ Adjustments that have to be made, otherwise • Postural pattern lurch all over generators all in ○ So the reflex makes fast, perfect accurate, fine brainstem, source of adjustment, micron level reticulospinal tracts • Turn off in swing phase – exaggerated in human • Grps of neurons in nuc, since walk flat on feet not toes; tendency when lift underneath 4 ventricle foot up for toe to drag against ground (cats don’t • Heavy projection down have this probably since walk on toes) spinal cord in ventral white ○ So need to lift toes up (dorsal flexion), flexes matter surrounding ventral ankle extensor muscles but must be turned off grey matter (containing all abruptly at onset of swing (since would move motornuclei) foot down into ground on activation and prevent • Bilateral projection, so on movement, counterproductive)
More Less

Related notes for PSL201Y1

Log In


Don't have an account?

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.