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Neurobio > unit 3 > Flashcards

unit 3 Flashcards

1
Q

what does each muscle contain

A

hundreds of muscle fibers (muscle cells)

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2
Q

how are muscle fiber organized?

A

into fascicles surrounded by connective tissue

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3
Q

muscle are attached to

A

bones

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4
Q

what are the two types of muscles?

A

striated and smooth

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5
Q

striated muscles

A

(striped) cardiac and skeletal muscle control function of the heart (involuntary) and movement of body (voluntary)

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6
Q

smooth muscle

A

line organs such as blood vessels, the guts and lungs (involuntary)

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7
Q

somatic motor system controls

A

voluntary muscle cells

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8
Q

autonomic motor system controls

A

involuntary muscle cells

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9
Q

why do skeletal muscles have stripes/striations?

A

due to the presence of a repeating contractile unit - the sarcomere

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10
Q

layout of the somatic motor system

A

2 neuron chain; upper and lower motor neurons

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11
Q

UPPER motor neuron

A

found in primary motor cortex (frontal lobe)
activates LOWER motor neuron by releasing glutamate

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12
Q

LOWER motor neuron

A

found in ventral horn of spinal cord (controls body movement) and brainstem (facial movement - cranial nerve)

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13
Q

LOWER motor neuron process

A

activates muscle cell by releasing ACh into skeletal muscle cells at the neuromuscular junction
mediated by activation of nicotinic receptors at NMJ
causes an influx of Na+ causing an EPSP = depolarization

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14
Q

why is there an influx of Na+ in nicotinic receptors?

A

other ions can flow through nonselective receptor (nicotinic receptor) BUT because Na+ has greater driving force and permeability its the primary ion

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15
Q

dorsal root/horn

A

incoming sensory info from periphery

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16
Q

ventral root/horn

A

outgoing motor info to the periphery; contains 2 types of motor neurons - alpha and gamma

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17
Q

white matter

A

info from UPPER motor neuron descends through white matter in spinal cord to LOWER

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18
Q

periphery nerves have both motor and sensory info because…

A

ventral and dorsal root come together into one

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19
Q

cervical

A

upper extremity

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20
Q

thoratic

A

trunk

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21
Q

lumbar and sacral

A

lower extremity

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22
Q

nerve plexus

A

intertwining of spinal nerves in PNS

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23
Q

brachial plexus

A

motor and sensory to upper extremity

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24
Q

lumbosacral plexus

A

motor and sensory to lower extremity

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25
Q

Upper and lower extremity muscle

A

appendicular muscle

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26
Q

trunk muscle

A

axial muscle

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27
Q

why is the size (relative) and shape of the ventral horn in the spinal cord relevent?

A

ventral horn in upper and lower extremities have a lot more to innervate
white matter: lot more in upper extremity vs. trunk and lower extremity BECAUSE all info travels through cervical region as it goes to and from CNS

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28
Q

signaling at NMJ

A

lower motor neurons release ACh
ACh binds to nicotinic ACh receptors; produces LARGE EPSP in muscle fiber
EPSP evokes muscle AP ALWAYS because of VG-channels
AP triggers Ca2+ release inside muscle fiber from the sarcoplasmic reticulum after traveling down t-tubule
fiber contracts
calcium reuptake (SERCA pump) puts Ca2+ back into sarcoplasmic reticulum

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29
Q

when ap propagates down t-tubule of muscle cells causes

A

calcium release from sarcoplasmic reticulum (via RYR) with help from DHP receptor on t-tubule (VG)

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30
Q

increased cytoplasmic calcium stimulates

A

shortening of sarcomere

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31
Q

calcium binds to…

A

troponin, causing a conformational change that exposes the myosin binding site on actin

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32
Q

exposing the myosin binding site on actin allows

A

myosin motor protein to interact with actin, ultimate resulting in shortening of sarcomere = CONTRACTION

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33
Q

flexion

A

making angle between two joints smaller

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33
Q

how does motor system facilitate movement?

