• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

Card Range To Study



Play button


Play button




Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

55 Cards in this Set

  • Front
  • Back

What is Synaptic Facilitation?

A rapid increase in synaptic strength that occurs when 2 or more action potentials invade the presynaptic terminal within a few milliseconds of each other.

What is facilitation a result of?

Prolonged elevation of presynaptic calcium levels following synaptic activity.

Calcium enters the presynaptic terminal quickly, but it takes a while for it to go back down to resting levels.

Thus, when action potentials arrive close together, calcium builds up inside of the terminal and allows more NT to be released.

What is Synaptic Depression?

The opposite of facilitation; causes NT release to decline during sustained synaptic activity.

What causes synaptic depression?

Depression depends on the amount of NT that has been released. For example, lowering the external calcium concentration to reduce the number of quanta released by each presynaptic AP, causes the rate of depression to be slowed.

What is the total amount of depression equal to?

Total amount of depression is proportional to the amount of NT released from the PS terminal.

Depletion of what pre synaptic site, is the cause of depression?

A progressive depletion of the pool of synaptic vesicles that are available for release.

What happens when rates of synaptic vesicle release are high?

Vesicles deplete rapidly, and cause a lot of depression.

What happens when the rate of synaptic vesicle release is slowed?

Less depression occurs, because the vesicle pool is able to keep replenishing itself.

State the vesicle depletion hypothesis:

Depression causes the strength of transmission to decline, until the pool is replenished by mobilization of vesicles from a reserve pool.

What is an observation that supports the vesicle deletion hypothesis?

More depression is observed after the size of the reserve pool is reduced by impairing synapsin (a protein that maintains vesicles in the reserve pool).

What is synaptic potentiation?

Elicited by repeated synaptic activity, and increase the amount of transmitter release from the presynaptic terminals.

Occurs late in the stimulus train.

--> Acts on a timescale of seconds to minutes. (Longer than augmentation)

What is synaptic augmentation​?

Elicited by repeated synaptic activity, and increase the amount of transmitter release from the presynaptic terminals.

--> Acts on a time scale of seconds.
(shorter that potentiation)

What is post tetanic potentiation (PTP)?

A result of the slow time course, potentiation that greatly outlasts the tetanic stimulus that induces it.

Although poorly understood, what is the current theory behind how potentiation and argumentation come about (specifically at the cellular level)?

Augmentation - Calcium enhancing the actions of munc-13

Potentiation - Calcium activates presynaptic protein kinases that go on to phosphorylate substrates (such as synapsin).

Describe (in graph form) what facilitation, augmentation, depression, and potentiation looks like.


Why was the marine mollusk, Aplysisa, used to study synaptic plasticity?

- Only has a small number of neurons.
-Neurons are very large.
- Many are in stereotyped (the same, predictable) locations within the ganglia that make up its nervous system.

The aplysia mollusk exhibits habituation. What is that?

A process that causes the animal to become less responsive to repeated occurrences of stimulus.
Ex.) We feel out clothes when we first put them on, but after that we don't feel the pressure of them anymore.

The aplysia mollusk exhibits sensitization. What is that?

A process that allows an animal to generalize an aversive response elicited by a noxious stimulus, to a variety of other non-noxious stimulus.
Ex.) In aplasia that have habituated to siphon touching, sensitization of gill withdrawal is elicited by pairing a strong electrical stimulus to the animals tail, with another light touch of the siphon. This pairing causes siphon touching to again, illicit a withdrawal response.

Describe the neuronal basis of aplysia habituation.

Transmission at the glutaminergic synapse between the sensory and motor neurons is depressed, and is responsible for the decreasing ability of the siphon stimuli to evoke gill contractions during habituation. This is presynaptic depression, caused by depletion of the number of synaptic vesicles available for release.

Describe the neuronal basis of aplysia sensitization.

- Function of the glutaminergic synapse between sensory and motor neurone is modified, by additional neurons being recruited.
- The tail shock that evokes sensitization, activates sensory neurons that innervate the tail. -These sensory neurons, in turn, excite modulatory interneurons that release serotonin onto the presynaptic terminals of the sensory neurons of the siphon.

