PHYS: Motor Systems + Skeletal Muscle Flashcards
1
Q
function of the posterior parietal cortex
A
- integrates sensory info and relays it to premotor and prefrontal cortices
2
Q
function of prefrontal cortex
A
- receives info from posterior parietal cortex
- makes decision to execute an action and communicates this to premotor cortex
3
Q
function of premotor cortex
A
- receives info from prefrontal cortex and plans the motor sequence
- communicates this to primary motor cortex
4
Q
primary motor cortex
A
- receives motor sequence from premotor cortex
- executes movement via UMNs, LMNs (alpha or gamma) > skeletal muscles
5
Q
2 main descending spinal tracts
A
- corticospinal: supplies body muscles
- corticobulbar: supplies face, head and neck muscles
6
Q
2 divisions of the corticospinal tract
A
- lateral (most fibres): supplies limb muscles
- anterior: supplies trunk muscles
7
Q
where are upper and lower motor neurons located?
A
- upper: originate in cerebral cortex or brainstem and synapse w/ LMN in motor nuclei of cranial nerves (brain stem) or ventral horn of spinal cord
- lower: nuclei of cranial nerves or ventral horn, terminate @ NMJ
8
Q
symptoms of an upper vs lower motor neuron lesion
A
- upper: hypertonia - spasticity (pyramidal), rigidity (extrapyramidal), hyperreflexia (inc. positive babinski reflex), clonus
- lower: hypotonia, hyporeflexia, muscle atrophy
9
Q
structure of the basal ganglia
A
- group of interconnected nuclei below the cerebral cortex:
- striatum (caudate and putamen)
- globus pallidus (internal and external) - suppresses movement
- subthalamic nucleus
- substantia nigra (pars reticulata and pars compacta)
10
Q
function of basal ganglia
A
- learn, plan and initiate voluntary movements
- evaluate rewards using previous experience
11
Q
direct and indirect pathways of basal ganglia
A
- direct: facilitates movement, inhibits global pallidus (normally suppresses movement) which allows thalamus to excite the motor cortex
- indirect: inhibits movement via longer pathway
12
Q
2 main types of symptoms re: damage to basal ganglia
A
- hyperkinetic: involuntary movement - reduced activity of the indirect (inhibitory) pathway e.g. Huntington’s chorea
- hypokinetic: increased activity of the indirect/inhibitory pathway e.g. Parkinson’s disease
13
Q
structure of cerebellum
A
- 2 lobes separated by vermis
- each lobe controls ipsilateral side of the body > damage causes ipsilateral loss of function
- grey matter on surface forms cerebellar cortex
14
Q
functions of cerebellum
A
- gait coordination
- maintenance of balance and posture
- muscle tone control and voluntary muscle activity
- REFINEMENT of motor commands to match sensory input (not initiation)
15
Q
motor unit vs motor pool
A
- unit: one alpha motor neuron + any muscle fibres that it innervates
- pool: one muscle + its associated nerves (consists of small and large motor units)
16
Q
alpha motor neurons:
- size
- myelination
- cell body location
- where are the cell bodies located for neurons that innervate more proximal muscles
A
- type of lower motor neuron
- larger
- more myelinated
- cell bodies in ventral horn
- a-motor neurons that innervate more proximal muscles have cell bodies more medially
17
Q
gamma motor neurons
- size
- myelination
- cell body location
- function
A
- type of lower motor neuron
- smaller
- less myelinated
- cell bodies in ventral horn
- involved in muscle spindles (proprioception)
18
Q
which motor units are more fatigue resistant?
