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Unit 3 Flashcards

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1
Q

Are there any absolutes in why we move?

A

no

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1
Q

What are the arguments for why we move?

A
  • shows the adaptive value of the advanced NS
  • moving in a coordinated manner lets us pursue mates and food as well as reacting to environmental stimuli (very adaptive for us)
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2
Q

What is the simplest explanation for why we move?

A
  • all movements are based on ion channel activity
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3
Q

How do paramecium move?

A
  • if it bumps into an object on anterior, Ca2+ channels open causing an AP and reversing motion
  • if it bumps into an object on posterior, K+ channels open, hyperpolarizing cell, causing forward movement
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4
Q

Is the primary motor cortex ipsilateral or contralateral?

A
  • contralateral
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5
Q

What broadmans’s area is the primary motor cortex?

A
  • broadmans area 4
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6
Q

Where in the brain is the primary motor cortex?

A

precentral gyrus (precentral sulcus on a gyrus)

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7
Q

What does the primary motor cortex do?

A

-executes the move
-population coding for direction of muscles

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8
Q

What are the UMN of the primary motor cortex?

A
  • pyramidal neurons in layer V
  • axons project to brainstem and spinal cord
  • each can influence multiple muscles
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9
Q

Where is the premotor area?

A

-in the premotor cortex

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10
Q

What broadman’s area is the premotor cortex?

A

6

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11
Q

What does the Premotor area do?

A

-plans movements, ideas for movement before movement happens
- Select appropriate movements based on external cues

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12
Q

Where are the premotor cortex and the supplementary motor area?

A

-anterior to M1

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13
Q

What is the order of activity between M1, SMA, PMA,

A
  • PMA,
  • SMA
  • M1
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14
Q

What broadman’s area is the supplementary motor area?

A

medial portion of Broadman’s area 6

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15
Q

What does the supplementary motor area do?

A
  • selects appropriate movements based on internal cues
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16
Q

What are the monkey motor experiments?

A

-Red light tells monkey where to hit
- Blue light tells them when to hit
- while it’s anticipating the movement we can see correlated activity in premotor cortex
- activity in M1 would correlate wit movement itself

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17
Q

What is apraxia?

A
  • selective inability to preform complex (but not simple) motor acts
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18
Q

Does damage to M1 cause Apraxia?

A

no, it would cause paralysis

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19
Q

Where does apraxia com from?

A
  • an inability to perform learned movements on command even tho the command is understood and there is willingness to preform the movement
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20
Q

What are the two types of apraxia?

A
  • ideomotor
  • ideational
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21
Q

What is the difference between paralysis and paresis?

A
  • paralysis there is no movement
    -paresis there is weak movement
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22
Q

What is ideomotor apraxia?

A
  • impaired ability to perform a skilled gesture with a limb upon verbal command and or/ imitation
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22
Q

What does ideomotor apraxia look like?

A
  • it can be shown with meaningful motor acts that don’t imply objects and gestures
    or that imply object use
  • different events based on the area affected
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23
Q

Are people with apraxia aware that they have it?

A

yes

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24
Q

What is ideational apraxia?

A
  • unable to plan movements related to interaction with objects because they’ve lost perception of the object’s purpose
    -disturbance in the concept of sequential organization of voluntary actions (no sequential actions)
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25
Q

What would idational apraxia look like?

A
  • “pick up something that would have coffee”
  • can’t pick up mug
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26
Q

How is the tomographic map of M1 organized?

A
  • movements and population coding more than muscles or body parts
  • not as cleanly segregated as S1
  • some organization (fingers grouped near hand)
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27
Q

Where does the basal ganglia receive input from?

A

-almost all of the cerebral cortex with most from the prefrontal cortex and motor cortex and least from sensory cortex

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28
Q

Where does the basal ganglia motor loop get projections from?

A
  • projections from basal ganglia, through the thalamus, back to the premotor cortex (area 6)
  • thalamic nucleus involved is a portion of the ventral lateral nucleus
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29
Q

Where does the basal ganglia motor loop project to?

A
  • superior colliculus to influence head and eye movements
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30
Q

What is special about the cerebellum?

A

-only part of the brain that gets to review itself

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31
Q

Where does the cerebellum get its projections from?

A
  • cerebellum, through thalamus, back to motor cortex
  • The thalamic nucleus involved is the caudal portion of the ventral lateral nucleus
    -cerebellum gets some sensory info more directly (vestibular and proprioceptive)
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32
Q

Where does the cerebellum motor loop project to?

