unit 3 Flashcards
1
Q
what does each muscle contain
A
hundreds of muscle fibers (muscle cells)
2
Q
how are muscle fiber organized?
A
into fascicles surrounded by connective tissue
3
Q
muscle are attached to
A
bones
4
Q
what are the two types of muscles?
A
striated and smooth
5
Q
striated muscles
A
(striped) cardiac and skeletal muscle control function of the heart (involuntary) and movement of body (voluntary)
6
Q
smooth muscle
A
line organs such as blood vessels, the guts and lungs (involuntary)
7
Q
somatic motor system controls
A
voluntary muscle cells
8
Q
autonomic motor system controls
A
involuntary muscle cells
9
Q
why do skeletal muscles have stripes/striations?
A
due to the presence of a repeating contractile unit - the sarcomere
10
Q
layout of the somatic motor system
A
2 neuron chain; upper and lower motor neurons
11
Q
UPPER motor neuron
A
found in primary motor cortex (frontal lobe)
activates LOWER motor neuron by releasing glutamate
12
Q
LOWER motor neuron
A
found in ventral horn of spinal cord (controls body movement) and brainstem (facial movement - cranial nerve)
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
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
15
Q
dorsal root/horn
A
incoming sensory info from periphery
16
Q
ventral root/horn
A
outgoing motor info to the periphery; contains 2 types of motor neurons - alpha and gamma
17
Q
white matter
A
info from UPPER motor neuron descends through white matter in spinal cord to LOWER
18
Q
periphery nerves have both motor and sensory info because…
A
ventral and dorsal root come together into one
19
Q
cervical
A
upper extremity
20
Q
thoratic
A
trunk
21
Q
lumbar and sacral
A
lower extremity
22
Q
nerve plexus
A
intertwining of spinal nerves in PNS
23
Q
brachial plexus
A
motor and sensory to upper extremity
24
Q
lumbosacral plexus
A
motor and sensory to lower extremity
25
Upper and lower extremity muscle
appendicular muscle
26
trunk muscle
axial muscle
27
why is the size (relative) and shape of the ventral horn in the spinal cord relevent?
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
28
signaling at NMJ
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
29
when ap propagates down t-tubule of muscle cells causes
calcium release from sarcoplasmic reticulum (via RYR) with help from DHP receptor on t-tubule (VG)
30
increased cytoplasmic calcium stimulates
shortening of sarcomere
31
calcium binds to...
troponin, causing a conformational change that exposes the myosin binding site on actin
32
exposing the myosin binding site on actin allows
myosin motor protein to interact with actin, ultimate resulting in shortening of sarcomere = CONTRACTION
33
flexion
making angle between two joints smaller
33
how does motor system facilitate movement?
muscle shortening/changing of joint position
34
extension
making angle between two joints bigger
35
muscles work in pairs
agonist and antagonist muscles
36
example: flex elbow
activate biceps = agonist
inhibit triceps = antagonist
37
frequency of motor neuron firing
increased AP frequency = increased muscle force (twitch vs. sustained contraction)
38
recruit additional synergic motor units
can increase activation of muscles
39
motor unit
an alpha motor neuron and all muscle fibers (cells) it innervates
40
recruit larger motor units
can increase activation of muscles
41
graded control of muscle function involves
frequency of motor neuron firing, recruiting addition and larger synergic motor neurons
42
synaptic input to alpha motor neurons
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
43
patellar (knee) tap
stretches muscle spindles, LOWER motor neuron activates quad muscles, inhibition of hamstrings (antagonist) muscles occurs via inhibitory interneuron
44
alpha lower motor neuron
bigger in diameter; activating skeletal muscle (extrafusal muscle)
45
gamma lower motor neuron
innervate muscles in muscle spindle (intrafusal muscle)
modulate the sensitively of muscle spindle to stretch by controlling intrafusal muscle
46
why is the gamma motor neuron important
when skeletal muscle contracts, muscle spindle gets squished so gamma keeps shape of muscle spindle so it can do it's job
47
prefrontal cortex
how should I behave/decide?
48
premotor cortex
area 6; how to move - "motor plan"; has the PMA and SMA; needs more stimulation but PMA and SMA can also activate movement
49
PMA controlled
distal musculature
50
SMA
proximal musculature
51
primary motor cortex (M1)
area 4; executing movement; requires the lowest level of stimulation to activate a particular movement
52
role of area 6 in motor planning
neurons in SMA area activate just before execution of a movement
identification of mirror neurons in PMA of monkey
53
how many layers does the primary motor cortex have?