A

muscle shortening/changing of joint position

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34
Q

extension

A

making angle between two joints bigger

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35
Q

muscles work in pairs

A

agonist and antagonist muscles

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36
Q

example: flex elbow

A

activate biceps = agonist
inhibit triceps = antagonist

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37
Q

frequency of motor neuron firing

A

increased AP frequency = increased muscle force (twitch vs. sustained contraction)

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38
Q

recruit additional synergic motor units

A

can increase activation of muscles

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39
Q

motor unit

A

an alpha motor neuron and all muscle fibers (cells) it innervates

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40
Q

recruit larger motor units

A

can increase activation of muscles

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41
Q

graded control of muscle function involves

A

frequency of motor neuron firing, recruiting addition and larger synergic motor neurons

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42
Q

synaptic input to alpha motor neurons

A

input from DRG axons from muscle spindle (1A) fibers initiates myotatic reflex, input from UPPER motor neurons, input from interneurons - local processing of motor information

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43
Q

patellar (knee) tap

A

stretches muscle spindles, LOWER motor neuron activates quad muscles, inhibition of hamstrings (antagonist) muscles occurs via inhibitory interneuron

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44
Q

alpha lower motor neuron

A

bigger in diameter; activating skeletal muscle (extrafusal muscle)

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45
Q

gamma lower motor neuron

A

innervate muscles in muscle spindle (intrafusal muscle)
modulate the sensitively of muscle spindle to stretch by controlling intrafusal muscle

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46
Q

why is the gamma motor neuron important

A

when skeletal muscle contracts, muscle spindle gets squished so gamma keeps shape of muscle spindle so it can do it’s job

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47
Q

prefrontal cortex

A

how should I behave/decide?

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48
Q

premotor cortex

A

area 6; how to move - “motor plan”; has the PMA and SMA; needs more stimulation but PMA and SMA can also activate movement

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49
Q

PMA controlled

A

distal musculature

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50
Q

SMA

A

proximal musculature

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51
Q

primary motor cortex (M1)

A

area 4; executing movement; requires the lowest level of stimulation to activate a particular movement

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52
Q

role of area 6 in motor planning

A

neurons in SMA area activate just before execution of a movement
identification of mirror neurons in PMA of monkey

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53
Q

how many layers does the primary motor cortex have?

A

6

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54
Q

in which layer are projection cells found in the primary motor cortex?

A

layer 5

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55
Q

how can you tell the areas of specific slices of the brain?

A

by the kind/density of neurons that are in it

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56
Q

somatotopic organization of motor cortex

A

motor homunculus (visual way); shows areas and size

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57
Q

who ‘discovered’ the motor homunculus?

A

wilder penfield

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58
Q

lateral corticospinal tract (LCST) function and location

A

voluntary appendicular movement
cell bodies in primary motor cortex and premotor cortex
also contains axons from primary somatosensory cortex

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59
Q

why does the LCST contain axons from primary somatosensory cortex?

A

sensorimotor cortex

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60
Q

LCST Pathway

A

i. cell in motor cortex
ii. axon descends through fiber bundles
iii. pyramidal decussation at bottom of brainstem/medulla
iv. descending in LCST
v. synapse in ventral horn of spinal cord

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61
Q

LCST lesion

A

“upper motor neuron syndrome”

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62
Q

what are the symptoms of LCST lesion?

A

NOT PARALYSIS; weakness, slowed movements that are less accurate and coordinated, loss of RISFMS (rapid individual finger movement), spasticity, hyperflexia, clonus, babinski sign
sometimes gradual improvement of syndrome over time

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63
Q

LCST lesion placement importance

A

lesion can happen in numerous different places in pathway so it can have ipsilateral or contralateral depending.