A
  • all UMN areas (not just cerebral cortex)
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33
Q

What does the basal ganglia do?

A
  • function varies by which part of the basal ganglia is being considered, but in general, it evaluates and modulates cortical commands
  • Evaluate and filter motor commands
  • consistent with lots of input from prefrontal cortex and association cortex (involved in planning)
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34
Q

Are the dorsal, caudate and putman area all together?

A
  • in humans they are all separate but animals have caudate and putamen together
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35
Q

What is required for normal initiation of voluntary movements?

A

dorsal, caudate, putamen area

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36
Q

What does the dorsal caudate putamen do?

A

helps in switching movement on and off and controlling and modulating various motor patterns

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37
Q

Is the basal ganglia bilateral or unilateral?

A

-bilateral, two different basal ganglia

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38
Q

What is disinihbition?

A

-limiting inhibition

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39
Q

What helps the basal ganglia function?

A

parallel circuits

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40
Q

What are parallel circuits involved in?

A
  • cognition (executive loop)
  • emotion (limbic loop)
  • ventral striatum and nucleus accumbens core and shell really help with this
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41
Q

What is the direct pathway?

A
  • acts to facilitate motor output and stimulate particular motor diagrams
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42
Q

What is the indirect pathway?

A
  • acts to inhibit motor output and suppress competing motor pathways
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43
Q

Why do the indirect and direct pathways happen at the same time?

A
  • to trigger wanted movements and supress unwanted ones
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44
Q

What causes the indirect and direct pathways to be different?

A

-its more about output, but indirect has an extra step that is going to change the result

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45
Q

What is the overall effect of dopamine in the direct pathway?

A

excitatory, encourages output

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46
Q

What is the overall effect of dopamine in the indirect pathway?

A
  • inhibition
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47
Q

What happens if you get rid of the SNPC in the direct and indirect pathway?

A
  • swings pathway to indirect and has an overall decrease in motor output
    -less excitation of direct
  • less inhibition of indirect
  • causes parkinsons
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48
Q

Describe dopamine?

A

-small NT
- catecholamine (like NE and E)
- reuptake is degraded in synaptic cleft
- 5 types of receptors

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49
Q

Describe the dopamine receptors?

A
  • 5 types
    -all metabotropic
  • d1 and d2 are highly expressed in striatum
  • cell bodies not in striatum just terminals
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50
Q

What does D1 activation cause?

A
  • increases in CAMP and is excitatory
51
Q

What does D2 activation cause?

A
  • decreases in Camp and is inhibitory
52
Q

What is parkinson’s caused by?

A
  • a loss of neurons in the SNPC, locus coerulus (NE) and dorsal raphe (serotonin)
  • not a decrease in tonic output of BG, but a change in the pattern of activity leading to increased synchronization of oscillatory discharge leading to a tremor
53
Q

What percentage of neurons are gone before a parkinson’s patient will have symptoms?

A

-typically 30-50%
- sometimes 70%

54
Q

When does parkinson’s typically onset?

A

60s

55
Q

What are the symptoms of parkinsons?

A
  • resting tremor
    -bradykinesia
    -loss of smell
    -cognition changes (depression)
  • mood disorders
  • loss of bowel control
    -akenisia
56
Q

What is bradykinesia?

A

-slow movements

57
Q

What is akenisia?

A
  • lack of movements/ difficulty starting movements
58
Q

What is the most common treatment for parkinsons?

A

LDOPA

59
Q

How does LDOPA work?

A
  • only works while there are still some neurons left
  • dopa decarbozylase bypases RLS compared to other products, producing dopamine
  • paired with a peripheral DOPA decarbozylase inhibitor becasue it can’t cross blood-brain barrier, limiting effects to brain only
60
Q

What are the problems with LDOPA?

A

-loses efficacy as neurons die
- side effects like dyskinesia, psychiatric disturbances, impulse control

61
Q

What is dyskinesia?

A

uncontrollable abnormal movements

62
Q

Why does LDOPA create impulse control problems?

A
  • due to synapse, circuit plasticity, and other dopamine pathways
63
Q

What are LDOPA alternatives?

A
  • transplants of Dopamine producing neurons from fetal tissue
  • inactive subthalmic nucleus or internal globus pallicidus (deep brain stimmulation
64
Q

Why can’t you use tyrosine for parkinsons?

