Notesale: Turn your study into money

Document Preview

Extracts from the notes are below, to see the PDF you'll receive please use the links above

---

BIO 3P3 EXAM WITH VERIFIED AND
CORRECT ANSWERS
...
= distance from S1 to S2/(ts2 - ts1)

Duchenne Muscular Dystrophy (DMD) - CorreCt Answers -point mutation
or deletion of gene for dystrophin protein (x-linked recessive)

dystrophin acts as shock absorbed during contraction

Why is Ca2+ a good 2nd messenger? - CorreCt Answers -small influxes of
Ca2+ lead to rapid & dramatic changes in intracellular [Ca2+]

Plasma membrane Ca2+ transports - CorreCt Answers -PMCA, NCX
exchanger, voltage-gated Ca2+ channels

Mitochondria Ca2+ transports - CorreCt Answers -calcium uniporter
(MCU) - brings Ca2+ into matrix 2Na:1Ca exchanger - releases Ca2+ from
matrix
Ca:2H exchanger

SR Ca2+ transports - CorreCt Answers -Ca2+ channels (for release)
SERCA (for reuptake)

SERCA vs
...
Increase in [Ca] causes
Ca2+ to bind to MICU & open MCU

Low affinity mechanisms for transporting bulk amounts of Ca2+ (fast &
urgent) - CorreCt Answers -exchangers, channels & uniporters

high affinity, fine-tuning transport of Ca - CorreCt Answers -ATPases

mitochondrial dysregulation of Ca2+ homeostasis - CorreCt Answers forms ROS, stimulates Kreb's cycle which increases e- flow through ETC
and stimulates NOS (NO inhibits ETC complex 1 & 4 causing more ROS)

dissociates cytochrome C and can trigger PTP opening -> apoptosis

accumulation of misfolded/unfolded proteins & ER stress - CorreCt
Answers -passage of calcium from ER to mitochondria is by a junction
formed by MAM complexes

accumulation of ROS can impair protein folding & suppress protein
synthesis

ER stress can lead to apoptosis

What happens to Ca2+ when cell is injured? - CorreCt Answers -plasma
membrane mechanisms are insufficient, so mitochondria accumulates large
amounts of Ca2+ through:

Limited loading: binding of Ca2+ to neg phospholipids in inner membrane

Matrix Loading: Ca enters through uniporter, driven by -180mv potential

Matrix loading - CorreCt Answers -phosphate is also imported to matrix,
calcium phosphate precipitates allowing mitochondria to bugger large
amounts of Ca2+ to allow cell time to repair

Once damage is repaired, mitochondria slowly releases Ca2+ via 2Na/Ca
exchanger at a rate compatible with Ca2+ plasma membrane export
3 important properties of ion channels - CorreCt Answers -1) conduct ions
across membrane

2) select specific ions
3) open/close in response to mechanical, electrical, or chemical signals

Even though Na+ is smaller than K+, why doesn't Na+ fit through highlyselective K+ channel (KcsA)? - CorreCt Answers -Na+ has stronger electric
field, so bigger hydration cloud, thus it behaves bigger than K+ and cannot
pass through the K+ channel pores

Which of the following types of ion channels is a monomeric protein?
Ligand-gated, gap-junction, voltage-gated
...


Triggered by high serum K+ levels & results in periodic muscle paralysis

What does the ion equilibrium potential (Eion) respresent? - CorreCt
Answers -when electrical gradient = chemical gradient (ie
...
04
Pcl = 0
...
Since
water follows Na, this causes swelling and possible rupture of cell
...


What is the role of the Na/K ATPase? - CorreCt Answers -maintain resting
Vm, maintain osmotic eqm, and prevent dissipation of ionic gradients
...
Action Potential - CorreCt Answers -Graded Potential:
- decays with distance
- can be inhibitory or excitatory
- amplitude proportional to duration & magnitude of stimulus
- no refractory period

AP
- no decay (self-regenerative_
- depolarizing
- triggered by net graded potential
- has threshold
- all-or-none
- refractory period

Why does AP peak never reach ENa? - CorreCt Answers -gK is still
substantial so K+ carries out charge brought in by Na+

What is threshold? - CorreCt Answers -depolarization that opens enough
Na+ channels to counter efflux of K+ (Pna > Pk)

Activation gate of Na channel? - CorreCt Answers -m-gate

Inactivation gate of Na+ channel? - CorreCt Answers -h-gate

Activation gate of K+ channel? - CorreCt Answers -n-gate

Voltage-clamping - CorreCt Answers -set membrane to "command
potential" and observe current changes

Tetrodotoxin (TTX) & Saxitoxin - CorreCt Answers -bind to outside of
voltage-gated Na channels so no inward Na current (can cause paralysis)

Tetraethylammonium (TEA) - CorreCt Answers -blocks voltage-gated K
channels

Anaesthetic - CorreCt Answers -blocks Na channels which reduces AP firing
frequency in dorsal root ganglia

