Topic F Flashcards
What are the four proteins needed for an action potential to occur?
- Na+ and K+ pumps
- K+ Leak Channels
- Voltage-gated K+ Channels
- Voltage gated Na+ Channels
What are the parts of a neuron?
- cell body
- dendrites
- axon (less than 1mm to more than 1m long)
- terminal branches of axons
- nerve terminal
What is the “usual” resting membrane potential
-70.0mV
An axon at resting membrane potential is more _____ on the inside and more ____ on the outside
negative; positive`
What is the resting membrane potential maintained by?
- Na+ & K+ pumps
- K+ Leak channels
Potassium channels are ______
Homotetramers
Sodium channels are ____ with ___ number of domains
monomers; 4
K+/Na+ channels in a neuron axon – Characteristics
shape: Channel
Energy - passive
Direction - uniport
Regulation: gated
Na+ channels open _____ in comparison to K+ channels when the membrane potential changes
Quicker
K+/ Na+ channels open at a membrane potential of ____
above -40 mv
(+) at the cytosol
(-) inside the neuron
Plasma membrane is depolarized
K+/ Na+ channels close at a membrane potential of ____
below -40 mv
(-) at the cytosol
(+) at inside the neuron
Plasma membrane is at rest
how do K+/ Na+ channels open
Gates of channels are wings that can rotate; (+) part of the wing moves towards (-) environment
What are the three phases of a sodium channel
- Closed: Plasma membrane at rest
- open: Membrane ois depolarized
- inactivated: Membrane is at refractory
What is the inactived stage of a voltage gated Na+ channel
(-) inside the neuron
(+) at inside the cytosol
membrane Refractory
Activity of Na+/K+ pumps
(few)
Always working
Activity of K+ leak channels
Open and close randomly (few)
Activity of Voltage gated K+ channels
close, open, close
Activity of Voltage gated Na+ channels
close, open, inactivate, close
What are the stages of an action potential
1) Subthreshold depolarization
2) Threshold depolarization
3) Depolarization Phase
4) Repolarization Phase
5) Refractory Period
Subthreshold depolarization
@ resting membrane potential
1 Na+ channel opens nothing happens b/c of the K+ leak channels thats already open
Threshold depolarization
Several Na+ channels open, an influx of Na+ overcomes the outflow of K+ allowing the threshold membrane potential to be reached (-40mV).
Depolarization phase
Once threshold membrane potential is reached (-40mV), all the Na+ channels open, Membrane potential rises to +40mV.
Repolarization Phase
Na+ channels inactivate, K+ channels open, this drives the membrane pot. back down
Refractory Period
nothing can happened b/c Na+ channels are inactive, K+ channels open
After Membrane potential is below -40mV for a time Na+ and K+ channels close
How does an AP travel on a regular axon
- voltage gated sodium channels allow Na+ to go into axon deploarizing the membrane causing passive depolarization to spread, which is followed by an outflow of K+ ions into the cytosol
Speed of travel – ~5m/s
How does an AP travel on a giant axon
Larger diameters of axons – quicker APs
Found in large invertebrates
Speed – ~100m/s
How does an AP travel on a myelinated axon
myelinated cells (myelin sheath) that wrap around the neurons axon insulating it
AP “jumps” between nodes of ranvier
speed ~100m/s
what is the function of SNAREs in Presynaptic Neurones
Activated by Ca+ (indirectly)
fusses synaptic versicle with presynaptic membrane
what is the function of Vesicles in Presynaptic Neurones
Carry neurotransmitters to presynaptic membrane
what is the function of SNAREs in Presynaptic Neurones
Activated by Ca+ (indirectly)
fusses synaptic versicle with presynaptic membrane to release neurotransmitters
what is the function of Acetylcholine receptors (AChR) in Postsynaptic Neurones
Ion channels or open adjacent ion channels
Made of negatively charged amino acid side chains
Open when neurotransmitters bind to it.
Electrical Synapses
Na+ moves through gap junctions
Advantages: speed
Chemical synapses
Neurotransmitters export from cell
Advantages: integration of multiple signals
what is the function of Acetylcholinesterase (AChE) in Postsynaptic Neurones
Degradation of ACh
removed Neurotransmitters from synaptic cleft
(break down with enzymes)
what is the function of Excitatory synapses in Postsynaptic Neurones
CASUES AN AP
synapse in which an action potential in a presynaptic neuron increases the probability of an action potential occurring in a postsynaptic cell
what is the function of inhibitory synapses in Postsynaptic Neurones
opposite to Excitatory synapses
what is the function of postsynaptic potentials in Postsynaptic Neurones
Each active synapse generates a tiny post synaptic potential (PSP) from excitatory and inhibitory synapses which then combine
what is the function of spatial summation in Postsynaptic Neurones
The combination of PSPs from DIFFERENT presynaptic neurons
what is the function of temporal summation in Postsynaptic Neurones
the combination of PSPs from ONE presynaptic neurons
what is the function of combined PSPs in Postsynaptic Neurones
TS and SS combined which then change the membrane potential of neurones
what is the function of encoding at the axon hillock in Postsynaptic Neurones
generates output of postsynaptic neurones
Magnitude of combined PSP –> frequency of axon potentials
low, medium, high combined PSPs
Cl- enters the postsynaptic neuron —>
Hyperpolairzation
Neurotransmitters are removed from synaptic cleft by..