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64
Q

lateral (corticospinal and rubrospinal tracts) pathways

A

voluntary movement of distal (far away)/appendage muscle (appendicular muscles)

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65
Q

distal muscles

A

limbs/far away

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66
Q

proximal muscles

A

torso and close to midline

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67
Q

appendicular muscles

A

appendages/limbs

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68
Q

axial muscles

A

torso/neck and head

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69
Q

ventromedial

A

postural control (axial muscles) and locomotion

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70
Q

tracts

A

collection of axons

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71
Q

corticobulbar tract function

A

voluntary facial movement; CN III and VII
same pathway as LCST but synapses in brainstem

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72
Q

corticobulbar tract pathway

A

i. cell in motor cortex
ii. axon descends through fiber bundles in corticobulbar tract
iii. synapses in brainstem

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73
Q

corticobulbar tract decussation

A

depending on which cranial nerve activating, decussation may or may not occur depending on such cranial nerve

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74
Q

anterior corticospinal (ACST) function

A

postural control; axial muscles

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75
Q

ACST pathway

A

i. cell in motor cortex
ii. axon descends through fiber bundles
iii. decussation and synapse in ventral horn of spinal cord

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76
Q

ACST decussation importance

A

decussates at spinal cord to provide bilateral input to lower motor neurons that innervate axial muscles –> postural control

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77
Q

rubrospinal tract (RST) function

A

voluntary appendicular movements
role of RST is minimal in humans because we have a much larger cortex than other animals - motor cortex provides significant input to red nucleus

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78
Q

RST pathway

A

i. ‘begins’ in red nucleus (brainstem)
ii. axons decussate immediately and descend through RST
iii. synapse in spinal cord

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79
Q

vestibulospinal tract function

A

regulates posture in response to vestibular input

80
Q

vestibulospinal tract start

A

vestibular nucleus

81
Q

vestibulospinal tract end/project target

A

regions of spinal cord to maintain upright posture - BILATERAL

82
Q

tectospinal tract function

A

reflexive orientation to visual and auditory stimulus

83
Q

tectospinal tract start

A

superior colliculus (midbrain)

84
Q

tectospinal tract end

A

decussation and synapse on LMN in cervical spinal cord

85
Q

facial muscles

A

collection of motor neurons (nuclei) in brainstem send their axons out thru cranial nerves to activate muscles of head/neck

86
Q

oculomotor nerve

A

III

87
Q

facial nerve

A

VII

88
Q

oculomotor nerve function

A

innervates 4/6 extraocular muscles
eye needs to be centered for light to hit retina, accommodation (lens shape),and pupillary size

89
Q

facial nerve function

A

controls muscles of facial expression and stapedius muscle

90
Q

facial nerve dysfunction

A

bells palsy: facial paralysis/dysfunction of CN VII
lower motor neuron synapses onto ipsilateral motor neurons - no decussator

91
Q

what is the basal ganglia

A

a collection of nuclei in the DEEP GRAY MATTER (lots of parts put into one

92
Q

basal ganglia is closer to the base of the brain than the surface… therefore…

A

basal

93
Q

motor function of nuclei/basal ganglia

A

is to initiate, stop and fine tune movements
also has functions related to learning and cognition

94
Q

striatum

A

caudate and putamen
input from cortex to basal ganglia (connects to GPI)

95
Q

thalamus

A

subdivisions: ventral anterior (VA) and ventrolateral (VL)
excitatory input to supplemental motor area

96
Q

thalamocortical excitation promotes…

A

initiation of desired movement (can also inhibit)

97
Q

general layout of circuitry

A

cortex -> striatum -> GPI -> thalamus -> cortex

98
Q

direct pathway function

A

enhances initiation of desired movements (GO signal)

99
Q

direct pathway PATHWAY

A

i. pre-frontal cortex stimulates striatum (activate) via glutamine connection
ii. striatum connects with GPI (inhibition) via GABA neuron
iii. GPI has GABA connextion with VL thalamus (activation)
iv. VL thalamus has glutamate project to pre-motor cortex (activation)
v. pre-motor cortex sends signal of motor output to spinal cord
————-> MOVEMENT

100
Q

disinhibition

A

turned off inhibition so activation

101
Q

indirect pathway function

A

stopping a movement (NO GO)

