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KIN 255 > Midterm Notes > Flashcards

Midterm Notes Flashcards

1
Q

Modulation of Stimulus Evoked Behaviour

What mechanisms can modify the stimulus-response relationship of a simple reflex?

A
  1. Change in gamma motor neuron activity
  2. Inhibit reflex
  3. Facilitate reflex
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2
Q

Modulation of Stimulus Evoked Behaviour

How do changes in gamma motor neuron activity modify a simple reflex?

A
  • Changes in muscle spindle receptor sensiticity
  • changing alpha-gamma relationship will alter taughtness if spindle (same stretch -> weaker afferent response)
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3
Q

Modulation of Stimulus Evoked Behaviour

Explain what inhibiting the relfex means.

A

Decrease the strength of the effect of the sensory afferent on the motor neuron (called gain)

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4
Q

Modulation of Stimulus Evoked Behaviour

Explain what facilitating the reflex means.

A

Increase gain at sensory motor synapse

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5
Q

Modulation of Stimulus Evoked Behaviour

What is the objective of modulating stimulus evoked behaviours?

like how are they modulated

A

Changing the probability of AP occuring without precluding that an AP could occur

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6
Q

Modulation of Stimulus Evoked Behaviour

What is spatial summation?

A

the aggregation of post-synaptic potentials arising from multiple separate synapses

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7
Q

Modulation of Stimulus Evoked Behaviour

What is temporal summation?

A

the aggregation of multiple post-synaptic potentials occuring close in time

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8
Q

What are the main neurotransmitters?

and which are the most common exitatory/inhibitory?

A
  • Glutamate (most common excitatory)
  • GABA (most common inhibitory)
  • Glycine (most common inhibitory in SC)
  • Acetylcholine
  • Dopamine
  • Serotonin
  • Norepinephrine
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9
Q

Receptors and ion channels

What is an ionotropic receptor?

A
  • A fast acting protein/receptor.
  • The neurotransmitter will bind directly to the channel.
  • Some are voltage gated.
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10
Q

Receptors and ion channels

What is a metabotropic receptor?

and what else is it known as?

A
  • aka 2nd messenger receptor
  • slow acting
  • neurotransmitter binds to a separate G protein-coupled receptor
  • This activates a second messenger system/ intermediary molecule
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11
Q

Receptors and ion channels

What what does voltage gated ion channel mean?

A

The ionotropic receptor wil not open right way once the neurotransmitter is bound. It requires the neurotransmitter and the internal voltage of the cell to be in a particular state (i.e depolarized)

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12
Q

Receptors and ion channels

What is a 2nd messenger?

A

an intracellular signaling molecule released by the cell when exposed to extracellular signalling (such as neurotransmitter)
[is released when neurotransmitte binds to metabotropic receptor, neurotransmitter binds outside cell, 2nd messenger is released and binds to ion channel inside cell]

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13
Q

Mechanisms of modulation

What is synaptic modulation

A

a change in the relationship between the pre-synaptic AP and post-synapitc potential

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14
Q

Mechanisms of modulation

what is pre-synaptic modulation?

A

change in the amount of neurotransmitter released by pre-synapic neuron

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15
Q

Mechanisms of modulation

What is post-synaptic modulation?

A

change driven by the post-synaptic neuron’s response to the neurotransmitter

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16
Q

Mechanisms of modulation

Explain baseline synaptic response

A
  1. Sharp burst of Na+ makes internal environment of pre-synaptic neuron near synapse for +
    • charged environment opens Ca2+ voltage gated ion channels allowing CA2+ to flow into neuron
  3. influx of Ca2+ signals vesicles holding glutamate NT to move to synapse & release their contents
  4. Glutamate binds to receptors attached to ion channels on post-synaptic neuron. Ion channels open, allowing NA+ to flow into post-synaptic neuron
  5. Na+ generates an excitatory post-synaptic potential (EPSP) that diffuses down the post-syn. dendrite. If EPSP is big enough, it will initiate AP
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17
Q

Mechanisms of modulation

Explain Pre-synaptic inhibition

at synapse

A
  1. Inhibitory neuron on pre-syp. neuron opens Cl- channels, making internal envionment of pre-syn. neuron more -
  2. Ca2+channels less likely to open, fewer vesicles move to expel glutamate
  3. Less glutamate = fewer receptors on post-syn. channels find a “friend” to bind to. Fewer ion channels open on post-syn. neuron
  4. Less open channels leads to smaller influx of Na+ into post-syn. neuron
  5. Smaller EPSP, less likely to be big enough to tigger AP
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18
Q

Mechanisms of modulation

Explain pre-synaptic facilitaion

at synapse

A
  1. facilitory neuron on pre-syn. neuron opens Na+ channels, so more Na+ and more + pre-syn. environment
  2. Ca2+ channels more likely to open, so more vesicles move to expel glutamate
  3. More glutamate means more receptor bind to ion channels. Thus more channels open
  4. Leads larger influc of Na+ into post-synaptic neuron
  5. Lager EPSP which is more likely to trigger AP
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19
Q

