Flashcards in Lecture 20 Deck (28):
How do different mechanism affect the pre-synaptic side?
Change the # quanta released per stimulus
How does facilitation affect vesicle release?
Increases the LIKELIHOOD that a vesicle's contents will be released
NO change to the size of each vesicle/amt of NT inside
Will one large stimulation cause facilitation?
NO - frequency dependent
More rapidly the nerve is stimulated - greater effect on EPSP
What is the mechanism that explains facilitation?
More stimuli = more depolarization = more Ca in pre-synaptic terminal
1. Lingering "on" machinery activated by Ca (priming)
2. Extra Ca adds to the depol of the next stimulus
What is depression?
Repeated pre-synaptic stimulation causes ever smaller EPSPs
↓# quanta released - again not about size
What mechanism explains depression?
Depleted pre-synaptic vesicles
Can you predict if depression of facilitation will be dominant at a synapse?
Both are present at varying degrees
Which one wins depends on the role of that synapse
Where on a neuron is a synapse a weak contributors to generating neuron depolarization?
Synapses on dendrites
Often far away from soma - signal becomes weaker the further it has to travel
Where on a neuron is a synapse a strong contributor to generating neuron depolarization?
Axon initial segment
What part of the neuron is the "detector" = determines whether a depolarization will occur? Why?
Axon initial segment
↑[Na channels] = low threshold
If depolarized, will send it down the length of the axon = myelinated
What is facilitation?
Rapid stimulation causes increasingly large sized EPSPs
What are passive electronic characteristics of the neuron that contribute to EPSP decay as it travels?
Current will escape through open ion channels as it travels
What is temporal summation?
2 potentials at same synapse in rapid succession
What is spatial summation?
2 potentials at 2 different synapses at the same time
How do neurons attempt to compensate for its own passive properties that lead to electronic decay of EPSPs with travel?
Add more Na channels to dendrites so that the signal can travel further
What is inhibition by shunting?
Inhibitory synapses near cell body
Will allow depolarizing (+) ions to leak out and it allows = ions to leak in
Loose current this way --> less excitatory input reaches the soma
"Prevents a depolarization"
Is the AMPA receptor excitatory or inhibitory? What is its NT?
What is long term potentiation? Are its effects transient or long lasting?
Elevated EPSP baseline (pre-stimulation)
Rapid stimulation --> gets progressive larger EPSPs --> then a SUSTAINED elevated baseline
What would block LTP?
Is a Ca2+ channel - block this = no change in baseline
What 3 factors make us think LTP is linked to memory?
2. Associative - requires events at both pre-synapse (glutamate release) and post-synaptic depol (via AMPA-R)
3. Specific - doesn't travel to affect neighboring synapses
What is LTP induction? Describe the process.
Detection of signal by NMDA receptor
1. MORE glutamate released than usual
2. Binds AMPA receptors --> STRONG post-synaptic depolarization
3. Remove Mg2+ NMDA receptor block
4. NMDA receptors open --> Ca2+ entry
How Ca2+ in the post-synapse cause LTP?
Activates protein kinases
With an elevated baseline from Ca2+ in the terminal, the synapse is now stronger meaning it can produced stronger depolarizations. How? (Hint: expression)
Insert new AMPA receptors into post-synaptic membrane
↑glutamate sensitivity of future stimuli
Where are new AMPA receptors often added for LTPs?
Makes sense - where most synapses occur
Where do these new AMPA receptors come from?
Were part of reserve normally used to replace worn out AMPA receptors
What are 2 other changes that must happen to accommodate the ↑# AMPA receptors?
↑size of dendrite spines
(Both of these indicate a stronger synapse in general)
How are the LTP changes from induction/expression maintained?
Change in protein translation and transcription