See page 168 for diagram.

What is the role of serotonin in Aplysia sensitization?

Serotonin enhances NT release from the siphon sensory neutron terminals, leading to increased synaptic excitation of motor neurons.

-This modulation in aplysia lasts about an hour.

State the 6 steps involved in the serotonin modulation of pre-synaptic enhancement underlying behavioural SHORT TERM sensitization (in other words why does touching aplysia with electrical shock what makes them funky)?

1.) Serotonin binds to g-protein coupled receptors on the PS terminals of siphon sensory neutrons.

2.) Production of 2nd messenger cAMP is stimulated by this.

3.) cAMP binds to regulatory subunits of protein kinase A (PKA).

4.) This liberates catalytic subbing of PKA which then are able to phosphorylate proteins including K+ channels.

5.) The net effect of of PKA action reduces the probability that K+ channels open during a PreSynaptic action potential, causing more Ca2+ channels to open up. There is evidence that Presynaptic calcium channel opening is also directly affected by serotonin.


See page 169 for diagram.

Explain how long term sensitization occurs.

Long term involves changes in gene expression, resulting in the synthesis of proteins that change PKA activity and lead to changes in synaptic growth.

--> With repeated tail shocks, serotonin activated PKA involved in short term sensitization phosphorylates (and activates) CREB.

See pg 169 for diagram.

- Creb then stimulates ubiquitin hydroxyls, which stimulates the degradation of the regulatory subunit of PKA, meaning it no longer requires serotonin to be activates.

How is CBEP (protein) involved in long term synaptic facilitation.

CBEP activates mRNAs and may be important for local control of protein synthesis. It also has self-sustaining properties, allowing it to always active, mediating permanent changes in synaptic structure.

What is the difference between short and long term sensitization?

Short: Rely on post translational modification of existing synaptic proteins.

Long: Requires changes in gene expression, protein synthesis, and growth and elimination of new and old synapses.

What is long term potentiation?

Long lasting increase in synaptic strength.

What is long term depression?

Long lasting decrease in synaptic strength.

Where has long term potentiation been most thoroughly studied?

In the mammalian hippocampus.

What does the electrical stimulation of the mammalian shaffer hippocampal cells do?

Generates EPSP's in the postsynaptic CA1 cells of the hippocampus.

How long can LTP's last (long term potentiation)

It is unknown, but at LEAST a year.

What characteristics of the collateral Shaffer hippocampal synapse makes in attractive to study LTPs (Long term potentiaions)?

- LTP requires strong activity in pre and post synaptic neurons, which shaffer cells have (depolarization occurs within 100ms of NT release).

-LTP is input specific: Only occurs when both synapses are active, and won't occur in other INACTIVE synapses even though they may touch the cell.

What is Hebbs theory of learning?

Hebb proposed that coordinated activity of a presynaptic terminal and a postsynaptic neuron, would strengthen the connection between them (1949).

This is exactly what happens in LTP!

What is a coincidence detector?

Allows LTP to occur only when both pre and postsynaptic neurons are active at the same time.

What is associativity?

Weak stimulation of a pathway will not, but itself, stimulate LTP. HOWEVER, if one pathway is weakly activated, while a neighbouring pathway onto the same cell is strongly activated, both will undergo LTP. This goes along with the idea that it takes 2 stimuli for learning to take place. ex.) PAVLOVS DOG!

Briefly explain the experiment about learning in the fruit fly (drosphilia).

Studies found that there a several gene mutations that disrupt learning and memory in flies.

They suggested that a central pathway for learning is signal transduction, mediated by cAMP.

Additionally, manipulation with the CREB transcription factor also inteferes with learning and memory in otherwise normal flies.

What was a key advance in understanding LTP (Hint, it's a type of receptor glutamate receptor that has a cool effect on LTP!)

NDMA receptor agonists prevent LTP, but have no affect on the response evoked by low frequency stimulation of the shaffer collaterals.

NMDA receptors are blocked by MAGNESIUM!
- Depolarization expels Mg2+ from the NMDA channel, allowing current to flow into the postynaptic cell. This leads to Ca2+ entry, which in turn, triggers LTP.

