Rhythmic movement 1 Flashcards
stepping, supraspinal control, spinal rehabilitation
the 2 theories on how rhythmic motor patterns are generated
- chain reflexes
- central model: CPGs (central pattern generators)
chain reflex theory
- rhythmic patterns arise through series of reflexes
-tactile and proprioceptive sensory reafference is NECESSARY for rhythmic movements
central model - CPGs
- rhythm is centrally generated NOT mediated by sensory reaffereance
- sensory reafference NOT necessary but is important to adjust motor patterns to external conditions
first demonstration of CPGs
- Graham Brown
- decerebrated cats and dorsal root cut (no sensory reafferance)
- found rhythmic flexors (TA) and extensor (GN) alternation still emerged: could still measure a rhythmic pattern
CPGs in a dish as evidence
- FICTIVE motor patterns or rhythmic firing patterns generated by nerous tissue ex-vivo that resembles those observed in-vivo
- when there is no muscle activation there is still a rhythm
fictive motor patterns also observed in-vivo (in cats) after neuromuscular blockers
where are CPGs located in humans
- brain stem (e.g. respiratory, chewing, swallowing)
- spinal cord (e.g. defacation, ejaculation, locomotion)
estimated based on animal models
what are the two main factors that the expression of rhythmic patterns by CPGs depend on the interaction between ?
- the circuitry
- the circuit elements
what is rhythm in relation to these 2 factors in CPGs
an emergent property
what is circuitry
the connectivity among cells in the network (synapses and gap junctions)
what are the circuit elements ?
the intrinsic dynamics of individual cells within the network
what are distinct CPGs for locomotion associated with
individual limbs
single limbs can generate rhythmic patterns
what does connectivity among CPGs for locomotion give rise to ?
limb co-ordination
e.g. alternating in walking
in locomototion, where does left-right co-ordination come from
commisural interneurons crossing the spinal cord midline
in locomotion for tetrapod animals (4 limbs), how is forelimbs-hindlimbs coordination achieved
long proprisonal descending neurons (LPDNs)
what do LPDNs do
connect cervical and upper thoracic segments with lumbar spine segments
first circuit model of CPGs
- Half Centres CPG model
- excitatory and inhibitory interneurons have reciprocal feedback which generates rhythm (back and fourth between them)
- rhythm provides alternate excitation of extensor and flexor motor neurons
brown downstream interneuron provide reciprocal inhibition of motor neur
by Brown and Lunderberg
what does the Half Centre CPG model fail to explain
- complexity of natural and fictive motor patterns
- effects of sensory reafference on phase and/or duration of locomotor patterns
what is not explained in observation for the Half Centre model about pattern complexity
some muscle activation does not follow strict extensor-flexor alternation
what is not explained in observation for the Half Centre model about reafference
- sensory afferent stimulation changes relative duration of flexor and extensor activation phase, but has no effect on overall cycle
Multilevel CPG model
- between rhythm generator (RG) level and motor neurons there is an intermediate level: PATTERN FORMATION (PF)
- RG level connects to multiple PF levels to achieve complex muscle activation
how does the mutilevel CPG model work
- RG provides rhythm, PF adjusts specific pattern of motor neuron activity
how does pattern formation adjust the pattern of motor neuron activity
by interacting with la and Renshaw interneuron cells so extensor and reflexor phases can be adjusted without affecting cycle duration
can then account for effect of these interneuron cells
Multiple interacting CPGs model
- no multilevel just multiple CPGs e.g.
- in each limb there are separate CPGs for each set of synergistic muscles
in the multiple interacting CPGs model, what does interaction among CPGs do
generate complex patterns of muscle activation
Classic individual cell properites (not connected to circuitry)
- endogenous bursting
- plateau potentials
- postinhibitory rebound
- spike frequency adaptation
endogenous bursting cell properties
e.g. pace-maker property
- generate bursts of charge
plateau potential cell properties
e.g. bistable cells
- can excite them and remain stable in this state until inhibited
postinhibitory rebound cell properties
rebound from inhibition
spike frequency adaptation
cells excited fire fast and channels mediate firing rate changes
- part of half centres model from Brown
what are the two main phases of locomotion
stance (foot contacts floor) and swing (no contact)
what does walking at higher speed or running do to stance duration
decreases it
what controls the timing of stance-to-swing transition
proprioception
what is stance-to-swing transition controlled by
sensory reafference at the spinal cord level
what is the stance associated with
activation of extensor muscles
extensor burst
(anti-gravity muscles)
what is swing associated with
activation of flexor muscles
flexor burst
what is the stance-to-swing transition ellicited by in extension
hindlimb extension
- muscle spindles
- extension of muscle initiates flexor burst (swing)
- CPGs in SC stimulate extensor muscles in stance and extension sensed by hip excite flexor muscles and so swing
what is stance-to-swing transition ellicted by in unloading
hind limb unloading
- swing intiated when leg is unloaded
- loading of extensors inhibits flexor burst
- effects mediated by Ib afferents