102
Q

indirect pathway PATHWAY

A

i. PFC has GLUT connections to striatum (activate)
ii. striatum sends GABA connection to GPE (inhibition)
iii. GPE sends GABA connection to STN (activate)
iv. STN sends GLUT connection to GPI (activate)
v. GPI sends GABA connection to VL thalamus (inhibition)
vi. VL thalamus sends GLUT connection to pre-motor cortex (inhibition)
————-> NO MOVEMENT

103
Q

substantia nigra pars compacta (SNpc) and dopamine function

A

influences direct/indirect pathways by releasing dopamine into striatum

104
Q

metabotropic dopamine receptors are…

A

differentially expressed on striatal neurons in indirect and direct pathway

105
Q

D1

A

excitatory; expressed in DIRECT pathway striatal neurons –> increased cAMP

106
Q

D2

A

inhibitory; expressed in INDIRECT pathway striatal neurons –> decreased cAMP

107
Q

dopamine inhibits…

A

striatal neurons in indirect pathway

108
Q

dopamine activates…

A

striatal neurons in direct pathway

109
Q

with dopamine if want to move

A

activates direct –> GO (activated), inhibits indirect –> NO GO (inhibited) = GO

110
Q

parkinson’s

A

dopaminergic neurons die = slowed/hard to initiate movements; treatment with L-DOPA, dopamine precursor

111
Q

cerebellum

A

laminar structure
gray-white-gray organization
diverse functions in motor and cognitive realm

112
Q

cerebellum function

A

coordinating precise control of motor function via corticopontocerebellar pathway

113
Q

how do we know what the cerebellum does

A

cerebellar lesions cause ataxia (clumbsiness)

114
Q

cerebellum gets input from…

A

upper motor neurons and muscle spindle

115
Q

cerebellum compares…

A

motor plan with sensory info (unconscious proprioception) to coordinate motor function

116
Q

if cerebellum needs to correct motor plan

A

communicated with M1 through Va/Vl thalamus

117
Q

corticopontocerebellar pathway PATHWAY

A

i. cell in M1 activated neurons in pons
ii. pons activates neurons in cerebellum after decussation

118
Q

corticopontocerebellar pathway function

A

sends info about motor plan to cerebellum
left M1 tells right cerebellum

119
Q

how an diseases of the nervous system be classified

A

by cause and by symptoms

120
Q

Classifying based on cause

A

genetic/familial, environmental (infectious), and gene and environmental/sporadic

120
Q

Classifying based on symptoms

A

psychological, neurological, motor, sensory, motor and sensory

120
Q

motor neuron diseases

A

are diseases that preferentially affects motor neurons, impacts ~5 in 100,000 individuals worldwide

120
Q

motor neuron disease can cause

A

dysfunction of UMNs, LMNs, both or other components of motor systems (basal ganglia/cerebellum)

120
Q

most motor neuron diseases are

A

sporadic/idiopathic

120
Q

lower motor neuron syndrome

A

paresis or flaccid paralysis, muscle atrophy, fasciculations, fibrillations - EMG, areflexia or hyporeflexia

120
Q

muscle atrophy

A

loss of muscle leading to its shrinking and weakening

121
Q

fasciculations

A

muscle twitch

121
Q

fibrillations - EMG

A

muscle cell firing abnormally - can only view thru EMG

122
Q

areflexia

A

muscles don’t respond to stimulus

123
Q

hyporeflexia

A

muscles overreact to stimulus

124
Q

upper motor syndrome

A

voluntary paresis (weakness), loss of RIFMS
due to dysfunction of a pathway originating in medulla: spasticity, hyperreflexia, clonus, babinski sign

125
Q

spinal muscular atrophy (SMA)

A

autosomal recessive motor neuron disease with incidence of 1 in 11,000 livebirths - familial
most common genetic cause of childhood mortality