Flushing toilets & AP - CorreCt Answers -1) threshold
2) all-or-none

3) refractory phase
4) uni-direction

absolute refractory period - CorreCt Answers -no AP can be triggered
during or immediately after an AP (this allows spacing between APs)

relative refractory period - CorreCt Answers -if a more intense stimulus is
delivered an AP may be triggered but w/ smaller amplitude

what is conduction velocity affected by? - CorreCt Answers -- axon diameter
& myelination

How does axon diameter affect conduction velocity? - CorreCt Answers larger diameter = decreased resistance = faster (could explain why squid
axon so big)

How does myelin increase conduction velocity? - CorreCt Answers insulates axon membrane, reduces current leak (less capacitance) to
facilitate saltatory conduction

Electrical vs
...
What happens to
EPC when Vm < resting Vm, etc? - CorreCt Answers -Vm more neg than
resting Vm = larger amp of EPC (inward flow)

Vm more + than resting = reversal in current flow (outward flow), current
is reduced

What is the reversal potential (Er)? - CorreCt Answers -Reversal potential is
the Vm where there is not net flow through the channel & EPC changes
direction

how to calculate magnitude of EPC? - CorreCt Answers -EPC = gach (Vm Er)

if df is neg, EPC is inward (depolarize)
if df is +, EPC is outward (hyperpolarize)

Bungarotoxin - CorreCt Answers -blocks neurotransmission by irreversibly
binding to nAChR (competitive inhibition)

Curare - CorreCt Answers -blocks nAChR via competitive inhibition

myasthenia gravis - CorreCt Answers -disease of the NMJ (neuromuscular
junction) which results in weakness of skeletal muscles
...
It does have an effect
on amount of NT that is released

Gray Type I synapse vs Gray Type II - CorreCt Answers -Gray type I =
excitatory
- asymmetrical membranes (e- dense at active zone of presynaptic, & more
dense at postsynaptic)
- rounded synaptic vesicles

Gray type II = inhibitory

- symmetrical membrane (less obvious difference)
- oval or flattened vesicles

Patellar Reflex - CorreCt Answers -stimulis: tap to tendon stretches muscle
receptor: muscle spindle stretches & fires
afferent path: AP travels through sensory neuron
integrating center: sensory neuron synapses in spinal cord
efferent path 1: somatic motor neuron -> quadriceps -> contract & lower leg
swings forward
efferent path 2: interneuron inhibiting somatic motor neuron -> hamstring
-> stays relaxed

Antagonistic muscle pairs - CorreCt Answers -As one muscle contracts, the
other relaxes
...


can sum with IPSP to reduce chances of reaching threshold

Why is the AP at axon hillock (trigger zone) of lower threshold? - CorreCt
Answers -because higher density of voltage-gated Na channels

Wave summation - CorreCt Answers -occurs from increase in repeated
stimulation (increase AP frequency) so less time for muscle fiber to relax
between stimuli

muscle tetanus - CorreCt Answers -if stimuli are fast enough, muscle will
contract completely & stay contracted until stimuli stops or muscle fatigues

4 criteria for a substance to be a NT - CorreCt Answers -1) must be
synthesized in presynaptic neuron
2) present in presynaptic terminal & is released in sufficient amounts to
exert effect
3) when administered exogenously, it mimics action of endogenous
transmitter
4) specific mechanism exists for removing it from synaptic cleft

How are small NT synthesized? - CorreCt Answers -synthesized at nerve
terminals, enzymes needed are synthesized in cell body & transported down
axon via slow axonal transport

packaged into small clear-core vesicles

How are peptide NT synthesized? - CorreCt Answers -synthesized in cell
body with enzymes for prescursors, transported via fast axonal transport

packaged into large dense-core vesicles

What does the SNARE complex do? - CorreCt Answers -SNARE proteins
partially zipper together and clamped by complexin
...
Inhibits muscle contraction = reduced muscle
tone (flaccid paralysis)

tetanus toxin - CorreCt Answers -Blocks the release of glycine
-patients unable to relax muscles

Funny Na current - CorreCt Answers -Na channels activated when cell is
hyperpolarized (instead of depolarized)

SNS on heart rate - CorreCt Answers -released noradrenaline which
increases Na & Ca2+ influx & increases HR

PSNS on heart rate - CorreCt Answers -releases Ach, increases K+
conductance & decreases Ca2+ conduction & decreases HR

GPCR structure/function - CorreCt Answers -7 transmembrane alphahelices, inactive when GDP bound

when NT binds, GDP is released & GTP binds, alpha subunit dissociates
from beta-gamma subunit

cAMP pathway - CorreCt Answers -norepinephrine binds B1 receptor, Galpha stimulates adenylyl cyclase to cataylyze synthesis of cAMP
...
PKA phosphorylates
calcium channels to increase calcium release (increases HR, & can also
phosphorylate SERCA to decrease relaxation time)

How do G beta-gamma subunits activate K+ channel? How do we know
this? - CorreCt Answers -ACh binds to muscarinic GPCR on cardiac tissue,
activated B-y subunits interact directly with K+ channels to increase efflux
which hyperpolarizes SA node & decreases HR
...


