lecture 19 - stuart baker Flashcards

1
Q

golgi tendon organ

A

sensing the force that a muscle is exerting
connects to interneuron which is inhibitory and inhibits motor neurone

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2
Q

1b inhibitory tendon reflex can become

A

excitatory
they can change depending on the state
feedback control loop during locomotion (movement)

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3
Q

cutaneous reflexes

A
  • skin is covered in cutaneous receptors
  • important for control of movement
  • electrodes on the finger stimulate the digital nerves that run along the finger
  • recording the activity of the muscle in the hand shows triphasic reflex
  • early excitatory component, middle latency inhibitory component, late excitatory component
  • E1 (spinal) , I1 and E2 (cortical) reflexes
  • the electrically stimulated reflexes are weak
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4
Q

people asked to grasp and lift an object
if the object slips from the grasp it stimulates to cutaneous receptors in the fingers
this caused a reflex increase in grip force
and this reflex was really powerful

A

natural stimulus causes strong reflex

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5
Q

pathway of cutaneous reflex

A
  • lab used genetic techniques to identify a particular class of interneurons in the spinal cord of a mouse called dI3 interneurons
  • showed that the dI3 interneurons receive input from cutaneous receptors and they project to motor neurons and they’re excitatory
  • they’re able to create a KO strain of the mice that lack the interneurons
  • when the KO mice are put in a cage and turned upside down they cannot grip and therefore fall out the cage
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6
Q

in the intermediate zone of the spinal cord there are corticospinal terminals which is where all the interneurons are
so all the spinal interneurons that are involved in controlling movement have input from the..

A

cortex
so theyre not just involved in reflexes theyre also involved in voluntary movements

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7
Q

we have a monosynaptic stetch reflex from muscle spindles which goes straight to a motor neurone and back to the same muscle
we also have a di synaptic inhibitory reflex which goes an inhibitory interneuon then motor neuron to the antagonist muscle and stops it contracting at the same time.
that inhibitory interneuron also gets input from the..

A

CS tract

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8
Q

interneurons are there to join the voluntary command with sensory inputs (reflexes) and give a coherent output

A
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9
Q

the cortex has multiple ways of sending information down to interneurons

A

can come via the brain stem
can come via propriospinal interneurons (C3-C4)
can come via segmental interneurons (C6-T1)
or via direct connections to motor neurones

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10
Q

C4-C5 CS lesion causes loss of direct connections but monkey can still do fine finger movement, suggest that…

A

interneurons can mediate fine finger movement

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11
Q

C2 corticospinal lesions causes the monkey not to be able to move fingers separately therefore…

A

brain stem pathways cannot mediate fine finger movements but to some extent the propriospinal interneurons can

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12
Q

spinal control of locomotion:
cat can speed up walking when treadmill pace increases even though it has a complete spinal section
therefore…

A

spinal cord is capable of driving a locomotion pattern (alternation between flexion and extension in a normal gait pattern that alternates between the two limbs) it can also integrate sensory input to adapt the gait without any connection to the cortex
(central pattern generator)

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13
Q

evidence that there is a central pattern generator in humans
electrodes are implanted into people that have a spinal cord injury
implanted over the spinal cord and boosted the activation of the spinal cord in a constant way and this caused production locomotor activity in the leg

A
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14
Q

the cerebellum:

A

small structure at the base of the brain in terms of volume but has large number of neurones

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15
Q

effects of cerebellar lesion

A

tremor and hypermetria (overreaching)
dysdiadochokinesia (inability to make rapid movements)
ataxic gait (walking looks like theyre drunk)

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16
Q

cerebellar anatomy

A

cortex (outer part)
inside the cerebellum are the deep cerebellar nuclei
there are different sections divided into the lateral part, the intermediate part and the medial part

17
Q

the sections of the cortex communicate down to the corresponding deep cellular nuclei:
the lateral part of the cortex connects to the…

A

dentate nucleus

18
Q

the intermediate part of the cortex connects to the…

A

interposed nuclei

19
Q

the medial part (also called the vermis) connects to the…

A

fastigial nucleus

20
Q

the lateral part of the cerebellum (aka the cerebrocerebellum) gets inputs from the…

A

cerebral cortex

21
Q

the cerebral cortex projects to the pontine nuclei which then projects to the cerebellum cortex which projects to the dentate nucleus which then projects to the thalamus and then back up to the cerebral cortex

