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Neuroscience > Exam 3: Motor system and Basal ganglia > Flashcards

Exam 3: Motor system and Basal ganglia Flashcards

1
Q

somatosensory system

A

controls striated skeletal muscles ⇒ this is how you move

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2
Q

2 components of the somatosensory system

A
  1. Moves the bones of your body around
  2. Controls posture, limbs, and face
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3
Q

autonomic motor system

A

sympathetic and parasympathetic control of heart, blood vessels, (GI) digestive tract ⇒ background processes

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4
Q

2 main sets of neurons

A
  1. upper motor neurons
  2. lower motor neurons
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5
Q

upper motor neurons (UMNs)

A

cell bodies are in the brain mostly that descend to various places in the brainstem and spinal cord
- start in the cerebral cortex and target the lower motor neurons
- Control lower motor neurons

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6
Q

Lower motor neurons (LMN’s)

A

actually leave the CNS and go out into the body and touch muscles to cause physical contractions
- start in brainstem (cranial nerves) or spinal cord (spinal nerves) and directly target muscles
- Brainstem is head and face while spinal cord is everything else

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7
Q

where do the soma of LMN’s sit and where do they synapse?

A

Their soma sit in the ventral horn of the spinal cord and brainstem cranial nerve motor nuclei
- these leave the spinal cord via the ventral root and make their way out to the periphery to contact a muscle in the tissue
- motor neurons synapse directly onto skeletal muscles

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8
Q

neuromuscular junction/synapse

A

the motor neuron muscle connection
- Similar to a synapse that happens in the brain between different neurons

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9
Q

how do motor neurons signal muscle contractions?

A

via acetylcholine

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10
Q

acetylcholine

A

neurotransmitter chemical release that acts on the muscle tissue to cause muscle contractions
- Like an action potential but instead is a muscle contraction

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11
Q

fascicles

A

large circles of what muscles are made up of and contain bundles of muscle fibers

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12
Q

fiber

A

small round portions that make up a fascicle unit in the muscles

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13
Q

how do muscles connect to bones?

A

via tendons

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14
Q

each adult muscle fiber is targeted by what?

A

by one neuromuscular junction

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15
Q

where are acetylcholine receptors concentrated?

A

on the muscle fiber membrane at the neuromuscular junction

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16
Q

what do muscle fiber membranes do?

A

allow the flow of ions in and out like normal cell membranes
- Muscle fibers are more than one cells but has a collective property of a membrane with cell like properties ⇒ mm-inches possible
- This limits the possibility of contraction because contractions have to spread throughout the whole muscle to contract at once

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17
Q

botox (botulism toxin)

A

blocks acetylcholine release at the neuromuscular junction
- Injection into muscles causes paralysis ⇒ cosmetic approach to reduce wrinkles

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18
Q

how does contraction work?

A
  • Acetylcholine released from the motor neuron activates acetylcholine receptors on the muscle
  • Acetylcholine receptors are ligand-gated ion channels
  • Activation of the receptor causes depolarization so sodium enters the muscle fiber and potassium exits
  • This spread across the fiber like an actin potential ⇒ calcium is released inside the fiber
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19
Q

ligand gated ion channels

A

determined by the presence of a certain molecule such as acetylcholine on the receptor which opens the depolarization of the muscle cell/other type of cell

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20
Q

what do muscle fibers contain?

A

alternating bands of motor proteins (actin and myosin) that form stripes in striated muscle

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21
Q

what is calcium released in response to?

A

acetylcholine binding to the muscle fiber activating the protein complex that causes muscle contraction
- Once acetylcholine binds then calcium can come into the cell to create the muscle contraction

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22
Q

how does myosin work in muscle contraction?