A
- smaller are more fatigue resistant
- therefore can be activated for longer periods of time compared to large motor units
19
Q
classes of muscle fibres
- speed (+ fatigue resistance)
- force
- function
A
- type I: slow, low force, postural muscles
- type IIa: fast and fatigue resistant, moderate force, non-postural
- type IIb: fast and fatiguable, high force, non-postural muscles
20
Q
3 layers of skeletal muscle connective tissue
A
- epimysium: strong connective tissue around the entire muscle
- perimysium: bundles muscle fibres into fascicles (contains blood vessels and nerves)
- endomysium: surrounds individual muscle cells
21
Q
myofibril
A
- muscle fibres contain cylindrical myofibrils which contain actin and myosin microfilaments
22
Q
sarcoplasm
sarcolemma
A
- cytoplasm of a muscle fibre
- plasma membrane of a muscle fibre
23
Q
sarcomere
sarcoplasmic reticulum
A
- smallest contractile subunit which extends from one Z-line to the next
- specialised smooth ER of a muscle fibre - stores calcium
24
Q
2 major striations in skeletal muscle
A
- A bands (anisotropic): dark, where actin (thin) and myosin (thick) bands overlap
- I bands (isotropic): light, contain actin (thin) filaments but no myosin
25
Q
H band
M line
A
- H band: area where there is myosin only, between 2 A bands, shortens during contraction
- M line is in the middle of H band
26
Q
structure of actin
A
- globular G actin polymerises to form an F actin chain
- 2x F actin chains interweave to form helix-like actin filament
- each G actin monomer has cross-bridge binding sites for myosin - these are blocked by tropomyosin when the muscle isn’t contracting
27
Q
structure of troponin
A
- 3 binding sites: tnI, tnT, tnC
- tnI (inhibitory): binds to actin, keeping tropomyosin in place which blocks myosin from binding, to stop muscle contraction
- tnT: binds to tropomyosin
- tnC: binds to calcium, causing tropomyosin to unblock actin binding sites, allowing myosin to bind for muscle contraction
28
Q
structure of myosin
A
- 2 heads w/ 2 binding sites each (1 for ATP, one for actin)
- neck made of myosin light chains: provides flexibility to move heads
- tail: gives rigidity + support
29
Q
structure of titin
A
- elastic filament attached to Z lines
- runs thru myosin for support + rigidity
30
Q
T (transverse) tubule
A
- located @ A-I junction
- invagination of sarcolemma (plasma membrane) with membrane on each side called terminal cisternae (forms triad)
- allows for electrical impulses to pass through deep into muscle cell for rapid contractions
- allows Ca2+ to be spread from NMJ for uniform contraction of the entire muscle cell @ once
31
Q
what happens in rigor mortis re: muscle tightness?
A
- after death, ATP stops being produced = cross bridges can’t detach
- actin and myosin stay bound > muscle stays tight and contracted
32
Q
3 phases of a muscle contraction
A
- delay: time taken for AP to arrive @ NMJ including refractory period
- contraction
- relaxation
33
Q
2 ways to increase muscle contraction force
A
- recruitment of more motor units from small to large
- rate-coding: firing another AP before the first twitch is completed > another twitch with increased force (summation > rough/unfused tetanus > smooth/fused tetanus)
34
Q
fused vs unfused tetanus re: rate-coding
A
- unfused tetanus: when we increase the rate of AP firing, resulting in lots of little contractions (but still greater force)
- fused tetanus: if we keep increasing the rate of AP firing, it results in one sustained contraction b/c Ca hasn’t had time to go back into sarcoplasmic reticulum > actin and myosin cross bridges stay > muscle stays contracted
35
Q
is the AP or muscle twitch longer in duration?
A
muscle twitch
36
Q
isotonic and isometric movements
A
- isotonic: tone stays same, muscle length changes
> concentric: contraction during shortening
> eccentric: contraction during lengthening - isometric: length stays same, tone changes
37
Q
excitation-contraction coupling
A
- ACh reaches NMJ > depol
- AP travels along sarcolemma and T tubules
- DHP receptor on T tubule membrane activates ryanodine receptor (RyR) on sarcoplasmic reticulum, causing Ca2+ release
- Ca2+ binds to troponin → displaces tropomyosin → exposes binding sites → actin and myosin can bind and sarcomere shortens
38
Q
crossbridge cycling mechanism
A
- Ca2+ binds to troponin-C, displacing tropomyosin from actin binding sites
- myosin heads are in a high energy state since ATP is hydrolysed into ADP + Pi
- when myosin binds to actin, Pi is released, triggering power stroke (myosin pulls actin towards M line and shortens the sarcomere)
- a new ATP binds to myosin > detaches crossbridge, Ca2+ actively pumped back to sarcoplasmic reticulum
- tropomyosin moves back to block binding sites > muscle relaxation