A
22
Q

the intermediate and medial parts of the cerebellum are often called the…

A

spinocerebellum

23
Q

they get inputs from…

A

parts of the cerebral cortex involved in somatic sensation but mainly from the spinocerebellar tract (sensory pathway from the periphery coming up the spinal cord to the cerebellum) projects to the intermediate and medial parts which projects down to the deep cerebellar nuclei (interposed and fastigial) and then that projects to the red nucleus and the reticular nuclei and then back to the spinal cord (it can also go up to the cerebral cortex as well)

24
Q

vestibulocerebellum which involes a small part of the cerebellum called the…

A

flocculonodular lobe

25
Q

input comes from the vestibular nuclei (about balance), projects to the cerebellar to the cortex and then back to the vestibular nuclei

A

cerebellar input/output circuits very often loop back

26
Q

cerebellar cortex microcircuit layers

A

top –> bottom
molecular layer
purkinje cells layer
granular layer
white matter layer

27
Q

what are the only output cells of the cerebellar cortex

A

purkinje cells (they project into the deep cerebellar nuclei)

28
Q

purkinje cells are GABAergic meaning they can only…

A

inhibit

29
Q

purkinje cells get input from…

A

climbing fibres (1:1 relationship, comes up the dendritic tree of the purkinje cell and winds around the dendrites and makes many synapses. they come from the inferior olive)
and parallel fibres (originate in the granular layer at the granule cells, they send an axon up to the molecular layer where in bifurcates and then the parallel fibres cross the dendritic tree of the purkinje fibres and right angles and then make synapses)

30
Q

the granule cells get their input from mossy fibres which come from pontine nuclei which get activated cerebral cortex or from the spinocerebellar tract

A
31
Q

there are inhibitory interneurons in the layers:

A

golgi cell - gets input from the parallel fibres and projects back to the granule cells. so the granule cells gets input from the mossy fibre and get inhibited by the golgi cell to keep activity at the right level
stellate and basket cells - get input from the parallel fibres and inhibit the purkinje cells

32
Q

purkinje cells have two different sorts of action potentials

A
  1. simple spike - normal APs, caused by activation of many parallel fibres adding up by temporal summation
  2. complex spike - come from the climbing fibres which cause massive depolarisation to the purkinje cells and that triggers a calcium spike which then causes a long lasting depolarisation and on top of that there is little bursts of sodium spikes. this doesn’t happen very often
33
Q

Marr and Albus:
- voluntary movement is produced by your voluntary intent from the cerebral cortex
- the voluntary activation of climbing fibres activates the purkinje cells
- the activity in the purkinje cells some how produces the movement
- some of the parallel fibres are active because of the sensory context
- the synapses between the parallel fibres and the purkinje cells will strengthen whenever theres paired activation of the parallel fibres and the purkinje cells (i.e when the purkinje cells are already active due to the climbing fibres)
- if the same sensory context happens again now because the parallel fibres are being activated and the synapses have been strengthened those parallel fibres could now automatically activate the purkinje cells (no need for climbing fibres)
- this is a way we can learn a movement (e.g driving a car, after time it becomes an automatic movement)

A
34
Q

evidence for this idea

A

they recorded from a purkinje cell and activate two parallel fibres (PF) that were connected to that purkinje cell
they activate PF1 and 2 separately and see EPSPs
they activated PF1 at the same time as activating the climbing fibre that goes to that purkinje cell (they do this a number of times)
then they go back and record the response to PF1 on its own and PF2 on its own and the EPSP gets smaller in PF1
so the one that was paired with activation of the climbing fibre changes the EPSP
evidence that cerebellar learning is happening

35
Q

evidence that this may occur in voluntary movements

A

trained a monkey to do a wrist movement
recorded from purkinje cells
when the monkey did the wrist movement there was activation of the purkinje cell
when there was weight added to the handle the monkey was moving so the monkey had to adapt to the fact that the handle was heavier
when they first recorded the purkinje cell started firing complex spikes around the time of the movement
after the monkey got used to the fact that the handle was not weight the activity in the complex spikes decreased
but also the firing rate of simple spikes had reduced
they thought that during the adaptation to the load the complex spikes served as some sort of training signal which caused a reduction in the firing rate of the simple spikes because it changes the synaptic weighting of the parallel fibre synapses and that lead to the monkey being able to do the monkey with a new load

36
Q
A