Mechanisms of modulation

Explain Post-synaptic Inhibition

at synapse

A

(Pre-synaptic behaviour is the same as the baseline)
1. Inhibitory neuron opens Cl- channels on post-synaptic neuron , making environment more -
2. -Cl- ions summate with + Na+ ions flowing in from pre-synaptic neuron
3. Opposing charges cancel each other to some extent, thus smaller EPSP
4. EPSP less likely to be big enough to trigger AP

More common than pre-synaptic

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20
Q

Mechanisms of modulation

Explain Post-synaptic facilitation

A

(pre-synaptic behaviour is the same as baseline)
1. Facilitatory neuron on post-synaptic neuron opens Na+ chnnels, making internal environment more +
2. Na+ ions summate with Na+ ions flowing from presynaptic glutamate release
3. Common charges add, increasing EPSP
4. EPSP more likely to cause AP

More common than pre-synaptic

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21
Q

Mechanisms of modulation

Explain the key points of pre vs post-synaptic interactions

(specificity, synaptic interactions)

A
  • Pre-synaptic interactions are more specific as it only affects one neuron/synapse (even if sensory neuron synapses with multiple other neurons)
  • Post-synaptic interactions will alter excitability of post-synaptic neuron, affecting every synapse even if it has multiple synapses with pre-synaptic neurons
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22
Q

Control of pre/post synaptic modulation

Where does the input that determines the activity of the inhibitory/facilitatory neurons come from?

2 sources

A
  1. Sensory inputs (centripetal)
    [inputs from primary afferent or interneurons mediated by afferent inputs]
  2. Central/Descending (centrifugal)
    [inputs arise from ‘higher’ centres like cortex/cerebellum/brain stem]
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23
Q

Control of pre/post synaptic modulation

What is the control reflex

Centripetal modulation

A

the muscle/reflex we are measuring alone (ex soleus influence on soleus reflex)

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24
Q

Control of pre/post synaptic modulation

What is the conditioned reflex

centripetal modulation

A

the muscle/reflex exerting influence over a difference muscle/reflex (ex tibialis anterior influence on soleus reflex)

25
Q

Control of pre/post synaptic modulation

What are the sources of descending modulatory input?

4 sources

post-synaptic centrifugal modulation

A
  1. Corticospinal tract
  2. Vestibulospinal
  3. Reticulospinal
  4. Rubospinal
26
Q

Control of pre/post synaptic modulation

How does the corticospinal tract modulate input

for reflexes

A

Adjusts reflex pathways to reduce conflict with voluntary movements

27
Q

Control of pre/post synaptic modulation

How does the vestibulospinal tract modulate input

for reflexes

A

Coordinate spinal reflexes with vestibular mediated responses, primarily for balance control

28
Q

Control of pre/post synaptic modulation

How does the reticulospinal tract modulate input

A

Adjusts reflex pathways during locomotion

29
Q

Control of pre/post synaptic modulation

How does the rubospinal tract modulate input

A

Modulates flexor reflex activity (eg withdraw reflex)
-midbrain

30
Q

Control of pre/post synaptic modulation

What neurons do descending tracts influence

A

Motor (directly and indirectly) and interneurons in spinal grey area

31
Q

Phase depentent reflex modulation

What is phase dependent modulation

A

The change (facilitation, inhibitions, complete reversal) of the response evoked by a specific stimulus depending on the phase of a movement

Think contraction/relaxation of soleus during stance vs swing phase and H-reflex graph

32
Q

Pain Perception

What is Nociception?

A

The neural process of detecting & processing noxious stimuli

33
Q

Pain Perception

What is Pain?

A

an unpleasent sensory & emotional experience associated with actual or potential tissue damage

34
Q

Pain Perception

What are the sources of afferent info that mediate pain perception

3 sources/typesof pain

A
  1. Nociceptive pain
  2. Neuropathic pain
  3. Other pain

both 2 & 3 are Non-nociceptive pain

35
Q

Pain Perception

What is Nociceptive pain

A

Pain arising from damage or potential damage to tissue (associated with activation of nociceptors)

36
Q

Pain Perception

What is neuropathic pain?

A

Pain arising from damage or insult to the NS that convey nociceptive info

37
Q

Pain Perception

What is other pain

(non-nociceptive)

A

Pain unrelated to nociceptor or related NS activity

38
Q

Motor control principles & supraspinal control

What is Goal-directed movement?