126
Q

60% of SMA patients suffer from

A

severe form, infantile-onset type I

127
Q

SMA is caused by

A

death of LMNs in ventral horn

128
Q

SMA symptoms

A

weakness, muscle atrophy, paralysis and respiratory failure in late stages

129
Q

95% of SMA cases are caused by (gene stuff)

A

homozygous deletion of SMN 1 gene leading to deficient production of SMN production
SMN 2 gene, c.280 C>T results in exclusion of exon 7, causing production of truncated RNA leading to a mostly nonfunctional protein

130
Q

amyotrophic lateral sclerosis (ALS)

A

progressive and fatal neurodegenerative disease that causes death of UMNs and LMNs
has symptoms of both upper and lower motor neuron syndrome: muscle atrophy is key symptom

131
Q

ALS familia cases vs. sporadic

A

familial cases (fALS) are 10% and the rest are sporadic (sALS)

132
Q

‘lateral sclerosis’

A

death of UMNs in motor cortex results in demyelination of lateral corticospinal tract

133
Q

pathological hallmarks of ALS

A

loss of UMNs and LMNs
the protein TDP-43 positive inclusion (clumping up) in amost all sporadic and most familial ALS

134
Q

the formation of protein aggregates (clumping)

A

unifying feature of many neurodegenerative diseases

135
Q

how did they find TDP-43 clumping?

A

immunohistochemistry

136
Q

ALS clinical presentation/diagnosis

A

UMN symptoms, LMN symptoms, bublar symptoms

137
Q

UMN symptoms for ALS

A

Babinski sign (foot reflex), hyperreflexia, spasticity, clonus

138
Q

LMH symptoms for ALS

A

atrophy, fasciculations, fibrillations, hyporeflexia - often present as limb weakness

139
Q

bulbar symptoms for ALS

A

tongue atrophy (CN XII), dysarthria, dysphagia, choking (late stage)
less common (20%)

140
Q

most common presentation of ALS

A

(80%) involves UMN and LMN symptoms in limbs with neurodegenerative spreading to other areas as disease progresses

141
Q

genetic basis of ALS

A

mutations in C9orf72, SOD1, TARDBP, FUS
usually dominant variants/inheritance, genetic mutations can be gain of function, loss of function or both (usually both)
sporadic ALS: essentially know nothing

142
Q

C9orf72

A

most commonly mutated

143
Q

SOD1

A

encodes superoxide dismutase ->oxidative stress

144
Q

TARDBP

A

encodes TDP-43; implicated in both ALS and FTD -> RNA transportation and binding

145
Q

FUS

A

encodes fused in sarcoma -> RNA transportation and binding

146
Q

potential pathogenic mechanisms of ALS

A

RNA transportation/binding impairments, oxidative stress, reduced GLUT reuptake, secretion of neurotoxic facto by reactive A1 astrocytes

147
Q

RNA transport/binding impairments

A

need to have RNA localized at axon because of length of motor neurons

148
Q

oxidative stress

A

SOD1 is endogenous and antioxidant that neutralizes superoxide - ROS

149
Q

reduced GLUT reuptake

A

excitotoxicity: overstimulation of NMDA receptors leads to increased Ca2+ an can lead to increased levels of ROS

150
Q

what system is the visceral motor system a part of?

A

autonomic system

151
Q

what is the visceral motor system?

A

controls organs by acting on smooth muscle in the wall of organs/cardiac muscle

152
Q

where as smooth muscles found?

A

in the gastrointestinal tract, cardiovascular (blood vessels), respiratory tract, sensory: ciliary muscles and iris

153
Q

which systems are CN III involved in

A

both voluntary and involuntary

154
Q

what ion is smooth muscle activation dependent upon and what structure does it come from?

