Neurophysiology Flashcards
Capacitance
of ions needed to change membrane voltage
Conductance
- ease of moving ions across membrane (how fast they can flow)
- representation of how many open channels there are on the cell (low conductance=less open channels)
Voltage (potential)
energy to move ions across cell membrane
Excitaton
-makes cell more positive=DEPOLARIZATION
think about de-polarizing or making the north pole less cold (polar-like) you would be increasing the temp. or making it more POSITIVE
Inhibition
-makes cell more negative=HYPERPOLARIZATION
Na/K Pump
- pumps Na out and K in
- against concentration gradient
- uses energy from ATP
- *Normally inside=low conc. Na and high conc. K
Uniport carrier
transports only one kind of substrate
Cotransporters (2 types)
- symport carriers
- antiport carriers
Symport carrier
move two or more substrates in the SAME direction across membrane
Antiport carrier
move substrates in opposite directions across membrane (one in, one out)
Primary active transport
- energy dependent (ATP)
- Na/K ATPase (antiport)
- Ca ATPase (uniport)
Secondary active transport
-uses energy(gradient) from primary active transport
Ex: sodium binds creating a spot for glucose to bind, when glucose binds, carrier changes formation
Gated channels (3 kinds)
- voltage=APs ad synaptic release
- ligand=chemical neurotransmitter
- mechanical deformation=hair cells in inner ear
- **gated channels are normally closed
Ionotropic recepters-ligand gated channels
Excitatory=ACh and glutamate-selective for Na and K ions
Inhibitory=GABA and glycine-selective for Cl ions
Graded potential
slow, analog, usually produced at synapses
- the more channels that are open, the greater the size of the potential
- decline exponentially as they travel along nerve fiber
- good at coding signal (b/c they can change size and frequency) but not good at transmitting over long distances (voltage gets smaller-# of Na ions decreases)
Action potential
fast, fixed size, digital signals, is regenerative
- *don’t change size based on size (amplitude) based on the strength of the stimulus, instead it changes its frequency
- produced if graded potentials are still at threshold when they reach the trigger zone (size of GP determines frequency of AP)
Trigger zone
location on neuron (between cell body and axon) where there is a high density of Na channels
-if GP is still at threshold when it gets to this location it will produce an AP (Larger GP creates greater frequency of APs-more APs which releases more neurotransmitter)
Depolarization
- make cell membrane potential more positive-bring in positive (Na) ions
- as you depolarize more and more, the probability that Na channels are open increases
Hyperpolarization
-make cell membrane potential more negative-bring negative ions in or let positive ions out
Rising phase of AP
-Na rapidly enters cell to depolarize it=Na channels opening
Falling phase of AP
- K moves out of cell to hyperpolarize it
- Na channels closing, K channels slowly opening
Peak of AP
- Na channels start to close while K channels start to open
- cell is close to the sodium equilibrium potential
How is acetylcholine transported from the presynaptic membrane to the postsynaptic membrane?
ACh diffuses across the synaptic cleft and binds to the ligand-gated channels on the postsynaptic neuron
What does the absolute refractory period cause
Action potential propagation to occur in one direction
What effect does acetylcholine have on the postsynaptic neuron
Ligand-gated sodium channels open and sodium flows in
What happens when an action potential arrives at the presynaptic terminal
Voltage-gated calcium channels open, causing calcium ions to flow into the cell
White matter of spinal cord contains
Ascending and descending tracts
The S4 transmembrane segment determines what property of the voltage gated sodium channel
Voltage sensitivity
Ionotropic vs metabotropic
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What channel event determines the absolute refractory period
Inactivation of the sodium channels
-have to wait for inactivation gate to be back in place before another AP can be generated
Botulinum toxin blocks proper synaptic signaling at the neuromuscular junction by doing what
Blocking vesicle fusion and transmitter release at the synapse
Myasthenia gravis
autoimmune disease
Slow pain fibers produce these two synaptic responses in the spinal cord
Excite ascending pain pathways and suppress inhibitory interneurons
Myelin
lowers capacitance of membrane so it takes less Na to produce same depolarization (easier to depolarize)
-if there was a missing myelin sheath segment, the Na would leak out of the axon and slow conduction-AP may not even be able to make it to next node
EX: multiple sclerosis=loss of myelin=slowed conduction
Hypokalemia
- low blood potassium
- neuron is less likely to fire b/c it is hyperpolarized since K flows out of cell to compensate for low K outside cell
Synaptic vesicle
package holding neurotransmitter
SNARE proteins
attach vesicle to presynaptic membrane
Botulinum toxins
interfere with SNARE proteins and prevent ACh vesicle fusion
Tetanus toxins
disrupts SNARE proteins to prevent fusion of glycine vesicles
-muscles contract too much
Synaptotagmin
binds to calcium and stimulates vesicle function
-changes conformation when it binds to Ca
Neurotransmitter deactivation
Can be:
1) returned to axon terminal for reuse or transported into glial cells
2) enzymes inactivate neurotransmitters
3) neurotransmitters diffuse out of synaptic cleft
