Unit 2 + Unit 3: spinal anatomy Flashcards
what other ion channel is similar in structure to a VG Na+ channel?
VG Ca2+ channel
also termed SLOW calcium channels
slow VG Ca2+ channels are blocked by:
dihydropyridine calcium channel antagnoists
Cl- permeability is adjusted to _____ or _____ electrical activity in excitable cells
hyperpolarize; suppress
these receptors typically open up Cl- channels in neurons
GABA receptors
Cl- influx typically makes the cell membrane more ____ and more ____ to excite
negative; difficult
permeability of Na+ _____ via opening of membrane Na+ channels; membrane potential becomes closer to nernst for Na+ during ______
increases; depolarization
why would a 2-way signaling process for depolarization along a cell be considered beneficial
if the AP can move in both directions, there would be a shorter time required to excite a cell
how is propogation of an AP in a VG Na+ channel considered a positive feedback loop?
the initial stimulus causes Na+ to come in, which then activates fast Na+ channels to allow more Na+ to come in until repolarization initiates
how does the motor neuron communicate with skeletal muscle if there is a “gap” between the two structures?
neurotransmitters
the gap is termed the neuromuscular junction (NMJ)
nicotinic-ACh receptor
found on skeletal muscles
(also on brain; think nicotine)
receptor has 2 binding sites
NT: ACh released from motor neurons and 1 receptor needs 2 ACh to bind
the inside of the receptor is negatively charged but the channel is specific for positively charged ions
which type of ions can pass through the nicotinic-ACh receptor?
the majority of the current is Na+ current; this means there is more Na+ influxing vs K+ effluxing (and Ca2+ influxing)
Ca2+ can also influx and depolarize the cell, but the majority of the influx is Na+
Ca2+ is a larger ion, which is why there isn’t as much Ca2+ influxing through the channel as there is Na+
aside from the n-ACh receptors found on skeletal muscle, how else do the skeletal muscles cells become more positively charged during depolarization?
after the initial depolarization through n-ACh receptors, nearby fast Na+ channels can open up to allow more Na+ to influx into the cell
paralytics work here
the neuromuscular junction
list out the steps to “excite” a nerve cell to cause skeletal contraction
- the brain sends “signal” to motor neuron to communicate with skeletal muscle cell
- the signaling molecules are the ACh neurotransmitters
- 2 ACh NTs bind to the nicotinic-ACh receptors
- the postively charged ion selective channel allows an influx of Na+ to flow into the cell
- depolarization occurs and activates nearby fast VG Na+ channels nearby to help propogate the AP across the skeletal cell leading to muscle contraction
which receptor types cause hyperpolarization in cardiac cells?
hyperpolarization makes cells more NEGATIVELY charged; this will suppress electrical activity in the cell
ex) muscarinic-ACh receptors
muscarine stimulates muscarinic-ACh receptors
where are m-ACh receptors found on the heart?
the “pacing centers”
SA and AV nodes
the RIGHT vagus nerve communicates with the ____ node
SA
the LEFT vagus nerve primarily communicates with the ____ node
AV
the vagus nerves communicate with the SA/AV nodes via this NT
ACh
the mACH-R has this type of protein structure
7TM (GPCR)
list out the mechanism of hyperpolarization in cardiac cells
- ACh binds to 7TM m-ACh-R
- alpha subunit and communicates with potassium channels (the effector protein) in the cell wall
- K+ channels now activated and effluxes K+ out of the cell
- increased EN makes the cell much more difficult to excite
- hyperpolarization (making the cell more negative past vrm) will make it so that it takes longer for the cell to become excited enough to fire off another AP
- this in turn will “keep the pace” of the heart (“70-72” BPM)
how does a vagal response cause a bradycardic response?
massive vagal stimulation causes potassium permeability to INCREASE, causing more K+ to efflux, causing hyperpolarization of pacemaker cells and causing the HR to slow down
describe what happens when an antimuscarinic drug inhibits pacemaker cell hyperpolarization
- antimuscarinic (antagonist) binds to active site of m-ACh-R
- alpha subunit is not active
- potassium channels close and cause cell to become more POSITIVE
- vrm is now more positive, and since our vrm has approached the threshold potential, it will take a SHORTER time to fire an AP
- shorter time to fire an AP means more APs fired AKA an elevated HR
give an example of a muscarinic-ACh-R antagonist
atropine