Functional plasticity and stretch reflexes Flashcards
Intro
Connecting synaptic plasticity to functional plasticity (Keck 2008)
Cerebral cortex can adapt to altered sensory inputs, a small lesion in the visual cortex retina causes the deprived cortical region to become responsive to adjacent parts of the visual field (topographic remapping is assumed to be mediated by rewiring of intracorticol connections – unknown dynamics)
Functional and structural alterations in adult mouse VC over months after a retinal lesion
Rate of dendritic spine lost and gained increased 3-fold after lesion incomplete replacement of spines in de-afferenated cortex in 2 months (this did not occur when all visual input was removed – activity-dependent new circuits)
Stretch reflex
Patello-femoral tendon and muscle stretch elicited, gravity mechanism (contract quad but relax hamstrings) – also seen in rapid dorsiflexion (short and medium latent reflexes)
1a (fast velocity – sensory afferents)
2 and GTO’s (respond to stretch)
Highlights simple reflex circuit is highly complex
Pre-synaptic inhibition 1a inhibitory interneuron, 1b IN and alpha-MN can inhibit itself via Renshaw cell inhibition act on agonist muscle – a few example connections
SC plasticity – early evidence believe SC can simply connect brain to limbs – but it can be plastic
SR can be elicited proximally and distally in upper and lower extremities
Easy to elicit in right place (biceps, triceps, brachioradialis, patellar, Achilles, plantar (Babinski)
Spasticity = hypereflexia – clonus – vibrations on hit
Mykleburst 1986
SR change throughout life
Infant – activity in both muscles = response immediate SR
Post-development – get normal soleud response but not in TA (develop not to respond) – highlights functional SR development
Spastic patients with cerebral palsy differ greatly from normal subjects or those with adult-onset CNS injuries (rapid dorsi can produce strong myotatic reflex EMG at 30-50msec in normal stretched soleus muscle – whilst antagonist TA muscle was quiet) – same true of spastic adult-onset injuries
CP patients this early response is found in both muscle groups – pattern of ‘reciprocal excitation’ us in contract to reciprocal inhibition normally seen
Reflex behavior suggests a developmental error in neuronal interconnection of SC in CS
Meyer-Lohmann (1986)
SR can change with motor learning
Effects of prolonged training of adult monkeys subject to random and brief perturbations of alternating elbow flexions and extensions – study over 4 years (1 year intensive training and 3 years with irregular long pauses)
Prolonged training with brief perturbations M2 component of EMG response of biceps and triceps become gradually smaller and disappear
M1 component progressively increased in amp until it dominated the EMG response
Training had similar effects of biceps to longer perturbations, only under certain conditions – all changes in earlier training occurred in flexor not extensor
Long-term functional plasticity of sensorimotor system of animal adults is evidence (growing role for fast segmental mechanisms in reaction to external disturbances as motor learning progresses) – SR changes = M1 changes, lack of M2 should or partially reflex on reduced cortical effect on a-MN and/or changes in spinal system processing afferent info
Hoffman reflex
Used to assess spinal excitability (important method in neuroscience) – took nerve bundle and shock – introduce AP into SN (1a afferent dorsal horn synapse with MN another contraction = H reflex) and MN (contraction quick = M wave)
Mixed nerve bundle stimulated EMG stimulus artefact MEP (M wave) H-reflex
Important experimental model of stretch reflex – not the same thing as it doesn’t stretch, but electric analogue of SR can control magnitude of M wave
M wave contraction = different H (something changed – one way to look at synaptic plasticity)
Nielsen 1993
• Human H-reflex can change with motor learning
o Assume ballet dancers don’t have SR – ballet V elite athletes (mainly footballers)
o H-reflex in ballet dancers is very low – learnt to suppress H reflex and SR
o Shown reflexes can be trained in monkeys and humans
o Size of maximal H-reflex measured at rest and expressed as a % of maximal M response – (untrained, mod, well trained and dancers)
o Hmax/Mmax sig larger in mod and well trained subjects than untrained but smaller in ballet dancers
o Suggests both amount and type of habitual activity may influence excitability of spinal reflexes
Changes in H-reflex
• Pavlovian conditioning – pre (bell = no salivation, food = salivation), conditioning (bell and food = salivation) and post (bell = salivation)
• Wolpaw (1997)
o Operant conditioning in white lab rats
o Wire electrode placed on head to assess stimulation and H-reflex of hind limb (record afferent stimuli and recording electrode in skin)
