Test 1, Deck 1 Flashcards
which action potential has the longest duration?
cardiac ventricle (200 ms, 10x longer)
which action potential beings and ends at -90mV?
skeletal muscle
what is a space constant
how easily an axon can conduct electrical activity
small axon = ___ membrane resistance= ___ internal resistance = ___ space constant = ___ conduction
small axon = higher membrane resistance (but overcome by the ->) = higher internal resistance= small space constant= slow conduction
at the depolarized region, there is a ___ in membrane polarity, which causes ___ to flow
reversal, current
depolarization is caused by
opening of of h & m** gates of sodium channels- rapid increase in Na+ channel conductance
repolarization is caused by
- delayed increase in K+ channel conductance;
- inactivation of Na+ channels (closing of h gate)
K+ channels deactivate by
repolarization of membrane potential
Na+ channels deactivate by
positive voltage of cell (one of few positive feedback loops)
channel properties (M & H)
resting- M closed, H open
activated- m open, h open
inactivated- m open, h closed
important difference between Na and K channels
K+ channels don’t have H gate, are inactivated by membrane repolarization
how does a more positive resting membrane potential affect the gating of Na channels?
H-gates begin to close as membrane becomes more positive; results in slow conduction & muscle weakness
absolute vs. relative refractory periods; what channel do they depend on
- absolute- h-gate is closed
- relative- hyperpolarization, where voltage difference is too great for another AP
NA CHANNELS!
how does calcium modulate sodium channel activity?
Ca binds to proteins surrounding Na channel, makes environment more positive, h-gate closes, less APs
hyperCalCemia
increased plasma Ca+, Na+ channels become inactive (less available), conduction slows
signs: weak reflexes
hyperventilation
blow off CO2, get less H+ in blood, get less binding of Ca2+ because of increased pH, increase membrane excitability
signs: agitation
hyperKalemia
increased plasma K+, less K+ leaks out of neuron, inside of the cell becomes more positive, h-gates close and get less APs
symptoms: slow mentation, muscle weakness
large differences in the diameter of unmyelinated axons do/don’t change conduction velocity
don’t
schwann cells increase the ______ by increasing _____
space constant; membrane resistance
where is the only place you see action potentials
nodes of ranvier
In MS, the space constant is
reduced
steps of synaptic transmission
- depolarization
- calcium enters
- synaptic vesicles fuse via SNARE
- transmitter released into synaptic cleft
- NTs bind or diffuse (NO)
- NTs cleared away
two types of post-synaptic events
ionotropic- quick- opening of ion channels
metabotropic- slow- GPCRs
BoTX mechanisms, symptoms
- cleaves SNAREs (synaptobrevin, SNAP-25, and syntaxin); prevents fusion of vesicles
- affects peripheral cholinergic fibers
- flaccid paralysis & autonomic symptoms
TeTX mechanisms, symptoms
- cleaves SNAREs (synaptobrevin); prevents fusion of vesicles
- taken up by inhibitory neurons in spinal cord
- spastic paralysis & death
types of cholinergic fibers
- all preganglionics
- postganglionics of parasympathetic NS
- basal forebrain
- brainstem
- NMJs
two types of Ach receptors
nicotinic- fast- ionotropic
muscarinic- slow- metabotropic
opening of ion channels (PSC) results in
PSP- postsynaptic potential (NOT AP)
types of excitatory NTs
Ach, glutamate
- inward Na, outward K= EPSC
what is an EPSP
