Nerve and Muscle Flashcards
1
Q
components of CNS
A
cerebral cortex
cerebellum
brainstem
spinal cord
2
Q
components of PNS
A
peripheral nerves
3
Q
neurons
A
10% of cells in CNS; 50% of volume
larger than glia
3 types: afferent, efferent, interneurons
4
Q
glia
A
90% of cells in CNS
provide physical and chemical support to neurons
5
Q
satellite cells
A
glial cells
provide structure/support isolating neurons from one another
6
Q
oligodendrocytes
A
glial cells
produce myelin in CNS
7
Q
Schwann cells
A
glial cells
produce myelin in the PNS
8
Q
radial glia
A
guide migrating neurons and direct axonal outgrowth during development
9
Q
astrocytes
A
glial cells
form the blood brain barrier
10
Q
afferent neurons
A
carry information from periphery to the spinal cord via dorsal roots
11
Q
efferent neurons
A
carry information from the spinal cord to the periphery via ventral roots
12
Q
interneurons
A
carry information between neurons
13
Q
spinal cord
A
contains white matter and grey matter
both dorsal horn (sensory) and ventral horn (motor)
14
Q
white matter
A
nerve fibres, glia
lots of axons - myelinated
15
Q
grey matter
A
neurons, glia, synapses
cell bodies - no myelin
16
Q
neuron structure
A
dendrites
cell body (nucleus)
axon hillock
axon
synaptic terminals
flow of information = down axon, away from cell body
17
Q
dendrites
A
receive stimuli through activation of chemically or mechanically gated ion channels
18
Q
cell body
A
receives stimuli and produces excitatory and inhibitory postsynaptic potentials through activation of chemically or mechanically gated ion channels
19
Q
axon hillock
A
trigger zone; integrates EPSPs and IPSPs → if sum causes depolarization that reaches threshold = initiation of action potential
site of action potential generation
20
Q
axon
A
propagates nerve impulses from initial segment to axon terminals in a self-reinforcing manner
impulse amplitude does not change as it propagates along the axon
21
Q
axon terminals
A
inflow of Ca2+ caused by depolarizing phase of nerve impulse triggers neurotransmitter release by exocytosis of synaptic vesicles
22
Q
types of neurons
A
anatomy of neuron is dictated by function
bipolar cell
pseudo-unipolar cell
multipolar cell
23
Q
bipolar cells
A
ex. retina
info from photoreceptors sent to retinal ganglion cells
24
Q
pseudo-unipolar cells
A
afferent neurons
ex. ganglion cell of dorsal root
no real dendrites; peripheral axon conducts input from skin and muscle to the cell body
central axon exists between cell body and axon terminals
25
multipolar cells
- motor - efferent - neuron of spinal cord (most typical representation of neuron)
- pyramidal cell of hippocampus
- purkinje cell of cerebellum
26
neuron structure
some neurons contain myelin sheath coating the axon = action potential is conducted faster
nodes of Ranvier are gaps in between myelin
27
membrane structure
phospholipid bilayer - impermeable barrier to ions
protein pumps and channels - control movement of ions through membrane
28
protein pumps
use energy by ATP hydrolysis for active transport
29
ion channels
are specific to ion
act as a door
do not require energy; move ions down electrochemical gradient
30
passive channels
leak channels
are open at rest
31
ligand-gated channels
closed at rest
ligand binds to receptor to open channel
32
voltage-gated channels
closed at rest
voltage change of neuron causes channel to open
33
resting membrane potential
steady state condition determined by relative permeability of membrane to to Na+ and K+
measure of electrical potential difference between intracellular environment and extracellular environment
resting membrane is approximately -70mV = inside the cell is ~70mV more negative than outside
34
Na+/K+ pump
sets net negative charge
electrogenic = moves charge across the membrane
requires energy (obtained from hydrolysis of ATP)
3Na+ molecules move out of cell and 2K+ molecules move in
35
mechanism of Na+/K+ pump
hydrolysis of ATP → P binds to pump on intracellular side = conformational change (close intracellular side of pump, open extracellular side)
3Na+ molecules are released outside of cell
2K+ molecules bind to inside of pump
phosphate is removed from binding site = conformational change (pump opens to inside of cell, closes to outside) → K+ moves into cell
36
Na+/K+ pump creates gradients
chemical: molecules want to maintain state of equilibrium
= K+ wants to diffuse out of cell; Na+ wants to diffuse into cell
electrical: intracellular environment wants to become more positive
37
leak channels
sets resting membrane
allow passive flow of ions into/out of neuron
selective for each ions
38
equilibrium potential
the membrane potential at which the chemical gradient is balanced
39
eq potential for K+