A

myosin molecules slide across actin molecules, shortening the muscle fiber
- Myosin requires energy (ATP) to produce muscle contraction
- The head of the myosin make contact with the fibers and they have a conformational change to physically pull the actin bands together
- The protein complexes synch together and there are millions collectively working together to pull the chunk of tissue together
- ATP is the rate limiting step since they need it for energy

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23
Q

type 1 muscle fibers

A

thin, slow, low force, and slowly fatigue

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24
Q

type 2A muscle fibers

A

thick, intermediate speed, intermediate force, intermediate fatiguability

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25
Q

type 2B muscle fibers

A

thick, fast, high force, and rapidly fatiguable

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26
Q

slow sustained exercise increases the proportion of which types of muscles?

A

type 1

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27
Q

short high intensity exercise increases the proportions of which types of muscles?

A

type 2 => A and B

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28
Q

motor unit

A

motor neuron and the muscle fibers it innervates

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29
Q

muscle groups with fine dexterity

A

(hands, face) have smaller motor units ⇒ more neurons devoted to these areas with fine level control than other types

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30
Q

course control muscles

A

(thighs, back) have large motor units

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31
Q

lower motor neurons are controlled by? (2)

A
  1. local circuits
  2. upper motor neurons
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32
Q

local circuits

A

LMN’s
- sensory neurons (reflexes)
- interneurons in the spinal cord

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33
Q

upper motor neurons contain? (2)

A
  1. cortical (pyramidal tracts) control
  2. noncortical control
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34
Q

cortical (pyramidal tracts) control

A

mostly voluntary motor control

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35
Q

noncortical control

A

mostly non voluntary motor control

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36
Q

types of noncortical control

A
  1. Vestibular nuclei
  2. Superior colliculus
  3. Red nucleus
  4. Reticular formation of the pons and medulla
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37
Q

reflex circuits

A

local and fast that don’t need a signal to come from the brain
- Triggers relapse circuits that go to the spinal cord and back out to the periphery as a reflex due to it happening so fast

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38
Q

why don’t reflex circuits use the brain?

A

If the brain came in to play it would be too slow

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39
Q

How does the motor cortex influence movement?

A

biggest descending input to lower motor neurons comes from upper motor neurons in layer V of the primary motor cortex

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40
Q

where is the primary motor cortex and what is it necessary for?

A

on the precentral gyrus of the frontal lobe
- necessary for voluntary movements
- organized somatotropically so more space is given to face and hands

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41
Q

what does the upper medial of the motor cortex control?

A

the lower body
- as you move down you get to hands and face

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42
Q

premotor cortex

A

essential for planning movements and executing learned movements
- your body is one step ahead of what movement you will do next

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43
Q

how does somatosensory cortex and association cortexes influence movement?

A

integrating other sense into movement and planning (such as somatosensation)

44
Q

how is the thalamus involved in movement?

A

relays basal ganglia and cerebellar information for movement coordination

45
Q

corticobulbar tract

A

control head and neck muscles ⇒ reference to brainstem

46
Q

components of the corticobulbar tract

A
  • Bilateral brainstem cranial nerve motor nuclei
  • Targets LMNs in cranial nerve nuclei in brainstem
  • All cranial nerves except olfactory, optic, and vestibulocochlear have a motor function
  • Control of the eyes, face, mouth, larynx, and neck
47
Q

corticospinal tract

A

control body/limb muscles

48
Q

components of the corticospinal tract?

A
  • lateral
  • ventral/anterior
  • Descending route from motor and premotor cortex
49
Q

lateral corticospinal tract

A

to entire contralateral spinal cord (mostly limb)
- Lateral tract crosses the midline (decussation)in lower medulla

50
Q

what is the descending route from the motor and premotor cortex through the corticospinal tract? (4)

A
  • Internal capsule
  • Cerebral peduncle (midbrain)
  • Pons
  • Pyramids (medulla)
51
Q

ventral/anterior corticospinal tract

A

to bilateral cervical and upper thoracic spinal cord ⇒ mostly central body
- ventral/anterior tract descends uncrossed
- controls muscles on both sides of the body compared to lateral which is contralateral
- depending on damage, it may affect different muscle groups ⇒ lateralization vs not

52
Q

everything neck down is controlled by which tract?