cation movement which depolarizes the cell to around ~0mv, ** increasing the probability that an action potential will be fired
inhibitory NTs; act on which channels
glycine, GABA; changes permeability to Cl, moves more towards -65mV and LOCKS- will always prevent AP
what does the ANS control
MOTOR SYSTEM- cardiac muscle, smooth muscle, glands
- has motor efferents and visceral afferents
function of ANS
homeostasis, respond to external stimuli
major autonomic neurotransmitters
** Ach and norepinephrine (NE)**
epinephrine is central NT, but in ANS is mainly hormone
differences between neuron-neuron (and neuron-SKM) and neuron-viscera (ANS)
- well defined vs en passant
- little vs. great distance
- ionotropic vs metabotropic
- direct effect vs. direct&neuromodulatory effect
effects of nerve gas (sarin)
inhibits Ache, prevent Ach degredation; have too much Ach in cholinergic synapse, overstimulate muscarinic receptors causing convulsions & paralysis
treatment of WMD gases
- diazepam: seizures
- atropine: blocks Ach receptors
- 2PAM (pralidoxime)- recover Ache function
NT for adrenergic neurotransmission; how its terminated; where degrading enzymes exist
NE synthesized in vesicles from DOPA; MAO and COMT; degrading enzymes in cytosol, mitochondria, circulation
location of pre-ganglionic cell bodies of sympathethic NS
C8
lateral horn of thoracics
upper lumbar
what do preganglionic sympathetic neurons secrete
Ach
- acts on nicotinic receptors- ionotropic, fast acting
location of post-ganglionic cell bodies of sympathethic NS
- para-vertebral (sympathetic trunk)
- pre-vertebral ganglia (abdomen)
sympathetic pre-ganglionic fibers are shorter/longer than parasympathetic preganglionic fibers
shorter
preganglionic neurons are mostly ipsilateral/contralateral except for ___, which are bilateral
ipsilateral; pelvic viscera/intestines
why is the adrenal medulla an exception
preganglionic neruons PASS THROUGH splanchnic; have NO post ganglionic neuron
- is nicotinic
- causes bolus release of NE/E into blood
why are sweat glands an exception
they’re sympathetic, but activated by Ach NOT NE
sympathetic post ganglionic fibers normally secrete
norepinephrine
autonomic centers in brain
pons (breathing)
medulla (blood vessels)
hypothalamus (master)
similarities between skeletal, smooth and cardiac muscle
all use Ca2+
all require actin & myosin
chemical energy comes from ATP
smallest to largest muscle components
myofilament -> sarcomere -> myofibril -> myofiber
what happens to the I, A, and H bands during contraction
A band (myosin) stays the same I band (actin) shrinks H band (between actins) shrinks
steps in EC coupling
- action potential goes down t-tubule
- depolarization activates DHPR
- DHPR activates ryanodine receptors
- ca2+ is released from SR
- ca2+ initiates muscle contraction
- SERCA pumps Ca2+ back into SR lumen
ways to regulate muscle contraction
fire successive APs (summate)
turn more/fewer fibers on
build bigger fibers
change resting length of fibers
sarcomeres in parallel add _____, but in series add _____
parallel/force
series/shortening
describe length-tension diagram
lots of stress-too short- sterics
no stress- too long- no overlap
isotonic contraction
muscle contracts and shortens- (includes concentric and eccentric contractions)- tension remains constant despite a change in muscle weights (bicep curls)
load < tension
isometric contraction
muscle contracts but does not shorten; muscle actively held at a fixed length, like when you flex to show your biceps, grip an object
load = tension
what counts for 50-70% of all ATP consumed? where is the rest used up?