approximately -90mV
40
eq potential for Na+
approximately +60mV
41
membrane potential rule
the more permeant the ion, the greater its ability to force resting membrane potential towards its own equilibrium potential
more K+ leak channels than Na+
permeability is 50-100x greater to K+ than Na+
42
specific membrane resting potential
determined by specific proportion of Na+ and K+ leak channels
43
at resting membrane potential
passive ionic fluxes are balanced so that there is charge separation and Em remains constant
44
disruption of membrane potential
specific stimuli disrupt this steady state by causing ion-selective channels in membrane to open
44
action potential
large change in membrane potential from -70mV to +30mV and back to resting over a period of a few ms
45
generation of action potential
electrical signal is generated due to activity of voltage-gated Na+ and K+ channels
opening of channels = ions flow + membrane potential changes
46
activation of afferents
muscle stretch or other sensory stimuli → increased opening of specialized Na+ receptors
= entry of Na+ into afferent fibre and depolarization of afferent neuron
if Na+ entry is sufficient to depolarize the neuron to its threshold, the Na+ channels will open = action potentiak
47
activation gate
removed by depolarization
= allow Na+ to flow into cell
influx of Na+ into cells → brings membrane potential closer to Na+ equilibrium potential
48
inactivation gate
closes channel a few ms after opened
49
action potentials - summary
1. rest
2. depolarizing input
3. start of action potential - depolarization
4. repolarization phase
5. end of action potential
6. rest
50
1. rest
relative permeability: K+ >> Na+
51
2. depolarizing input
sensory or synaptic stimulus changes potential
relative permeability: increases to Na+
52
3. start of action potential - depolarization
Voltage-gated Na+ channels open
relative permeability: Na+ >>>> K+
53
4. repolarization phase
voltage gated K+ channels open and Na+ channels inactivate
relative permeability: K+ >>>> Na+
54
5. end of action potential
voltage gated Na+ channels at rest; voltage gated K+ channels still open
relative permeability: K+ >>>> Na+
55
6. rest
voltage gated K+ channels at rest
relative permeability: K+ >> Na+
56
action potentials: transmission
activation results in opening of voltage-gated Na+ channels = local depolarization of membrane
→ causes adjacent voltage-gated Na+ channels to activate
new action potential is generated in adjacent membrane
action potential only travels in one direction due to refractory period
57
electrotonic conduction
spread of current inside axon
action potential initiated at one point in membrane
current spreads electrotonically to adjacent membrane
adjacent membrane depolarizes to threshold
new action potential generated in adjacent membrane
58
speed of electrotonic conduction
current flow is fast but action potential must be regenerated at every point on the membrane = requires opening + closing of channels
slower than necessary for body functions
59
myelination
increases speed of action potential propagation
only axon is myelinated
60
myelin
fatty substance; acts as insulator → current can't escape through channels in membrane
formed from Schwann cells in PNS; oligodendrocytes in CNS
61
Nodes of Ranvier
small unmyelinated regions along axon
(myelination is discontinuous)
voltage-gated Na+ channels are clustered at nodes = where the action potential will need to be regenerated
62
Schwann cell ensheathing
single Schwann cell generates single myelinated segment
= many Schwann cells required to ensheath one axon in the peripheral nervous system
63
oligodendrocyte ensheathing
one oligodendrocyte ensheaths many axons in the CNS
a single oligodendrocyte lays down multiple segments of myelin on each fibre, on multiple fibres
64
saltatory conduction
action potential is regenerated at nodes of Ranvier
current flows electrotonically between the nodes
65
afferent fibre types
classification based on how fast they propagate action potentials:
- thickness of nerve fibre (axon)
- is it myelinated
66
group I afferent fibres
diameter: 12-20 microns
conduction speed: 20-120 m/s
sensory receptors: skeletal muscle proprioceptor (ex. stretch reflex)
67
group II afferent fibres
diameter: 6-12 microns
conduction speed: 35-75 m/s
sensory receptors: skin mechanoreceptor (touch/pressure afferents)
68
group III afferent fibres
diameter: 1-5 microns
conduction speed: 5-30 m/s
sensory receptors: pain/temperature (quick + sharp pain)
69
group IV afferent fibres
diameter: 0.2-1.5 microns
conduction speed: 0.5-2 m/s
sensory receptors: pain/itch/temperature (dull + throbbing pain)
70
why does action potential conduct in only one direction?
