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PSL300 > Lesson 4- Synaptic Potentials: Ionotropic & Metabotropic > Flashcards

Lesson 4- Synaptic Potentials: Ionotropic & Metabotropic Flashcards

1
Q

where does the transmitter thats emitted from the presynaptic receptor go to?

what does the binding of the transmitter do to the protein?

A
  • Transmitter agent diffuses across synapse from the pre-synaptic neuron and binds to a specific receptor site on the postsynaptic membrane
  • Binding of transmitter causes a change in shape of the receptor protein
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2
Q

what are the types of receptors on the postsynaptic neuron? (2)

A
  • Receptors are either:
  • Ionotropic (directly opens channels)
    – Metabotropic (initiates a metabolistic cascade to activate enzymes)
  • Receptor determines the effect, not the transmitter
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3
Q

What happens when the transmitter ligand binds to the ionotropic receptor on the post-synaptic membrane?

how long does the PSP last?

What ion channels open and what is it called if the ESP is depolarized vs hyperpolarized?

A
  • When the transmitter binds to an ionotropic receptor on the post-synaptic membrane it results in the opening of an ion channel and changes the post-synaptic membrane potential (PSP)
  • as long as the transmitters are present, the PSP will last around 20-40 ms long
  • if the binding of the transmitters on the post synaptic membrane results in depolarization (more positive PSP) –> Na+ and K+ ion channels will open –> this is called EPSP (excitatory PSP)
  • if the binding of the transmitters on the post synaptic membrane results in hyperpolarization (more negative PSP) –> Cl- and K+ ion channels will open –> called IPSP (inhibitory PSP)
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4
Q

example of ionotropic receptors with acetylcholine transmitter and nicotinic receptor

A
  • acetylcholine is transmitted and binds to the nicotinic receptors on the post-synaptic membrane
  • this results in a conformational change on the receptor causes the cation channel to open
  • since the cation channel opens, an EPSP is conducted and Na+ and K+ ion channels are open
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5
Q

what are the transmitter ligands that can act on ionotropic receptors?

A

– Acetylcholine (Ach)
– Glutamate
– GABA (used for generating an IPSP)
– Glycine

  • All these ligands can act on the metabotropic receptors; It’s the receptor that determines the effect and not the transmitter
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6
Q

how are benzodiazepines (affect GABA levels) used to treat anxiety

A
  • benzodiazepines are used to treat anxiety and more
  • common name is lorazepam etc.
  • they work by increasing the brain chemical GABA –> this decreases the excitability of neurons (IPSP) –> reduces the communication between neurons –> thus has a calming effect on the brain
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7
Q

What happens when the transmitter ligand binds to the metabotropic receptor on the post-synaptic membrane? what is produced or destroyed as a result?

A
  • Binding of the transmitter ligand to the post-synaptic metabotropic receptor activates an enzyme that is usually G-protein coupled
  • The enzyme facilitation will result in either inc. production or destruction of 2nd messengers
  • this will then sometimes result in opening of ion channels (not guaranteed - may be internal metabolic effect)
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8
Q

how are metabotropic effects different than ionotropic effects in terms of speed?

A
  • Ionotropic effect is much more immediate (opens ion channel directly as soon as ligand binds - fast EPSP, fast IPSP)
  • The metabotropic receptor activation takes time
  • If you influence an ion channel through the metabolic effect (i.e. through phosphorylation), the change in MP will develop slowly (slow EPSP, slow IPSP)
  • Change is slow because of it has to go through all the enzyme activity first before influencing the ion channels
  • Moreover, it is not necessary that there is any change in the MP, it might be all internal metabolic effect
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9
Q

what are the three types of 2nd messengers for metabotropic receptors and what is their function? what does their function do for ion channels?

A

2nd messengers are either: cAMP, cGMP, or InP3
* 2nd messenger then activates other enzymes, e.g. phosphokinases which
phosphorylate membrane proteins or other proteins in the cytoplasm
* If you phosphorylate membrane proteins (i.e. ion channels) > result in opening of ion channels

2nd step involved for metabotropic receptors which is the involvement of 2nd messengers

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10
Q

example of metabotropic receptors with B-adrenoreceptor (beta receptor) and Noradrenalin transmitter

B = beta symbol

A
  • B-receptor is a metabolic receptor for Noradrenalin (NA)
  • Binding of NA to B-receptor activates adenylyl cyclase via G-protein alteration
  • adenylyl cyclase increases the production of cAMP (2nd messenger)
  • cAMP then activates kinases which phosphorylate membrane Ca++ channel
  • Phosphorylation of the Ca++ channel –> increase in Ca++ influx (important in heart muscle for an increase in contractility)
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11
Q

how are beta blockers used at the NA and adrenoreceptor site? what ion and function does this effect

A
  • beta blockers work at the site
  • they blocks the interaction of NA to the B-receptor
  • this results in decrease in the Ca++ availability (calcium is involved in the contractility of the heart)
  • thus less Ca++ = dec. contractility of the heart
  • used clinically to reduce excessive contractility of the heart
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12
Q

what is used in the endocrine system that is also used in the nervous system as metabotropic transmitters?

list some examples

how is acetylcholine binding differ in ionotropic receptors and metabotropic receptors?
- what does specific receptor does it bind to in each case?