A

-involved in rate limiting step

65
Q

Why can’t you just inject more dopamine to fix parkinon’s?

A

-blood-brain barrier problems

66
Q

What does a lesion that diminishes the indirect pathway do?

A
  • increases motor output
67
Q

How does deep brain stimulation work?

A
  • disrupts the atypical electrical patterns in a way that allows the neurons to communicate more smoothly to lessen symptoms
  • especially helps resting tremors and muscle stiffness (another Parkinson’s symptom), bradykinesia, and gait problems
  • can be long-lasting but there is still a debate on when to do it
68
Q

What are the drawbacks to deep brain stimulation?

A
  • expensive and invasive
69
Q

What is Huntington’s caused by?

A
  • caused by a loss of neurons that project from striatum to external GP
  • mutant form of HTT gene leads to neuronal death
70
Q

How long until huntingtons causes death?

A

10-20 years

71
Q

When does huntington’s onset?

A

50s-40s

72
Q

What does huntington’s cause?

A
  • chorea
  • death of neurons elsewhere (frontal and temporal lobe) leading to personality disorders and dementia
  • death due to associated complications (pneumonia, heart failure, choking, malnutrition) and increased risk of suicide
73
Q

What is chorea?

A
  • involuntary, rapid, jerky movements
    -more subtle than dyskinesia
74
Q

Compare ballism and huntingtons?

A
  • Ballism: much more violent involuntary sudden movements
  • Huntington - starts more subtle and increases intensity overtime, chorea, involuntary, rapid jerky movements
75
Q

What is ballism?

A
  • violent, involuntary (but you can try and direct) limb movements usually caused by a stroke
76
Q

Where does the cerebellum develop from?

A

-hindbrain

77
Q

Where does the cortex develop from?

A

-diencephalon

78
Q

Why does cerebellum structure differ from species to species?

A

-different origins so different structure

79
Q

What is unique about the electric fish cerebellum?

A

-cerebellum hypertrophies
- they sense prey and communicate through electrical signals and the cerebellum has to process sensory signals

80
Q

What does the cerebellum do?

A

-process sensory signals and tell the brain when movement has occured

81
Q

What is the cerebellom made of?

A

-3 layers
- 2 hemispheres, vermis along midline, deep cerebellar nuclei

82
Q

What creates cerebellar layers?

A

purkunje fibers

83
Q

What are the three layers of the cerebellum?

A
  • purkunje cells/layers
  • granule cells/layer
  • molecular layer
84
Q

What is the molecular layer of the cerebellum?

A
  • outermost layer
  • has dendritic arbors of purkunje fibers
85
Q

What are dendritic arbors of purkunje fibers?

A
  • dendrites covered with dendritic spines
  • a Purkinje neuron receives as many synaptic inputs as any other neuron in the NS
  • fan-shaped, almost 2D
  • 100,000s of synapses
86
Q

What do different regions of the cerebellum do?

A

serve different functions

87
Q

What kind of somatotopic map does the cerebellum have?

A
  • a fractured one
    -maps are typically of ipsilateral body
88
Q

Where does the cerebellum get its info from?

A
  • ipsilateral sensory cortex
89
Q

Where do parallel fibers come from?

A

granule layer

90
Q

Describe parallel fibers?

A
  • from the granule layer
  • run perpendicular
  • synapse onto many Purkinje fibers
91
Q

How do climbing fibers work?

A
  • go from contralateral inferior olivary nucleus in the brainstem then leading to one synapses many times onto a single purkunje cell leading to a very strong excitatory output
92
Q

What is the difference between parallel and climbing fibers?

A
  • carry proprioceptive info from muscles while parallel fibers carry info from cerebral cortex
93
Q

What happens when climbing gibers and parallel fibers are active at the same time?

A
  • parallel synapses et weaker and less effective, a form of LTD
94
Q

What is parallel fiber input specificity?

A
  • only parallel fiber synapses that are active at the same time as climbing fibers show LTD
    -80% of purkunkje fibers are for error correction, primary role of cerebellum is error reduction
  • error reduction happens during a given moment and is a part of learning overtime
95
Q

What is cerebellar ataxia?

A
  • jerky inaccurate, poorly coordinated movements
96
Q

What kind of causes does cerebellar damage have?

A

-many causes with many different effects
- autoimmunity to purkunje fibers, stroke, toxin damage, genetic disorders

97
Q

What is an intention tremor?