A
  • an expression of thought through action that is organized around a specific behavioural goal and environmental context
  • requires coordination of neural processes controling many small movements that are incorporated into larger action
39
Q

Motor control principles & supraspinal control

What is coordination

A

the organization of different elements of a complex body or activity so they work together

40
Q

Motor control principles & supraspinal control

What is the Motor Program Theory

A

hypothesize goal-directed movements were based on motor programs developed through prior experience

41
Q

Motor control principles & supraspinal control

What is a motor program

A

An organized set of muscle commands sent to the muscles to generate a predetermined sequence of actions carried out in the absense of sensory feedback

42
Q

Motor control principles & supraspinal control

What are the main challenges with the motor program theory

3 challenges and what they each are

A
  1. the storage problem (brain does not have enough neurons for unique combos of each goal directed movement)
  2. The novelty problem (how do we produce a goal directed movement without a preexisting motor program)
  3. the generalization problem (general features of movements seem to transfer across effectors)
43
Q

Motor control principles & supraspinal control

What is a generalized motor program

A

an abstract representation of goal-directed movement that results in the production of a coordinated movement sequence

44
Q

Motor control principles & supraspinal control

What is an invarient feature

generalized motor program

A

a movement element that is consistent across all different attempts of the goal-directed movement regardless of varience or effector

For example, the swing of the racket in tennis

45
Q

Motor control principles & supraspinal control

What is a surface feature

generalized motor program

A

a movement element that varies across all attempts of the goal-directed movement

for example, the angle to place your wrist to hit the ball in tennis dur

46
Q

Motor control principles & supraspinal control

Controlling movement when relying on generalized motor programs dependent on

A
  1. Setting parameters (prediction of expected action)
  2. Feedback to make corrections (internal errors - incorrect parameters; exteral errors - unexpected environmental events)
47
Q

Methods to study supraspinal motor control (imaging)

That are the methods to study supraspinal motor control (assess the role of the cortex in motor control)?

8 methods, 2 invasive, 6 non-invasive

A
  • Single cell studies
  • Lesion studies
    Non-invasive:
  • fMRI
  • PET
  • fNIRS
  • EEG
  • MEG
  • TMS
48
Q

Methods to study supraspinal motor control (imaging)

Explain EEGs

How it works

A
  • uses electrodes bridged to scalp to quantify the activity of large populations of neurons over time
  • AP are too fast to measure w EEG, instead signal is releated to the post-syn. potential generated by a pre-syn. AP
  • Quantify activity measured at one electrode by subtracting out the electrical signal from an inert/reference electrode

Electroencephalography

49
Q

Methods to study supraspinal motor control (imaging)

What are examples of measures of brain activity to processes stimuli we can get from EEGs

A
  1. Event-related potential (ERP) or Evoked potential (EP)
50
Q

Methods to study supraspinal motor control (imaging)

Explain fMRI

A
  • MRI uses strong magnetic fields to distinguish b/w substances w different structures/properties in the brain
  • change in Blood Oxygen Level Dependent (BOLD) response is correlated to the concurrent behaviour to draw conclusions about the role of a brain area to the behaviour

Functional Magnetic Resonance Imaging

51
Q

Methods to study supraspinal motor control (imaging)

What do fMRIs exploit

A
  1. the relationship b/w neural activity, metabolic demand and blood flow
  2. Different magnetic properties of oxygenated/deoxygenated blood
52
Q

Methods to study supraspinal motor control (imaging)

Explain TMS

A
  • Uses magnetic fields to induce AP in underlying cortex
  • rarely excites corticospinal neuron directly, instead genereates AP in excitatory interneurons that synapse on corticospinal neuon
  • Descrete single or pairs of TMS stimuli are used to assess the excitability of the corticospinal neurons or the intereurons that influence corticospinal neuon
  • Trains of stimuli can be used to induce short periods of change (plasticity) in cortex excitability. This is transient and will reverse within minutes-hours
  • the trains that induce periods of plasticity are sometimes called ‘virtual lesions’

Transcranial Magnetic Stimulation

53
Q

Primary Motor Cortex (M1)

Explain Primary Motor Cortex (M1) organization

A
  • Somatotopic organization
    (fine structure is far more complex)
  • Homonculus (motor)
  • Evidence that cells code for movements rather than simply individual muscles
54
Q

Primary Motor Cortex (M1)

Explain the corticospinal tract

A
  • Starts in cortex, ends in spinal cord
  • Synapse into ventral horn and also intermediate zone of spinal cord
  • Majority of corticospinal tract crosses at level of medulla
  • Primary Motor Cortex is source of most corticospinal projections
  • Corticospinal neuron integrates info from many different sources that shape movement (both feedforward and feedback pathways)
55
Q

Primary Motor Cortex (M1)

Explain Feedforward control

A

Generated motor commands based upon a prediction of the resulting outcome from executing a motor plan given current body state

56
Q

Primary Motor Cortex (M1)

Explain feedback control

A

reacts to deviations from the planned outcome during/after the movement

57
Q

Primary Motor Cortex (M1)

where do corticospinal neurons project

A
  • they only project to a subset of alpha motor neurons innervating a muscle
  • Axon of a single AMN branches to innervate many muscle fibers, however, each muscle fibre is only innervated by a single nerve
  • Muscle fibres are recruited in a specific order to provide fine control vs. brute force
58
Q

Primary Motor Cortex (M1)

Explain force, timing, direction and task type importance for activityof a cortcospinal neuron

A
  • Force: activity reflects how much force is required to achieve the desired movement goal
  • Timing: activity precedes movement onset
  • Direction: activity has a directional preferece
  • Task type: activity has a task/type preference (ex grip type)

KIN 255 (6 decks)

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