o Stim rats to produce M wave (constant) measure H size
o When H threshold increases = food pellet (similarly seen when H below certain threshold = down-regulation)
o Corticospinal tract probably has essential role in producing this plasticity – firing threshold likely to contribute to rewarded behavior (primary plasticity), others might preserve previously learned behaviours (compensatory plasticity), or are simply activity-driven products of changes elsewhere (reactive plasticity)
o Complex pattern of plasticity is necessary and inevitable for outcome of simplest learning
Wolpaw 2010
• Cellular work – down-conditioned MN have slower CV and more GABAergic terminals
• CV shifted – made slower due to downconditioning SC plasticity
• Decreased GABAergic receptors on post-membrane (less likely to produce AP)
• Activity-dependent CNS plasticity has many different mechanisms and involves every region from cortex to SC (new knowledge – explain complex learning and memory and increases SC relevance)
• SC key role
o Final common pathway for behavior and is site of plasticity
o Simple, accessible and distant from rest of CNS, connected to behavior, uniquely suited for identifying sites and mechanisms of plasticity (how they account for behavioural change)
o Offer new approaches to guiding activity-dependent plasticity so as to restore functions lost to injury or disease
Chen (2010)
- Operant conditioning of the rat H-reflex carries over to EMG activity during locomotion
- Assessed upconditioning effects on SOL and TA function after sciatic nerve transection and repair – EMG electrodes and stim cuff on post tibial nerve – 120 days control (TC), sol H-reflex, up conditioning (TU) rats
- SOL and probably TA background EMG activity recovered faster in TU than TC, and final recovered sol H-reflex was sig larger in TU than TC
- TU and TC has sig fewer labelled MN and higher props of double-labelled MN than untransected – supports hypothesis SOL H-reflex up-conditioning strengthened primary afferent reinnervation of SOL MN (H UC may improve functional recovery after injury and repair)
Thompson 2009
- Operant conditioning of human H
- 6 baseline and 24 conditioning sessions (soleus H measured HRup or HRdown) over 10 weeks – given visual feedback to see whether size criterion had been satisfied
- Task-dep appeared in 4-6 sesions and persisted (around +/-15% in both)
- Long-term changes began after 10 sessions and increased gradually
- H-reflex acquisition consists of 2 phenomena (task-dep and long-term change) new motor skill
- Brain and SC plasticity underlies acquisition and maintenance of motor skills
- Levels not as good as rats – not same training volume (rats stim unexpectedly for 24/day hundreds of times), humans 30 min sessions (limited by amount of training needed to make it efficacious)
Yamanaka 1999
- Inactivity decreases excitability of H-reflex (space program)
- H and MEP induced by TMS in soleus of normal subjects before and after 20 days 6° head down bed rest – soleus H during standing following bed rest decreased in all 5 subjects (size of Hmax expressed as % of maximum M response), decreased from before BF to after (no significant differences between MEP’s before and after (MEP/Hmax after bed rest was larger than before in all subjects)
- Strong inhibition of H and no adaptation of MEP in soleus during standing post-BR
Ung (2005)
- Backward walking (TMS applied to leg area of motor cortex) – MEPS recorded from soleus and TA in untrained at different cycle phases (hyp = if SOL MEPS could be elicited mid-swing, while soleus is inactive, strong evidence for increased post-synaptic excitability of alpha-motor neurone
- Untrained – no soleus MEPS even though large H in mid-swing (unexpected) – sol MEPS increased more rapidly as function of EMG activity during voluntary activity than during backwards walking
- Conditioning stim to MC facilitated soleus H-reflex at rest and voluntary plantar but not midswing
- Daily backward training, time at which H-reflex began to increase was progressively delayed until it coincided with onset of solues EMG, and amp reduced compared with its value on first experimental day (no timing or amp MEP change with training)
- Possibility large amp of H in untrained and its adaptation with training are due to control of pre-inhibition of 1a afferents by other descending tracts
Chen (2010)
- Hierarchy of brain and SC plasticity underlies H-conditioning
- Definite or probable plasticity sites = MN membrane (firing threshold and CV), MU props, main corticospinal tract, IN and GABA IN, GABAergic inhibitory terminals, 1a afferent synaptic connection, terminals conveying disynaptic group 1 inhibition or excitation to MN and sensorimotor cortex
- SP directly responsible for H-conditioning appears to be induced and maintained by corticol plasticity that itself depends for its long-term survival on the cerebellum