6
54
in which layer are projection cells found in the primary motor cortex?
layer 5
55
how can you tell the areas of specific slices of the brain?
by the kind/density of neurons that are in it
56
somatotopic organization of motor cortex
motor homunculus (visual way); shows areas and size
57
who 'discovered' the motor homunculus?
wilder penfield
58
lateral corticospinal tract (LCST) function and location
voluntary appendicular movement
cell bodies in primary motor cortex and premotor cortex
also contains axons from primary somatosensory cortex
59
why does the LCST contain axons from primary somatosensory cortex?
sensorimotor cortex
60
LCST Pathway
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
61
LCST lesion
"upper motor neuron syndrome"
62
what are the symptoms of LCST lesion?
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
63
LCST lesion placement importance
lesion can happen in numerous different places in pathway so it can have ipsilateral or contralateral depending.
64
lateral (corticospinal and rubrospinal tracts) pathways
voluntary movement of distal (far away)/appendage muscle (appendicular muscles)
65
distal muscles
limbs/far away
66
proximal muscles
torso and close to midline
67
appendicular muscles
appendages/limbs
68
axial muscles
torso/neck and head
69
ventromedial
postural control (axial muscles) and locomotion
70
tracts
collection of axons
71
corticobulbar tract function
voluntary facial movement; CN III and VII
same pathway as LCST but synapses in brainstem
72
corticobulbar tract pathway
i. cell in motor cortex
ii. axon descends through fiber bundles in corticobulbar tract
iii. synapses in brainstem
73
corticobulbar tract decussation
depending on which cranial nerve activating, decussation may or may not occur depending on such cranial nerve
74
anterior corticospinal (ACST) function
postural control; axial muscles
75
ACST pathway
i. cell in motor cortex
ii. axon descends through fiber bundles
iii. decussation and synapse in ventral horn of spinal cord
76
ACST decussation importance
decussates at spinal cord to provide bilateral input to lower motor neurons that innervate axial muscles --> postural control
77
rubrospinal tract (RST) function
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
78
RST pathway
i. 'begins' in red nucleus (brainstem)
ii. axons decussate immediately and descend through RST
iii. synapse in spinal cord
79
vestibulospinal tract function
regulates posture in response to vestibular input
80
vestibulospinal tract start
vestibular nucleus
81
vestibulospinal tract end/project target
regions of spinal cord to maintain upright posture - BILATERAL
82
tectospinal tract function
reflexive orientation to visual and auditory stimulus
83
tectospinal tract start
superior colliculus (midbrain)
84
tectospinal tract end
decussation and synapse on LMN in cervical spinal cord
85
facial muscles
collection of motor neurons (nuclei) in brainstem send their axons out thru cranial nerves to activate muscles of head/neck
86
oculomotor nerve
III
87
facial nerve
VII
88
oculomotor nerve function
innervates 4/6 extraocular muscles
eye needs to be centered for light to hit retina, accommodation (lens shape),and pupillary size
89
facial nerve function
controls muscles of facial expression and stapedius muscle
90
facial nerve dysfunction
bells palsy: facial paralysis/dysfunction of CN VII
lower motor neuron synapses onto ipsilateral motor neurons - no decussator
91
what is the basal ganglia
a collection of nuclei in the DEEP GRAY MATTER (lots of parts put into one
92
basal ganglia is closer to the base of the brain than the surface... therefore...
basal
93
motor function of nuclei/basal ganglia
is to initiate, stop and fine tune movements
also has functions related to learning and cognition
94
striatum
caudate and putamen
input from cortex to basal ganglia (connects to GPI)
95
thalamus
subdivisions: ventral anterior (VA) and ventrolateral (VL)
excitatory input to supplemental motor area
96
thalamocortical excitation promotes...
initiation of desired movement (can also inhibit)
97
general layout of circuitry
cortex -> striatum -> GPI -> thalamus -> cortex
98
direct pathway function
enhances initiation of desired movements (GO signal)
99
direct pathway PATHWAY
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
disinhibition
turned off inhibition so activation
101
indirect pathway function
stopping a movement (NO GO)
102
indirect pathway PATHWAY
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
substantia nigra pars compacta (SNpc) and dopamine function
influences direct/indirect pathways by releasing dopamine into striatum
104
metabotropic dopamine receptors are...
differentially expressed on striatal neurons in indirect and direct pathway
105
D1
excitatory; expressed in DIRECT pathway striatal neurons --> increased cAMP
106
D2
inhibitory; expressed in INDIRECT pathway striatal neurons --> decreased cAMP
107
dopamine inhibits...