- actomyosin ATPase (crossbridging)
- SERCA CA2+ ATPase
- Na/K ATPase
sources of ATP for muscle metabolism
- creatine phosphate- 1st used and depleated
- oxidative phosphorlation
- glycolysis (anerobic exercise)
types of muscle fibers
type 1- slow- oxidative phosphorylation- postural muscles- lots of blood vessels/mitochondria
type 2- fast- glycolysis- fast & forceful
difference in E-C coupling between skeletal muscle and cardiac muscle
DHPR
physical coupling vs Ca2+ induced Ca2+ release
weight training increases
the number of myofibrils
endurance increases
the number of mitochondria
relationship between alpha and beta adrenergic receptors and smooth muscle activation
- alpha decreases cAMP and beta increases it
- cAMP stimulates PKA to phosphorylate MLCK, resulting in RELAXATION
relationship between nitric oxide and smooth muscle contraction
vagal stimulation increases Ach in blood, which binds to endothelial cells, causing them to release NO; NO increases cGMP which stimulates the MLCP, resulting in de-phosphorylation of the light chain and relaxation of blood vessels
sequence of electical activity
SA AV His Bundle branches Purkinje
two reasons for deviation of membrane potential from Nernst equation
1) small sodium influx
2) decrease in potassium permeability (inward rectification)
two causes of inward rectification
1) chemical- decrease in extracellular K+
2) electrical- depolarization of the membrane
channels during fast action potential
0- fast Na channels let Na in
1- transient Ito channels let K+ out
2- slow calcium channels let calcium in, transient channels close, trapping K+ in
3- delayed potassium channels open, letting K+ out
4- K+ equilibrates (IK1’s are open)
how hypokalemia affects resting membrane potential
get no net change in voltage
how hyperkalemia affects membrane potential
membrane potential becomes more positive
channels during slow AP
4- funny channels let more Na in than K+ out
2- voltage Ca2+ channels open, and Ca2+ goes in
3- K+ channels open, K+ leaves, get repolarization
slow vs fast AP in heart
slow- pace maker (e.g. SA cells)
fast- contractile cells
what does TTX do?
block fast Na+ channels, turns contractile cells to slow conduction
3 types of junctions found at intercalated disks
fascia adherins
macular adherins
gap junctions (connexons)
what are gap junctions sensitive to
Ca2+ and H+
properties of pacemaker cells
function: pace make
small diameter
few gap junctions
few myofibrils
properties of atrial and ventricular muscle cells
function: contraction
medium diameter
abundant gap junctions
abundant myofibrils
properties of His/bundle branches/Purkinjes
function: rapid conduction
large diameter
abundant gap junctions
few myofibrils
2 factors that determine cardiac conduction
1) space constant ((Rm/Ri)^1/2)
2) rate of rise and amplitude of action potential
membrane resistance is ___ related to K+ permeability
inversely
internal resistance is ____ related to number of gap junction connections and ______ related to cell diameter
inversely related
conduction is strictly related to which part of the action potential?
upstroke- sodium channels
conditions that can change RMP
hyperkalemia
premature excitation
ischemia - build of of K+ in tissue
P-R interval
conduction time from atrial muscle-AV node-his-purkinje- 200 ms
QRS interval
conduction time from endocardial to epicardial surface- 100 ms
AV nodal conduction abnormalities- type 1
abnormal prolongation in P-R interval (1:1 conduction)
AV nodal conduction abnormalities- type 2
some atrial impulses fail to activate ventricles; not all P waves followed by QRS (e.g. 2:1 conudction)
AV nodal conduction abnormalities- type 3
complete AV block; no consistent P-R interval
sympathetic innervation to the heart
- NE
- acts on beta adrenergic receptors
- increases speed of all things in the heart
- increases cAMP and inward calcium
parasympathetic innervation to the heart
- Ach (vagal)
- acts on muscarinic receptors
- acts on everything up to AV node
- increases K+ permeability
supraventricular tachycardia
- narrow QRS
- normal sequence, just rapid
- CO not affected
- filling time decreased
ventricular tachycardia
- QRS is abnormally prolonged
- impulse originates in ventricle and skips His-Purkinje; goes in circular pattern
- conduction is slow
- CO compromised
atrial fibrillation
- absence of P-waves (like static where they should be), R-R are irregular
- non leathal
ventricular fibrillation
lots of random electrical activity; is probably the end
how to spot AV conduction abnormalities on EKG
look for how QRS follows p-wave
what does digitalis inhibit and what can it cause
- inhibits Na/K pump, reverses Na/Ca2+ pump
- DADs by abnormally increasing intracellular Ca2+