Know this by inside-out patch clamp (place in bath with beta-gamma
subunit & observed K+ conductance)

inositol phospholipid pathway - CorreCt Answers -Gq (alpha) activates
phospholipase C (PLC) which cleaves PIP2 which leads to the production of
DAG & IP3

What does IP3 do? - CorreCt Answers -Triggers release of Ca2+ from SR

What does DAG do? - CorreCt Answers -activates PKC

Calcium-induced calcium release (CICR) - CorreCt Answers -low cytosolic
[Ca2+] increases opening of IP3-gated channels (calcium moves into the
cell and stimulates release of calcium from the SR)

Negative feedback of calcium release - CorreCt Answers -high [Ca2+]
inhibits IP3-induced Ca2+ release (IP3 receptor has Ca2+ binding sites)

Calcium blips - CorreCt Answers -Ca2+ release from SR by SINGLE IP3
receptor calcium channel (occurs in response to low IP3 levels)

Calcium puffs - CorreCt Answers -Ca2+ release through CLUSTERS of Ip3
receptor calcium channels

DHPRs & RYR - CorreCt Answers -DHPRs are L-type Calcium channels
(long lasting voltage-gated) in T-tubule membrane
...


Overall leads to muscle weakness & fatigue

Nitric Oxide (NO) pathway - CorreCt Answers -Ach acts on muscarinic
AChR in IP3 pathway (calcium activates calmodulin which leads to NO
synthase)

NO diffuses through membrane to activate guanylate cyclase which
stimulates cGMP production which activates PKG

Causes muscle relaxation & vasodilation

Regulated by PDEs (phosphodiesterases) which degrade cGMP

Viagra - CorreCt Answers -developed for hypertension by targeting PDE5
for inhibition (would increase cGMP), PDE5 was believed to be found in all
blood vessels but is predominantly in lungs and penile tissue
...
Made up of
myofilaments (thin actin & thick myosin)

Sarcomere - CorreCt Answers -repeated units of myofibrils

membrane of Muscle fibre (cell) - CorreCt Answers -surrounded by
sarcolemma then endomysium

membrane of muscle fascicle (many cells) - CorreCt Answers -surrounded
by perimysium

membrane of skeletal muscle (many fascicles) - CorreCt Answers surrounded by epimysium

Muscle contraction (cross-bridge) cycle - CorreCt Answers -1) Ca2+ is
released from SR & binds to troponin causing tropomyosin to shift from
active sites on actin
2) myosin heads (ADP + Pi) bind to actin binding sites, forming crossbridges
3) energy (ADP + Pi) is released as myosin head pivots toward M-line, ATP
binds to myosin head breaking the cross-bridge

4) ATP provides energy to reactivate myosin heads and return them to
original positions

What is a twitch? - CorreCt Answers -single stimulus-contractionrelaxation sequence in a muscle fiber

latent period - CorreCt Answers -AP moves through sarcolemma, Ca2+ is
being released

Motor unit - CorreCt Answers -A motor neuron and all of the muscle fibers
it innervates

motor nucleus/pool - CorreCt Answers -A group of motor neurons that
innervates particular group of muscles

motor nerve - CorreCt Answers -a nerve that transmits information from
the central nervous system to the muscles

Which NT/aa stimulates motor neuron? - CorreCt Answers -glutamate

Which NT is released at motor neuron terminal? - CorreCt Answers -ACh

Central pattern generator (CPG) - CorreCt Answers -central neuronal
network in spinal cord that controls repetitive motor activity

produces rhythmic patterned outputs to coordinate antagonistic muscle
pairs through:

- bursting neurons (APs in periodic groups)
- interactions between cells consisting of mix of excitatory & inhibitory
synapses

under descending inhibition (brain prevents CPG from being active during
periods of rest)

silicon CPG chips - CorreCt Answers -electronic chip acting as CPG,
possibility for spinal cord injuries

Upper motor neurons - CorreCt Answers -in premotor cortex, control lower
motor neurons

lower motor neurons - CorreCt Answers -in spinal cord & brain stem,
directly innervate skeletal muscle

2 diseases that target motor neurons - CorreCt Answers -1) ALS
2) SMA (mostly inherited)

amyotrophic lateral sclerosis (ALS) - CorreCt Answers -fasciculations
(involuntary twitches) = inabiliy to couple contraction of muscle

leads to loss of motor neuron function & wasting of muscles

most patients die from respiratory failure

bladder & eye muscles are unaffected

Familial ALS - CorreCt Answers -mutation of SOD1 gene

SOD1 is antioxidant of cell (converts ROS to H2O2 or O2)

mutation leads to: hyperactivation of motor neurons, ER stress,
proteosome inhibition, mitochondria dysfunction, superoxide production,
altered axonal transport & synaptic vessel defects

Spinal muscular atrophy (SMA) - CorreCt Answers -autosomal recessive
inheritance of mutated SMN1 gene, motor neuron doesn't survive (inability
to produce enough neuron transcription factor)

muscle weakness & wasting



---