by the time the absolute refractory period is over, the action potential is between 2 and 20 cm down the axon
action potential conduction:
- myelinated axons = 12-130 m/s
- unmyelinated axons = 0.5-2 m/s
absolute refractory period lasts almost 2 ms
71
action potential transmission
sensory neuron fires action potential in response to physical stimulus → receptor potential → nerve ending is depolarized to threshold → action potential is generated in sensory neuron
72
electrical synaptic transmission
physical channel connects two cells; physical coupling
no neurotransmitters; movement of molecules between cells
synchronize large groups of neurons to fire, especially during development
fast
bidirectional - no clear pre or post synaptic cell
73
electrical synapses
gap junctions: small gap between the two cells is bridged by connexons → open or close to control the free flow of ions
communication between cytoplasm for sharing regulatory signals
inflexible - stereotypical behaviours, difficult to change response
74
chemical synaptic transmission
release and binding of neurotransmitters between cells
75
chemical synapses
much larger gap than electrical synapses
2 types:
- directly gated
- indirectly gated
flexible
inhibition, specificity, complexity, plasticity
76
directly gated chemical synapse
1. transmitter binds
2. receptor channel located directly on ion channel opens
3. ions pass through channel
receptor and effector are same molecule
effects: fast onset, short lasting
77
excitatory transmission
glutamate: excitatory neurotransmitter
Na+ (+ K+) channels open → ions enter cell
78
inhibitory transmission
GABA + glycine: inhibitory neurotransmitters
Cl- or K+ pass through = hyperpolarization of cell → no action potential
79
indirectly gated chemical synapse
1. transmitter binds
2. activation of second messenger system
GPCR → G proteins → adenylyl cyclase → cAMP = second messenger
3. cAMP activates protein kinases
→ phosphorylation of ion channel → opens/closes + change in membrane permeability
4. ion influx → depolarization or hyperpolarization
effects: slow onset, long lasting
receptor and effector are different molecules
80
ionotropic receptor
in directly gated synapses
receptor is located on ion channel
81
metabotropic receptor
in indirectly gated synapses
receptor is not directly located on effector; binding of transmitter induces intracellular cascade of events
82
chemical synapse specificity
specific transmitters have specific effects on postsynaptic membrane
83
chemical synapse complexity
response can vary in type, timecourse, strength, location, etc
84
chemical synapse plasticity
changes in synaptic structure and function associated with development, aging, learning, etc.
indirectly gated synaptic transmission
85
synaptic transmission
1. action potential arrives in presynaptic terminal
2. presynaptic terminal depolarizes
3. voltage-gated Ca2+ hannels open
4. Ca2+ influx into presynaptic terminal
5. Ca2+ causes synaptic vesicles to fuse with presynaptic membrane
6. transmitter released by exocytosis → diffuses across synapse → binds to receptor + opens ligand-gated ion channels
7. ions flow across membrane as dictated by their concentration gradients and depolarize or hyperpolarize postynaptic cell
8. transmitter removed from receptor → recycled or degraded
ion channel closes and PSP ends
86
excitatory presynaptic neuron
release of glutamate from presynaptic cell → binds to glutamate receptor on Na+ ion channel
channel opens → influx of Na+ = EPSP
87
EPSP
excitatory postsynaptic potential
small depolarization resulting from influx of Na+
subthreshold (requires many to reach depolarization threshold)
88
inhibitory presynaptic neuron
release of GABA or glycine from presynaptic cell → binds to Glu/gly receptor on Cl- ion channel
channel opens → influx of Cl- = IPSP
89
IPSP
inhibitory postsynaptic potential
small hyperpolarization resulting from influx of Cl-
prevents generation of action potential
90
synaptic potentials decay with distance
the potential of a depolarization loses amplitude as it travels down the dendrite - current leaks out membrane
the farther from the axon hillock the PSP's site of origin is, the smaller it will be once it reaches the axon
91
summation of PSPs
individually, a PSP is insufficient to generate an action potential
small PSPs can summate to reach threshold at axon hillock and trigger action potential
temporal and spatial summations occur simultaneously in the CNS
92
temporal summation
PSPs from single presynaptic axon overlap in time → add together
93
spatial summation
PSPs generated in different regions of the postsynaptic neuron are added together
the PSPs must also overlap in time
94
spatial summation of EPSP and IPSP
IPSP cancels out the EPSP = very small potential
95
synaptic integration
excitatory and inhibitory signals are integrated into a single response by the postsynaptic neuron
process of summing together all the inputs into an action potential output in the postsynaptic cell
96