A

corticospinal tract

53
Q

initiation of voluntary movement control comes from what?

A

upper motor neurons

54
Q

internal capsule

A

white matter tract in the brain that helps connect parts of the brain including the cortex
- The descending motor system is important coming from the primary motor cortex

55
Q

where does the internal capsule tract go?

A

They keep going to the cerebral peduncle which is another band of axon fibers connecting the brainstem and the cerebrum together

56
Q

are more neurons in the lateral corticospinal tract or the ventral?

A

more neurons in the lateral

57
Q

where does the corticospinal tract cross the midline and synapse on?

A

crosses the midline at the lower medulla, descends in the spinal cord, and synapses on LMNs in the ventral horn of the spinal cord ⇒ go down the other side of the spinal cord

58
Q

what does the lateral corticospinal tract mainly control?

A

limb muscles

59
Q

how do LMNs receive information via the corticospinal tract?

A

the muscles are receiving information in a very controlled and specific way (lateral on outside and midline on inside)
LMNs for limb muscles are in the lateral ventral horn (targeted by the lateral corticospinal tract)
- LMNs for the trunk muscles are in the medial ventral horn (targeted by the ventral/anterior corticospinal tract)

60
Q

damage to the motor cortex produces paralysis ___ vs. damage to the spinal cord produces paralysis primarily ____

A

contralateral; ipsilateral

61
Q

4 non pyramidal motor pathways for unconscious movements?

A
  1. rubrospinal
  2. vestibulospinal
  3. reticulospinal
  4. tectospinal
    → mixture of crossed and uncrossed pathways
62
Q

rubrospinal tract

A

red nucleus to spinal cord for coordinating fine limb movements

63
Q

vestibulospinal tract

A

vestibular nucleus to spinal cord for balance and head position adjustment

64
Q

reticulospinal tract

A

reticular formation to spinal cord for postural control and learned limb movements

65
Q

tectospinal tract

A

superior colliculus to cervical spinal cord for coordinating head and eye movements

66
Q

amyotrophic lateral sclerosis (ASL) aka Lou Gehrig’s disease

A

progressive loss of motor control due to degeneration
- Symptoms follow from which motor neurons die

67
Q

primary lateral sclerosis

A

affects only UMNs

68
Q

progressive muscle atrophy

A

affects only LMNs

69
Q

paralytic polio

A

motor neurons are directly targeted and killed by the virus, causing muscle atrophy and paralysis

70
Q

basal ganglia

A

subcortical nuclei critical for information processing related to decision making and movement selection (diencephalon)

71
Q

components of the basal ganglia function (3)

A
  • Sit in the middle of the brain under cortex
  • Relay and process information but also regulate output as the animal experiences the world
  • Important for decision making, movement, action, motivation, learning, etc.
72
Q

structures in the basal ganglia (4)

A
  • striatum (caudate, putamen, nucleus)
  • globus pallidus
  • sub thalamic nucleus
  • substantia nigra
73
Q

what is the main input and output to and from the basal ganglia?

A

input is from the cortex and main output is thalamus

74
Q

general functions of the basal ganglia (3)

A
  • Voluntary movements and action selection
  • Skill learning
  • Motivation and emotion ⇒ to express this we must move
75
Q

where is the nucleus accumbens?

A

only present in the anterior/rostral striatum

76
Q

striatum

A

receives dense inputs from cortex and dopamine neurons in the midbrain
- anterior and a big entry part for BG

77
Q

internal capsule

A

divides the striatum and is a white matter tract with axons from cortex

78
Q

2 divisions of the globus pallidus?

A
  1. external (GPe) => intrinsic nucleus
  2. internal (GPi) => part of the output of the basal ganglia
79
Q

globus pallidus

A

control conscious and proprioceptive movements
lies medial to the putamen and is part of the diencephalon

80
Q

2 divisions of the substantial nigra?