striatal neurons in indirect pathway
108
dopamine activates...
striatal neurons in direct pathway
109
with dopamine if want to move
activates direct --> GO (activated), inhibits indirect --> NO GO (inhibited) = GO
110
parkinson's
dopaminergic neurons die = slowed/hard to initiate movements; treatment with L-DOPA, dopamine precursor
111
cerebellum
laminar structure
gray-white-gray organization
diverse functions in motor and cognitive realm
112
cerebellum function
coordinating precise control of motor function via corticopontocerebellar pathway
113
how do we know what the cerebellum does
cerebellar lesions cause ataxia (clumbsiness)
114
cerebellum gets input from...
upper motor neurons and muscle spindle
115
cerebellum compares...
motor plan with sensory info (unconscious proprioception) to coordinate motor function
116
if cerebellum needs to correct motor plan
communicated with M1 through Va/Vl thalamus
117
corticopontocerebellar pathway PATHWAY
i. cell in M1 activated neurons in pons
ii. pons activates neurons in cerebellum after decussation
118
corticopontocerebellar pathway function
sends info about motor plan to cerebellum
left M1 tells right cerebellum
119
how an diseases of the nervous system be classified
by cause and by symptoms
120
Classifying based on cause
genetic/familial, environmental (infectious), and gene and environmental/sporadic
120
Classifying based on symptoms
psychological, neurological, motor, sensory, motor and sensory
120
motor neuron diseases
are diseases that preferentially affects motor neurons, impacts ~5 in 100,000 individuals worldwide
120
motor neuron disease can cause
dysfunction of UMNs, LMNs, both or other components of motor systems (basal ganglia/cerebellum)
120
most motor neuron diseases are
sporadic/idiopathic
120
lower motor neuron syndrome
paresis or flaccid paralysis, muscle atrophy, fasciculations, fibrillations - EMG, areflexia or hyporeflexia
120
muscle atrophy
loss of muscle leading to its shrinking and weakening
121
fasciculations
muscle twitch
121
fibrillations - EMG
muscle cell firing abnormally - can only view thru EMG
122
areflexia
muscles don't respond to stimulus
123
hyporeflexia
muscles overreact to stimulus
124
upper motor syndrome
voluntary paresis (weakness), loss of RIFMS
due to dysfunction of a pathway originating in medulla: spasticity, hyperreflexia, clonus, babinski sign
125
spinal muscular atrophy (SMA)
autosomal recessive motor neuron disease with incidence of 1 in 11,000 livebirths - familial
most common genetic cause of childhood mortality
126
60% of SMA patients suffer from
severe form, infantile-onset type I
127
SMA is caused by
death of LMNs in ventral horn
128
SMA symptoms
weakness, muscle atrophy, paralysis and respiratory failure in late stages
129
95% of SMA cases are caused by (gene stuff)
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
amyotrophic lateral sclerosis (ALS)
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
ALS familia cases vs. sporadic
familial cases (fALS) are 10% and the rest are sporadic (sALS)
132
'lateral sclerosis'
death of UMNs in motor cortex results in demyelination of lateral corticospinal tract
133
pathological hallmarks of ALS
loss of UMNs and LMNs
the protein TDP-43 positive inclusion (clumping up) in amost all sporadic and most familial ALS
134
the formation of protein aggregates (clumping)
unifying feature of many neurodegenerative diseases
135
how did they find TDP-43 clumping?
immunohistochemistry
136
ALS clinical presentation/diagnosis
UMN symptoms, LMN symptoms, bublar symptoms
137
UMN symptoms for ALS
Babinski sign (foot reflex), hyperreflexia, spasticity, clonus
138
LMH symptoms for ALS
atrophy, fasciculations, fibrillations, hyporeflexia - often present as limb weakness
139
bulbar symptoms for ALS
tongue atrophy (CN XII), dysarthria, dysphagia, choking (late stage)
less common (20%)
140
most common presentation of ALS
(80%) involves UMN and LMN symptoms in limbs with neurodegenerative spreading to other areas as disease progresses
141
genetic basis of ALS
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
C9orf72
most commonly mutated
143
SOD1
encodes superoxide dismutase ->oxidative stress
144
TARDBP
encodes TDP-43; implicated in both ALS and FTD -> RNA transportation and binding
145
FUS
encodes fused in sarcoma -> RNA transportation and binding
146
potential pathogenic mechanisms of ALS
RNA transportation/binding impairments, oxidative stress, reduced GLUT reuptake, secretion of neurotoxic facto by reactive A1 astrocytes
147
RNA transport/binding impairments
need to have RNA localized at axon because of length of motor neurons
148
oxidative stress
SOD1 is endogenous and antioxidant that neutralizes superoxide - ROS
149
reduced GLUT reuptake
excitotoxicity: overstimulation of NMDA receptors leads to increased Ca2+ an can lead to increased levels of ROS
150
what system is the visceral motor system a part of?