PSPs vs APs
PSP:
graded ~1mV
msec-sec
dendrites and soma of postsynaptic cell
passive
AP:
all-or-none
msec
initiated at axon hillock
active
97
smooth muscle
walls of hollow organs
contraction reduces size of structures
not under voluntary control
98
cardiac muscle
striated muscle
walls of the heart
no under voluntary control
99
skeletal muscle
striated muscle
contraction is under voluntary control
100
motor neuron
stimulates skeletal muscle cells to contract
1 efferent contacts lots of muscle cells
101
motor unit
motorneuron + muscle fibres it activates
functional unit of motor system
smallest increment of force that can be generated
102
synaptic transmission at neuromuscular junction
1 action potential in motor neuron = generation of 1 action potential in muscle cell (no PSPs)
each muscle fiber is only innervated by one presynaptic axon
always release of excitatory NT = Acetylcholine
axons are not myelinated = electrotonic conduction
103
excitation contraction coupling
electrical signal of action potential is converted to mechanical force
104
neuromuscular junction at rest
polarized = resting membrane potential
negative in cell; positive outside of cell
105
release of acetylcholine
contained in vesicles
released into synaptic cleft by exocytosis
Ca2+ ions are pumped out of axon terminal
106
contraction of muscle cell
1. muscle action potential propagated down tranverse tubule → activates DHP receptor (bound to ryanodine receptor) = opening of Ca2+ channel
2. Ca2+ released from sarcoplasmic reticulum into cytosol of cell
107
DHP receptor
dihydropyridine receptor
voltage gated channel
108
muscle fiber
myofibrils contain muscle filaments
sarcolemma: muscle fiber membrane
sarcoplasmic reticulum wraps around myofibrils; transverse tubules are in between SR
109
sarcomere
segment of myofibril, in between two z disks
contains thick and thin filaments (alternate)
shortens during muscle contraction
110
H zone
space between thin filaments
muscle contraction = shortening of H zone
111
myosin
bundled together to form thick filaments
single molecule = tail + two globular heads (cross bridge)
112
myosin cross bridge
two binding sites: ATP and actin
low energy state = bent, ATP is bound
high energy state = flat, ATP is hydrolyzed into ADP + P
113
actin
primary component of thin filament
actin subunits are twisted into double helical chain
each subunit has myosin binding site
114
tropomyosin
regulatory protein
entwines actin
at rest: tropomyosin covers myosin binding sites on actin subunits = cross bridge cannot bind
115
troponin
attaches to tropomyosin strand
moves tropomyosin aside to expose myosin binding sites
has binding site for Ca2+
116
sliding filament theory of muscle contraction
1. influx of calcium triggers exposure of binding sites on actin
2. myosin binds to actin
3. power stroke of cross bridge
4. ATP binds to cross bridge → disconnects from actin
5. hydrolysis of ATP
6. transport of Ca2+ into SR
117
1. exposure of binding sites on actin
Ca2+ ions flood into cytosol after release from SR → bind to troponin = change in conformation of troponin-tropomyosin complex
→ exposes binding sites on actin
118
2. binding of myosin to actin
high energy state myosin = cross bridge can bind to exposed actin site
119
3. power stroke
ADP + P are released from cross bridge (myosin is in low energy state)
cross bridge flexes → pulls thin filament inward toward center of sarcomere
H-zone shortens
= chemical energy → mechanical energy
120
4. disconnection of cross bridge from actin
ATP molecule must bind to site on myosin cross bridge to release myosin from thin filament
121
5. hydrolysis of ATP
ATP is hydrolyzed → ADP + P
re-energizing + repositioning of cross bridge
myosin = high energy state
122
6. removal of Ca2+ ions
active transport from cytosol into SR by calcium pumps (membrane of SR) → energized by ATP
calcium is removed → troponin-tropomyosin complex covers binding sites on actin
123
multiple cross bridge cycles
during a contraction, all cross bridges are neither bound nor disconnected at the same time
124
role of ATP in muscle contraction
1. energizing power stroke
2. disconnecting cross bridge from actin
3. pumping Ca2+ back into SR
125
white muscle fiber
large
light in colour → reduced myoglobin
few capillaries
few mitochondria
high glycogen content
glycolysis: anaerobic process to generate large amounts of ATP fast
quickly depleted
126
red muscle fiber
half the diameter of white fibers
dark red → lots of myoglobin
many capillaries
lots of mitochondria
low glycogen content
oxidative phosphorylation + Krebs cycle: aerobic processes to generate ATP (slower process)
slower deletion of ATP
127
fast twitch fibers
white muscle fibers
power and speed; short duration
glycolysis = quick synthesis of ATP
fast contractions
large number of myofilaments
fatigue rapidly - build up of lactic acid, depletion of glycogen
128
slow twitch fibers
red muscle fibers
endurance, continuous contraction
Krebs cycle + oxidative phosphorylation
slower contractions
