Neuro B5 Flashcards
Ionotropic Receptor
Receptor that, when activated by an appropriate agonist, functions as an ion channel when appropriately stimulated.
Metabotropic Receptor
Receptor that, when activated by an appropriate agonist,interacts with a G protein to produce a change of enzyme activity within the postsynaptic cell
AMPA receptor
ionotropic glutamate receptor that is activated selectively by the agonist alpha-amino-3-hydroxy-5methyliosxazole-4-propionic acid (often called a non-NMDA receptor)
NMDA receptor
ionotropic glutamate receptor that is activated selectively by the agonist N-methyl-D-aspartate
Excitatory Postsynaptic Potential (EPSP)
excitatory depolarizing graded potential driving membrane potential towards the threshold for action potential
Inhibitory Postsynaptic Potential (IPSP)
inhibitory hyperpolarizing graded potential driving the membrane potential away from threshold for action potential
why is there a small synaptic delay between arrival of the impulse and a postsynaptic response?
time required for release, diffusion and binding of transmitter, opening of ion channels, movement of ions and changes in enzyme activity.
Exocytosis or quantal release of transmitter is governed by what?
P- probability that the contents of a given vesicle will undergo release
N- number of vesicles available for release
Therefore the number of vesicles participating in exocytosis is given by pn
Can the value of p be non zero even in the absence of impulses in the nerve terminal?
yes due to the increase with Ca2+
small spontaneous (without nerve stimulation) transient depolarizations can happen where? (Also called minEPPs)
at the muscle end plate
What is a standard way of lowering P (probability of release) at the NMJ (neuromuscular junction)?
replace Ca2+ with Mg2+ —-> this will reduce influx of Ca2+
When the P (probability of release) is low, what do the EPPs (end plate potentials) look like?
have amplitudes that are multiples of a set minimum (referred to as quantal fluctuations)
Quantal Size
number of transmitter molecules in a vesicle
Quantum Content
The number of quanta released by a single impulse
Mean Quantum Content
mean size of EPP (end plate potential) / mean size of MinEPP
Is Botulinum Toxin considered a protease?
YES :)
What is Botulinum Toxin produced by?
produced by Anaerobic Bacillus Clostridium botulinum
What is the mechanism of action of botulinum toxin?
Prevents vesicular release of ACh irreversibly. does this by binding to the cholinergic nerve endings, entering the cell and suppressing the docking mechanism by breaking down synaptobrevin (remember that is a v-SNARE protein)
What are some signs and symptoms of a patient several hours after ingestion of botulinum toxin?
double vision, dysphagia, dry mouth, and dysarthria followed by weakness of limbs and trunk
what are some clinical uses of Botulinum Toxin?
treatment of destinies (muscle contractions) or wrinkle reduction
Is Tetanus Toxin considered a protease?
Yes of course :)
What is Tetanus Toxin produced by?
by the anaerobic bacillus Clostridium tetani (from soil)
Does tetanus toxin enter the PNS or CNS?
PNS via a cut or wound then passes to CNS by retrograde axonal transport
What is the mechanism of action of Tetanus Toxin?
Enters glycinergic interneurons and suppresses the docking of vesicles by breaking down synaptobrevin. The suppression of glycine release disinhibits lower motor neurons.
What is the mechanism of action of aminoglycoside antibotics? (neomycin and streptomycin)
Inhibit exocytosis of ACh at motor nerve terminals by blocking presynaptic calcium channels. Therefore raising extracellular calcium
What is the mechanism of action of the drug aminopyridine?
K+ channel blocking drug prolongs the duration of the impulse and thereby enhances Ca2+ entry tin the motor nerve ending. Hence enhancing quantum content
Explain what happens in EPSPs? (excitatory post synaptic potentials)
positive charge flows into the neuron at the dendrite and sonata and passes to adjacent cellular surfaces
As the current spreads further from the synaptic sites do depolarizations decline or increase?
decline, duh! (EPSPs spread with decrement) ;)
Where is the density of voltage-gated sodium channels the highest?
At the axon hillock (therefore this is the initiation zone for action potentials)
Where is the initiation zone for sensory neurons?
close to the sensory ending rather than at the junction of the cell body and axon
Explain spatial summation
more then one input into the same cell, however, we are adding inputs from different parts of space( could be sufficient to provoke an action potential)
Explain temporal summation
perhaps 10 impulses at 20ms intervals that serially arrive at the excitatory synapse on a motor neuron
The firing rate of a neuron is dictated by what?
by the combined effect of the spatial and temporal summation of EPSPs (excitatory post synaptic potentials) and IPSPs (inhibitory post synaptic potentials)
Do both the transmitter release and the cellular effects of transmitters occur briskly?
No, transmitter release occurs briskly but cellular effects of transmitters may linger for 20ms or far longer
The transmitter, glutamate, is rapidly removed from the synapatic cleft by transporters, explain the process
Glutamate when taken up by transporters into astrocyte, is metabolized to glutamine, which has its own neuronal transporter
Are peptide transporters found in blood brain barrier cells?
yes
How are norepinephrine, epinephrine, dopamine, and serotonin (5-HT) absorbed and then degraded in the outer membrane of mitochondria in the nerve endings?
absorbed via transporters and then degraded by monoamine oxidase (MAO). NOTE—> can also be degraded by COMT