How exactly does the NMDA receptor cause LTP's?

Both AMPA and NMDA receptors bind glutamate, but NMDA is blocked by magnesium. NMDA is voltage dependent, so when the voltage is high enough to get the Mg2+ out, calcium ions can then flow in!

What are 2 requirements for the NMDA receptor to open?

1.) Glutamate has to bind, causing a conformational change in the protein.

2.) Sufficient amount of voltage depolarization has to occur, in order for Magnesium to exit from blocking the channel, so calcium can flow through.

What is the most abundant postsynaptic protein at shaffer collateral synapses, and what is its role in LTP?

CaMKII - enzyme that is activated during stimuli that induce LTPS. Inhibition prevents LTP.

What does the strengthening of synaptic transmission during LTP arise from?

Increase sensitivity of the postsynaptic cell to glutamate. ex.) New AMPA receptors can e added to 'silent' synapses that did not previoulsy have AMPA receptors.

What causes the "expression" of LTP?

Insertion of AMPA receptors where the previously were none.

What causes "induction" of LTP?

Activation of NMDA receptors.

What are silent synapses and when are they most prevalent?

Silence of synapses is due to the blockage of NMDA receptors by magnesium. When the presynaptic cell releases glutamate, it binds to NBDA receptor, but if the Postsynaptic cell is at resting membrane potential, nothing happens because it is blocked by magnesium UNTIL it is sufficiently depolarized.

Some neurons ONLY HAVE NMDA receptors, and this occurs most during development, but decreases in adults.

When are AMPA receptors abundant?

AMPA receptors are scarce in babies, but prevalence increases with age.

How are re AMPA receptors inserted?

1.) During glutamate release, and sufficient stimulation, NMDA receptors open up.

2.) Calcium ions enter the neon.

3.) Calcium activates protein kinease C and CaMKII.

4.) These cause substrate phosphorylation that lead to the insertion of more APMA receptors.

What happens when you block protein synthesis during LTP?

Doesn't affect the LTP measured a few minutes after, but affects LTP measured hours after.

Late phase LTP is initiated by protein kinase A, which goes on to active transcription factors such as CREB, which stipulate the expression of other proteins (hey hey, AMPA receptor insertion, remember!?!)

When does LTD occur (long term depression) occur? (Hint, what kind of stimulus, and for how long)

When shaffer collateral are stimulated at a low (1hz) rate, for long periods.

In neuronal terms, small and slow rises in Ca2+

When does LTP occur? Hint (what kind of stimulus and for how long?)

Brief high frequency stimulation.

In neuronal terms, large and fast increases in Ca2+

True or false, LTD can erase the effects of LTP?


How are AMPA receptors involved in LTD?

Calcium enter the excited cell through NMDA receptors, which activates protein phosphotasesm which dephosphorylate substrates, and the amoa recruits are removed from the membrane and go back into the dendritic spine (opposite of how LTP works!!!!! AHHHH) :)

This is due to the same clathrin dependent endocytosis mechanisms important for synaptic vesicle recycling.

How is cerebellar LTD different that hippocampal LTD?

-The difference is found within the parallel and climbing fibres of the cerebellum. Glutamate binds to the glutamate receptor on the post synaptic neuron.

-Does not involve the entry of calcium.

- requires the activity of a protein kinase, rather than a phosphatase.

-NMDA receptors are not present in the cerebellum purkinjie cells.

What is spike timing dependent plasticity?

Precise timing of pre and post synaptic activity determining polarity. ( depression or potentiation)

What happens if a postsynaptic action potential occurs before a presynaptic action potential in spike-timing dependent plasticity?

Post before pre, she wants the D (LTD)

What happens if a presynaptic action potential occurs before a postsynaptic in spike timing dependent plasticity?

Pre before post, Potentiation occurs most (LTP)

What is kindling? (Hint: Epilepsy)

Seizure production, by insertion of an electrode into the amygdala.

Weak stimulation produces no effect, but repeated weak stimulation every day for weeks, soon causes full blown seizures. Eventually, even the weak stimulus applied after a year will still illicit a full blown seizure. (Kindling - a single match growing to start a HUGE fire).