A
  • many peptides and hormones that are used in the endocrine system are used as metabotropic transmitters in the nervous system

ex.
* ACh: Muscarinic receptor
* Peptides: substance P,  -endorphin, ADH
* Catecholamines: noradrenaline, dopamine
* Serotonin
* Purines: adenosine, ATP
* Gases: NO, CO

  • we have seen ACh - acetylcholine when bound to the nicotinic receptor (an ionotropic receptor) produced an inotropic effect
  • but when acetylcholine is bound to muscarinic receptors (metabotropic receptor) then this will lead to a metabotropic effect
  • reinforces the idea that its the receptor that causes the effect not the neurotransmitter
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13
Q

what is the difference between an action potential and a graded potential

  • what generates an AP or GP?
  • where is an AP or GP generated
  • is there a loss of voltage of an AP or GP as it moves along the cell?
A

GP:
- EPSPs generate graded potentials
- these are generated at the synapse that connects the pre and post synaptic neurons (before the trigger zone)
- there is a loss in voltage as the EPSP moves along the cell body of the neuron

AP:
- depolarizing currents generate action potentials
- these are generated at the trigger zone at the end of the neuron
- there is no loss of voltage as the AP moves along the axon because of the all-or-nothing principle (maintains a consistent amplitude and speed as it propagates along the axon)

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14
Q

Why can a graded potential not fire an action potential

A

the energy at the synapse cannot fire an AP because the dendrites and cell body are non-excitable (don’t have many Na+ ion channels)

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15
Q

How do EPSPs work to signal for an eventual AP?

A
  • If an EPSP is generated at the post synaptic neuron, it must pass through passive conduction across the soma to get to the trigger zone of the axon
  • we hope that when it reaches the trigger zone, there will be enough depolarization left over so that the trigger zone can reach threshold from -70mV to -55 mV and fire an AP
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16
Q

explain signal degradation with EPSPs

how does this effect APs

how do we combat this with summations?

A
  • if the trigger zone is too far from the synapse, you will get signal degradation - you will loose depolarization as you move away from the synapse
  • thus a single depolarizing EPSP will not be enough to bring the trigger zone to threshold for an AP
  • we need lots of EPSPs working together to depolarize the membrane from -70 to -55 mV
  • this process of adding a bunch of PSPs together is called PSP summation
17
Q

what are the two types of EPSP summations

A
  • Spatial summation: many different synapses are working together making a synchronous EPSP
  • temporal summation: few active synapses, but all generating EPSPs at a very high frequency
18
Q

what is spatial summation

A
  • a large number of EPSPs are working together simultaneously on the dendritic tree
  • even if their voltage alone is not large enough to bring the trigger zone to threshold, summated it will be able to fire an AP
  • for this to work they must act in synchrony and be activated at the same time
19
Q

what is temporal summation

A
  • EPSPs last for about 30-40 ms in duration before dying out
  • thus, successive inputs of EPSPs must be given before the previous input dies out, in order for the voltages to stack on each other in a staircase pattern and eventually reach the threshold potential of -55 mV –> generates AP (eg. EPSP delivered 10 ms apart)
  • important for high frequency of EPSP rather than number of synapses
20
Q

where are IPSPs located on the cell and how is this a strategic advantage

A
  • IPSPs tend to be preferentially located on the cell soma, interposed 1⁄2 way between the site where EPSP is generated and the trigger zone
  • IPSPs have strategic advantage: due to its location in the middle between the EPSP and the trigger zone –> it can stop the depolarizing EPSP current from reaching the trigger zone
21
Q

How do IPSPs shunt or kill the depolarizing EPSP current?

A
  • we have to make the membrane more negative
  • IPSP involves the opening of the Cl- channel
  • Cl- are located more on the out than the inside because they are repelled by the negatively charged protein
  • The equilibrium potential for Cl- is very close to the resting MP (-70 mV)
  • Therefore at rest, opening of the Cl- channel would result in little change
  • However, when the membrane is depolarized through EPSPs (more positive), opening of the Cl- channel will bring the MP back down to -70 mV
  • The net affect of Cl- is basically to ‘clamp’ the membrane potential to -70 mV, which is preventing excitation, thus preventing successful depolarization by EPSP –> inhibitory effect
  • These IPSPs are very strategically located and they completely block any signal coming from EPSPs simply by positioning right on the soma between EPSP and trigger zone
22
Q

why are IPSPs more important than EPSPs in the nervous system?

A
  • This is because it controls all the information
  • shapes the information
  • IPSPs tend to be very specific and precise, whereas EPSPs are all over the place and not accurate
  • we are defined by how we inhibit ourselves (okay freud)
23
Q

what is a spike train?

A
  • suprathreshold stimulus results in more AP firing within a time period = inc. frequency
  • we want this strong input that lasts a long time to be translated in a continuous stream of APs called a spike train
  • telling the brain that this is a powerful and long stimulus
24
Q

how do we generate a spike train?

A
  • if we recall, when we have a stimulus that reaches above threshold and fires an AP, we can only fire another AP once the membrane is polarized again below threshold and reopens the shut voltage sodium channels (refractory period)
  • in order to generate a spike train we need to hyperpolarize the membrane to restore the Na+ channels asap so that the next AP can be generated
25
Q

what will happen if we have a powerful suprathreshold stimulus and it lasts a very long time (around 500 ms)? how will we generate multiple APs within this 500 ms frame to generate a spike train?

A
  • if we have a powerful suprathreshold stimulus and it lasts a very long time (ex. 500 ms), we can generate multiple APs within 500ms instead of just generating one and waiting for the membrane to fully polarize 500 ms later for the next AP to be generated
    –> wasted energy and potential
  • to generate more than one, ie create a spike train, we have to overcome the depolarization ‘block’
  • with the addition of voltage gated K+ channels that open when the membrane is depolarized, we can use these ‘extra’ K+ channels to quickly re-polarize the membrane below threshold level –> this is called after-hyperpolarization
  • this will allow the voltage gated Na+ channels to be reconfigured quickly, so that they can generate another AP, even within the 500 ms

PSL300 (22 decks)

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