A

Ca2+; sarcoplasmic reticulum

155
Q

path for activating smooth and cardiac muscles

A

i. ACh with mAChR activates and Gaq unit dissociates
ii. dissociation activates PLC leading to an increase in IP3
iii. IP3-gated Ca2+ channels on sarcoplasmic reticulum open
iv. Ca2+ is released and CONTRACTION

156
Q

how many neurons do the sympathetic and parasympathetic systems have

A

2 neuron systems: pre and post-ganglionic neurons

157
Q

sympathetic system has

A

a short pre- and long post- neurons

158
Q

where are the pre-ganglionic neurons in the sympathetic system

A

in the lateral horn of the thoracolumbar region of the spinal cord

159
Q

thoracolumbar region

A

in thoratic and part of lumbar spinal cord (middle of it)

160
Q

where are the post- neurons of the sympathetic nervous system

A

just outside the spinal cord in the sympathetic chain ganglion

161
Q

sympathetic pre- to post- synapse

A

ACh released onto nAChR
Na+ influx -> DEPOLARIZATION/EXCITATION onto post-

162
Q

sympathetic post- to target organ synapse

A

stimulate target organ with norepinephrine using metabotropic adrenergic receptor

163
Q

parasympathetic system has

A

a long pre-ganglionic and short post-ganglionic neuron

164
Q

where are the parasympathetic pre- neurons

A

found in the craniosacral regions of NS

165
Q

craniosacral region

A

cranio = brainstem and sacral = bottom of spinal cord

166
Q

where are parasympathetic post- neurons

A

found within the wall of target organ and synapse onto it

167
Q

CNs in parasympathetic

A

III - oculomotor
X - vagus

168
Q

vagus nerve

A

X - controls most organs

169
Q

parasympathetic pre- to post- synapse

A

ACh released onto nAChR; Na+ influx = depolarization/excitation onto post-

170
Q

parasympathetic post- to target organ synapse

A

synapse onto target organ ACh with mAChR

171
Q

nicotinic ACh receptors

A

ionotropic, ligand-gated, change membrane potential via ionic currents (Na+ influx) = ACT FASTER
used in both systems on post- neuron

172
Q

muscarinic ACh receptors

A

used in parasympathetic nervous system
metabotropic, couples to g-proteins, involve 2nd messenger activation - signal amplification = act slower

173
Q

which mAChR are stimulatory

A

Gaq coupled
M1R, M3R, M5R

174
Q

which mAChR are inhibitory

A

Gai coupled
M2R, M4R

175
Q

what special about M1, 4, and 5 receptors

A

found primarily in brain/CNS

176
Q

M3R

A

Gaq; causes smooth muscle contractions

177
Q

how does M3R stimulate digestion in the gut

A

peristalsis

178
Q

how does M3R work in the lungs

A

bronchoconstriction

179
Q

M2R

A

Gai; slows heart rate

180
Q

how does Gai coupled with M2R work

A

have Gai,b,y
i. beta and gamma (ligand-gated) will stimulate K+ channel
ii. K+ leaves cell = HYPERPOLARIZATION = decreased heart rate

181
Q

adrenergic receptors

A

used in sympathetic system
AR respond to epinephrine and norepinephrine
intracellular effect mediated by g-protein coupled receptors

182
Q

where does epinephrine come from

A

adrenal gland

183
Q

Gas –>

A

increase AC –> increase cAMP

184
Q

Gai –>

A

decrease AC –> decrease cAMP

185
Q

what do ai AR do

A

smooth muscle contraction; coupled to Gaq
will cause vasoconstriction = increase BP = decrease blood flow - also cause hair to stand up, pupils widen, etc

186
Q

where are ai AR found

A

in blood vessels in skin and GI tract

187
Q

what do B2 AR do

A

smooth muscle relaxation; increase blood flow; cause bronchodilation

188
Q

where are B2 AR found

A

found in blood vessels in skeletal muscle to increase blood flow

189
Q

how can epinephrine and norepinephrine stimulate cardiac function

A

by binding B1 receptors in heart

190
Q

central control of autonomic function

A

brain has control; numerous parts. ex: hypothalamus

191
Q

visceral nervous system has efferent and afferent components because

A

can tell brain somethings wrong and fix it = reflexes

Neurobio (6 decks)

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