autonomic system
151
what is the visceral motor system?
controls organs by acting on smooth muscle in the wall of organs/cardiac muscle
152
where as smooth muscles found?
in the gastrointestinal tract, cardiovascular (blood vessels), respiratory tract, sensory: ciliary muscles and iris
153
which systems are CN III involved in
both voluntary and involuntary
154
what ion is smooth muscle activation dependent upon and what structure does it come from?
Ca2+; sarcoplasmic reticulum
155
path for activating smooth and cardiac muscles
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
how many neurons do the sympathetic and parasympathetic systems have
2 neuron systems: pre and post-ganglionic neurons
157
sympathetic system has
a short pre- and long post- neurons
158
where are the pre-ganglionic neurons in the sympathetic system
in the lateral horn of the thoracolumbar region of the spinal cord
159
thoracolumbar region
in thoratic and part of lumbar spinal cord (middle of it)
160
where are the post- neurons of the sympathetic nervous system
just outside the spinal cord in the sympathetic chain ganglion
161
sympathetic pre- to post- synapse
ACh released onto nAChR
Na+ influx -> DEPOLARIZATION/EXCITATION onto post-
162
sympathetic post- to target organ synapse
stimulate target organ with norepinephrine using metabotropic adrenergic receptor
163
parasympathetic system has
a long pre-ganglionic and short post-ganglionic neuron
164
where are the parasympathetic pre- neurons
found in the craniosacral regions of NS
165
craniosacral region
cranio = brainstem and sacral = bottom of spinal cord
166
where are parasympathetic post- neurons
found within the wall of target organ and synapse onto it
167
CNs in parasympathetic
III - oculomotor
X - vagus
168
vagus nerve
X - controls most organs
169
parasympathetic pre- to post- synapse
ACh released onto nAChR; Na+ influx = depolarization/excitation onto post-
170
parasympathetic post- to target organ synapse
synapse onto target organ ACh with mAChR
171
nicotinic ACh receptors
ionotropic, ligand-gated, change membrane potential via ionic currents (Na+ influx) = ACT FASTER
used in both systems on post- neuron
172
muscarinic ACh receptors
used in parasympathetic nervous system
metabotropic, couples to g-proteins, involve 2nd messenger activation - signal amplification = act slower
173
which mAChR are stimulatory
Gaq coupled
M1R, M3R, M5R
174
which mAChR are inhibitory
Gai coupled
M2R, M4R
175
what special about M1, 4, and 5 receptors
found primarily in brain/CNS
176
M3R
Gaq; causes smooth muscle contractions
177
how does M3R stimulate digestion in the gut
peristalsis
178
how does M3R work in the lungs
bronchoconstriction
179
M2R
Gai; slows heart rate
180
how does Gai coupled with M2R work
have Gai,b,y
i. beta and gamma (ligand-gated) will stimulate K+ channel
ii. K+ leaves cell = HYPERPOLARIZATION = decreased heart rate
181
adrenergic receptors
used in sympathetic system
AR respond to epinephrine and norepinephrine
intracellular effect mediated by g-protein coupled receptors
182
where does epinephrine come from
adrenal gland
183
Gas -->
increase AC --> increase cAMP
184
Gai -->
decrease AC --> decrease cAMP
185
what do ai AR do
smooth muscle contraction; coupled to Gaq
will cause vasoconstriction = increase BP = decrease blood flow - also cause hair to stand up, pupils widen, etc
186
where are ai AR found
in blood vessels in skin and GI tract
187
what do B2 AR do
smooth muscle relaxation; increase blood flow; cause bronchodilation
188
where are B2 AR found
found in blood vessels in skeletal muscle to increase blood flow
189
how can epinephrine and norepinephrine stimulate cardiac function
by binding B1 receptors in heart
190
central control of autonomic function
brain has control; numerous parts. ex: hypothalamus
191
visceral nervous system has efferent and afferent components because
can tell brain somethings wrong and fix it = reflexes