A

-only a tremor when making movements, an expression of ataxia

98
Q

What do lesions of the vestibulocerebellum lead to?

A

-impaired eye function

99
Q

What is korsakoff’s syndrome?

A
  • due to alcohol abuse
  • degeneration of the lower body (anterior spinocerebellum)
  • results in wide, staggering gait, later difficulty with walking at all
100
Q

What are the four groups of UMNs?

A
  1. body posture (axial and proximal limb muscles)
  2. movements of the arms (Proximal arm muscles)
  3. orienting movements of eyes and head
  4. complex sequences of voluntary movements
101
Q

Describe the body posture UMN group?

A
  • axial and proximal limb muscles
  • vestibular nuclei in brainstem (Feedback)
  • axons run vestibulospinal tract
  • axons run reticulospinal tract to spinal cord
  • reticular formation in brainstem (Feed foward)
102
Q

Describe the arm movement UMN group?

A
  • proximal arm muscles
  • red nucleus in midbrain
  • axons run rubrospinal tract
103
Q

Describe the orienting movements of head and eyes UMN?

A
  • superior colliculus (optic tectum) in midbrain
  • axons run in tectospinal tract
104
Q

Describe the complex sequences of voluntary movements UMN?

A
  • cell bodies in the contralateral frontal lobe
  • primary motor cortex
  • axons project to the spinal cord in corticospinal tract
105
Q

Describe alpha motor neurons?

A
  • LMN
  • cell bodies arse in the ventral horn of the spinal cord
  • axons in ventral roots and then spinal nerves
  • typically innervate a large number of muscle fibers
106
Q

What is ALS?

A

-neurodegenerative neuromuscular disease that causes muscle weakness and atrophy

107
Q

How long does ALS take?

A

over 1-6 years voluntary movement is lost

108
Q

Does ALS affect cognition, sensation, or intellect?

A

no

109
Q

How does ALS cause death?

A
  • failure of respiratory system
110
Q

What is the main pathology of ALS?

A
  • death of AMN, death before axon retraction occurs 1st
  • in some cases UMn in M1 also dies, but axon retraction occurs first
111
Q

What causes ALS?

A
  • in 10% of cases its inherited, the rest are environmental/ unknown
  • environmental cases are well documented (such as exposure to pesticides and cyanobacteria, most causes are not)
  • ELEVATED GLUCOSE LEVELS IN THE SPINAL CORD, excitotoxicity caused death of MN
  • anything that can slowly and selectively kill alpha MN can induce ALS
112
Q

Why are ventral horns larger at enlargements?

A
  • there are more alpha motor neurons there, thoragic region has small ventral horns and fewer AMNS
113
Q

Why is there less white matter at the lumbar level than the cervical level?

A

-fewer axons

114
Q

What do MN that innervate the same muscle have in common?

A
  • cell body together in nuclei
  • MN location represents an orderly representation of muscles innervated
115
Q

What is a motor unit?

A

smallest functional unit of the skeletal motor system

116
Q

What is the motor neuron pool?

A
  • group of MN cell bodies that innervate a given muscle
117
Q

What properties to motor units vary in?

A

-fatiguabilty
- speed of contraction
- size

118
Q

How do motor units vary in size?

A
  • fine motor control is optimal in small MU
  • small MU tend to get recruited first and larger MU later
  • more moter units= stronger contraction
119
Q

What are the types of motor unit stimulation?

A
  • muscle twitch
  • summation of contractions
  • sustained contraction (tetanus)
120
Q

What system are muscle spindles a part of?

A

proprioceptive

121
Q

What is the strect reflex innervated by?

A

-1A afferents

122
Q

Do reflexes involve the brain?

A

no

123
Q

How does the stretch reflex work?

A
  • stretch activates mechanically gated channels in 1A afferents that are Na (possibly Ca) permeable
  • contains small muscle fibers (intrafusal muscle fibers)
124
Q

What are intrafusal msucle fibers)

A
  • small muscle fibers
  • innervated by gamma MN
  • don’t directly contribute to muscle contraction
  • critical
  • to stretch receptor function, maintains tension on spindles for stretch detection
    monosynaptic
125
Q

What is an agonistic muscle?

A
  • generates desired movement
126
Q

What is an antagonistic muscle?

A
  • opposes movement
127
Q

What type of synapses are ipsilateral flexion and contralateral extension?

A

not monosynaptic

Neuro Biology (4 decks)

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