diffusion – Wonder away
degradation – Break down w/ enzymes
Reuptake – import back into a cell
Low combined PSP
No action potential
Voltage Gated Na+ and K+ channels are closed
Minimal axon membrane potential (mV)
High combined PSP
Lots of action potential
Voltage gated Na+ and K+ channels are open
Many axon membrane potential (mV)
Moderate combined PSP
action potentials are possible but iinfrequent
____ refractory periods when combined PSP is ___ above threshold
extend; Slightly
What are the steps in activating a skeletal muscle cell?
1) Voltage Gated Ca+2 open with the activation of the nerve impulse resulting in a release of ACh
2) ACh binds to AChR —> localized memb. depolarization
3) Voltage gated Na+ opens –> entire surface including T-tubules depolarizes
4) Voltage Gated Ca+2 open
5) Mechanically gates Ca+2 –> Ca+2 enter cytosol
The Binding of ___ to the troponin complex exposes the ____ ____ site.
Ca+2; myosin binding
What are the steps in activating a skeletal muscle cell?
1) Voltage Gated Ca+2 open with the activation of the nerve impulse resulting in a release of ACh
2) ACh binds to AChR —> localized memb. depolarization
3) Voltage gated Na+ opens –> entire surface including T-tubules depolarizes
4) Voltage Gated Ca+2 open
5) Mechanically gates Ca+2 –> Ca+2 enter cytosol
steps for recovery of an activated skeletal muscle cell…
- ACh removed from synapse
- Channels close
- Ca+2 removed from cytosol
- Tropomyosin block myosin binding sites
Ca+2 removed from cytosol with ____ & ____ Ca+2 transporters
ATP powered; Na+ gradient powered
How are skeletal muscles controlled
Need multiple signals/APs (temporal summation) to contract a muscle
Do muscle cells also do spatial summation?
No, only temporal
What is one motor unit?
1 motor neuron and several muscle cells
cardiac muscle cells vs skeletal muscle cell
- cardiac muscle cells are controlled by pacemaker cell not motor neuron – sends pulses of (+) ions
- wave of contractions to heart muscle cells – spreads across heart
- Connected with electrical synapses –gap junctions
- Brain and adrenaline control the heart rate
- cardiac muscle cells contract for a longer time
steps for recovery of an activated skeletal muscle cell…
- ACh removed from synapse
- Channels close
- Ca+2 removed from cytosol
- Tropomyosin block myosin binding sites
Agonist
Activates
Antagonist
Blocks
Activator toxin
normal binding to site of enzyme; Increases activity
Competitive inhibitor toxin
Binds to active site of enzyme to decreases activity
Noncompetitive inhibitor
decreases activity
Noncompetitive inhibitor
binds at an allosteric site separate from the active site of substrate binding to decreases activity
Toxin: BoNT/A
Enzyme that cleaves SNAREs – cuts SNARE thats necessary for release of ACh vesicles
(Prevents release of neurotransmitters)
Toxin: Sarin
Competitive inhibitor – mimics ACh and Inhibits AChE
Involuntary muscle contractions
(Prevents removal of neurotransmitters)
Toxin: Charybdotoxin
AChR Antagonist – Blocks certain AChRs
Muscle paralysis
(prevents activation of receptors)
Toxin: Nicotine
AChR Agonist – mimics ACh and activates certain AChRs
Increases activity in brains pleasure center – produces euphoria feeling and adrenaline response
(inappropriate activation of receptors)
Humans have __ different AChRs
11
Toxin: BoNT/A
The effect?
- Enzyme that cleaves SNAREs – cuts SNARE thats necessary for release of ACh vesicles
- Muscle paralysis; Treat people who have uncontrolled muscle contractions; Botox
(Prevents release of neurotransmitters)
Toxin: Sarin
The effect?
- Competitive inhibitor – mimics ACh and Inhibits AChE
- Involuntary muscle contractions
(Prevents removal of neurotransmitters)
Toxin: Charybdotoxin
The effect?
- AChR Antagonist – Blocks certain AChRs
- Muscle paralysis
(prevents activation of receptors)
Toxin: Nicotine
The effect?
- AChR Agonist – mimics ACh and activates certain AChRs
- Increases activity in brains pleasure center – produces euphoria feeling and adrenaline response
(inappropriate activation of receptors)
most dangerous neurotoxin? why?
BoNT/A; enzyme–> 1 molecule within a cell of the toxin can get rid of all the SNAREs
Nicotine activates AChRs on ____ and ___ cells
brain; adrenal
Nicotine activates AChRs which Causes voltage gates Ca+2 channels to ____ and ____ exocytosis of adrenaline
open; causes