A
  • pars compacta (SNc) => major dopamine center
  • pars reticulata (SNr) => part of the output of the basal ganglia
81
Q

substantia nigra

A

important for connectivity and communication
- part of the midbrain/mesencephalon
- positioned between the subthalamic nucleus and cerebral peduncle
- dopamine neurons are concentrated in the SNc where they project to the dorsal striatum
- SNc dopamine neurons contain high levels of neuromelanin, pigment them black/brown

82
Q

where is the striatum located compared to substantial nigra and sub thalamic nucleus

A

striatum is telencephalon and the other two are in the diencephalon

83
Q

where in the basal ganglia do cortical neurons project to?

A

to the striatum and then to the internal unit which has specific output to the thalamus (SNr and GPi)

84
Q

corticostriatal neurons

A

signal with glutamate to excite medium spiny neurons (MSNs) in the striatum ⇒ excitatory cortex info

85
Q

striatal MSN’s

A

project to multiple BG structures for information processing
- MSNs signal with GABA to inhibit target neurons
- Dopamine input from SNc can modify MSN activity ⇒ different kind of neurotransmitter that sends dopamine (can have different effects) => excitatory via D1Rs and inhibitory via D2Rs

86
Q

what are the main output centers for the BG?

A

the GPi and SNr which signal ventral anterior and ventral lateral nuclei of the thalamus with GABA

87
Q

what integrates BG signals and sends excitatory projections to the cortex; what is it critical for?

A

the thalamus
- Activity in cortico-strioato-thalamic loops is critical for movement and control and basic learning/motivational processes

88
Q

general functions of the basal ganglia? (3)

A
  • learning
  • motivation
  • action selection
89
Q

what can BG pathology result in?

A

cognitive and learning deficits that contribute to psychiatric diseases

90
Q

hypokinesia

A

reduced movements

91
Q

akinesia

A

impaired initiation ⇒ can’t start a movement vs expression as it moves

92
Q

bradykinesia

A

slowed and reduced ⇒ cannot make fluid movements vs control

93
Q

rigidity

A

stiffness and resistance

94
Q

hyperkinesia

A

increased movements

95
Q

chorea

A

rapid/jerky movements

96
Q

athetosis

A

slow writhing

97
Q

ballism

A

flailing

98
Q

nigrostriatal dopamine neurons

A

are concentrated in the SNc, where they project to the dorsal striatum
- Goes from SNc to striatum in the caudate and putamen area
- These are what die off in parkinson’s disease

99
Q

Parkinson’s disease

A

(hypokinesia) symptoms arise from degeneration of dopamine neurons in substantia nigra pars compacta ⇒ substantia nigra are the dark band (light in parkinson’s bc they died)

100
Q

symptoms of Parkinson’s

A

(dopamine neuron dies) Impaired movement in 1% of people over 60
- Akinesia
- Bradykinesia
- Resting tremor
- Muscle rigidity

101
Q

Oral levodopa (L-DOPA)

A

dopamine precursor molecule that crosses the blood brain barrier and is converted to dopamine
- Less effective in late stage Parkinson’s and can produce unwanted involuntary movements
- Parkinsons has no cure but there are treatment options that improve motor control

102
Q

deep brain stimulation

A

surgical treatment for Parkinson’s, OCD, and other diseases
- Stimulating electrodes are implanted usually into the GPi or subthalamic nucleus
- Can restore movement control in Parkinson’s patients

103
Q

Huntington’s

A

degeneration of medium spiny neurons in striatum ⇒ dying of striatal neurons
- Genetic origin from inheritance of a dominant mutation producing a mutant protein that kills MSNs
- Produces hyperkinesia ⇒ involuntary random, rapid movements
- Gets worse over time and ends up being deadly

104
Q

tourettes syndrome

A

dysfunction in striatal and frontal cortical circuits ⇒ hyperkinesia (more promising research)

105
Q

dystonia

A

uncontrollable sustained muscle rigidity and contortions

106
Q

how do most BG diseases progress?

A

from motor impairments to cognitive/decision making deficits
- basal ganglia systems are critical for learning, reward, cognition, in addition to movement

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