Cellular Physiology Flashcards
The gap between myelin sheaths is named this
Node of Ranvier
What is the the Node of Ranvier?
The gap between myelin sheats
This is the start area of the axon and the initiation site of action potentials (APs)
Axon hillock
These contact neurons and wrap around synapses
They also wrap around the blood vessels in the brain, where they act as a conduit for nutrients from the circulatory system to the neurons
Astrocytes
Astrocytes are linked to each other by these
Gap junctions
Small mobile cells in the CNS that act as the brain’s host defense system
When parts of the brain are damaged, these accumulate at the site of injury to remove the damaged tissue via phagocytosis
Microglial cells
These are responsible for the myelination of axons in the CNS
Oligodendrocytes
These are responsible for the myelination of axons in the PNS
Schwann cells
Oligodendrocytes form the myelination of axons in the CNS or PNS?
CNS
Schwann cells form the myelination of axons in the CNS or PNS?
PNS
The cells that line the ventricular areas of the brain and the central canal of the spinal cord, help in the circulation of the CSF
Ependymal cells
Refers to the movement of ions through the membrane through ion channels
Current
This is the result of the movement of several different ion species through various ion channels and transporters in the plasma membrane
Resting membrane potential
This equation defines the equilibrium potential of a specific ion separated by a cell membrane
Nernst equation
This is the typical resting membrane potential for neurons
-60 to -70mv
In depolarization, is Vm more positive or negative than RP?
Positive
In hyperpolarization, is Vm more positive or negative than RP?
Negative
Will the membrane potential depolarize or hyperpolarize when the external concentration of K+ is increased?
Depolarize
(Vm becomes more positive than RP)
A cell’s resting membrane potential is very sensitive to changes in extracellular concentrations of this ion
Potassium
Do changes in extracellular potassium concentrations affect resting membrane potential?
Yes!
Increase [K+] = depolarization
Do changes in extracellular sodium concentrations affect resting membrane potential?
No
Sodium channels are closed under resting conditions
This refers to the number of channels that are open in a membrane
Conductance
This is the membrane potential at which the occurrence of the action potential is required
Threshold potential
Resting potential is due to these channels
Ungated K+ channels that are almost fully open
Depolarization is due to these channels
Opening of Na+ channels and Na+ entry
Repolarization is due to these channels
Delayed opening of K+ channels, and K+ efflux and Na+ channel inactivation
After-hyperpolarization is due to these channels
Slow closing of K+ channels, and opening of additional K+ channels
Tetrodotoxin blocks this channel
Sodium
Tetraethylammonium blocks this channel
Potassium
Lidocaine blocks this channel
Sodium
This is the period after AP initiation and just after the peak when a stimulus (no matter how strong) will not initiate another AP due to Na+ channel inactivation
Absolute refractory period
This is the period when Na+ channels are recovering from the inactivation, but a strong stimulus can produce another AP
Relative refractory period
What effect does demyelination have on action potential conduction velocity?
Decreases
Do action potentials decay as they travel down the axons?
No
Conduction velocity is positively correlated to this characteristic of the fiber
Diameter
These form a complex and tether the vesicle to the plasma membrane for docking and priming
SNAREs
SNAP-25, syntaxin, synaptobrevin are this type of compound
SNAREs
Increased levels of this in the presynaptic terminal stimulates acetylcholine release from synaptic vesicles into the synaptic cleft
Calcium
Influx of this causes local depolarization of the postjunctional membrane of the neuromuscular junction
Sodium
Bolutinum toxin blocks release of this at the neuromuscular junction
Acetylcholine
What effect does botilunum toxin have at the neuromuscular junction?
Total blockade
Paralysis of respiratory muscles, death
Curare competes with this for receptors on motor end plate
Acetylcholine
What is the effect of Curare at the neuromuscular junction?
Decreases size of end plate potential
May produce paralysis of respiratory muscles and death
Neostigmine is an inhibitor of this
Acetylcholinesterase
What is the effect of Neostigmine at the neuromuscular junction?
Prolongs and enhances action of acetylcholine at the motor end plate
Hemicholinium blocks reuptake of this into presynaptic terminal
Choline
What effect does Hemicholinium have at the neuromuscular junction?
Depletes acetylcholine stores from presynaptic terminal
Excitatory synapse releases excitatory neurotransmitters, such as this
Glutamate
Excitatory synapse releases excitatory neurotransmitters that triggers opening of these channels
Sodium
Inhibitory synapse releases inhibitory neurotransmitters, such as this
GABA
Inhibitory synapse releases inhibitory neurotransmitters triggers opening of these channels
Chloride
Is glutamate an excitatory or inhibitory neurotransmitter?
Excitatory
In this part of the body, acetylcholine is a neuromodulator
Brain
In this part of the body, acetylcholine is a neurotransmitter
Neuromuscular junction
In the brain, is acetylcholine a neuromodulator or neurotransmitter?
Neuromodulator
In the neuromuscular junction, is acetylcholine a neuromodulator or neurotransmitter?
Neurotransmitter
Do ionotropic or metabotropic receptors form ion channels?
Fast responses
Ionotropic
Do ionotropic or metabotropic receptors use second messengers (i.e. G protein)?
Slow responses
Metabtropic
Are NMDA and AMPA receptors considered ionotropic or metabotropic?
Ionotropic receptors
AMPA transports these ions
Sodium and potassium
NMDA transorts these ions
Sodium, potassium, and calcium
Are NMDA and AMPA receptors excitatory or inhibitory?
Excitatory
Is NMDA a ligand-gated or voltage-gated ionotropic receptor?
Both
This usually blocks the NMDA receptor during normal function
Magnesium
Silent synapse contains this type of receptors only
NMDA
(no AMPA)
Type of excitatory synapse in the brain that are initially inactive but can become active under certain conditions
Contains NMDA receptors only
Silent synapse
Is GABA-A or -B considered a ligand-gated ionotropic receptor?
A
Is GABA-A or -B considered a metabotropic receptor?
B
Benzodiazepines bind to these subunits of GABA-A
Alpha and gamma
Barbiturates bind to these subunits of GABA-A
Alpha and beta
Alcohol binds to these subunits of GABA-A
Alpha and delta
Benzodiazepines, barbiturates, and alcohol have this effect on GABA
Are positive allosteric modulators of GABA-A = enhance receptor function indirectly
This is used as an antidote in the treatment of benzodiazepine overdoses
Flumazenil
This compound decreases GABA function by blocking the pore
Picrotoxin
This compound is a competitive GABA receptor antagonist
Bicuculline
Six connexins form a channel (pore) called this
Connexon
What forms a connexon?
6 connexins
These have an important role in synchronizing neuronal activity and propagation of seizures
Are found in neurons and astrocytes
Can spread electrical current
Electrical synapses (Gap junctions)
Astrocytes maintain homeostasis of this in the CNS
Glutamate
These cells provide net synthesis of glutamine
Astrocytes
Long-term potential involves insertion of AMPA receptors to these membranes
Postsynaptic
Long-term depression involves removal of AMPA receptors to these membranes
Postsynaptic
