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Brain And behaviour (BIBB109) > Chapter 4 - Synaptic Transmission > Flashcards

Chapter 4 - Synaptic Transmission Flashcards

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1
Q

Define electrical synapse

A

Ion channels connect cytoplasm of pre- and post-synaptic cells

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2
Q

Define chemical synapse

A

Neurons are separated by synaptic cleft

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3
Q

Briefly explain the chemical synapse. SIMPLY

A

AP leads to real ease of neurotransmitters that diffuse across the synaptic cleft.
Neurotransmitter interacts with receptors on postsynaptic cell causing either depolarization or hyperpolarization

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4
Q

What is a gal junction?

A

A gap junction is the channel at the electrical synapse comprised of 2 connexons with 6 connexins each

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5
Q

What contains neurotransmitters?

A

Synaptic vesicles

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6
Q

What are the three types of synapses?

A
  • axodendritic
  • axosomatic
  • axoaxonic
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7
Q

What is another way of differentiating synapses (not axoaxonal,…)?

A

The symmetry of the membranes :

  • asymmetrical membranes (Gray’s Type 1) —> round vesicles —> excitatory
  • symmetrical membranes (Gray’s type 2)
    —> flattened vesicles—> inhibitory
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8
Q

What the different types of neurotransmitters?

Give one example per nt.

A
  • Amino acids : glutamate, GABA, glycine
  • Amines : acetylcholine (ACh)
  • Peptides (molecule of different amino acids) : dynorphin
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9
Q

Where and how are large peptides formed?

A

1) large peptides are formed in the ribosomes in the rough endoplasmic reticulum.
2) Thé Golgi apparatus folds the newly formed, PRECURSOR, peptide
3) The active peptide neurotransmitter is packaged into secretory granules for transport and ease

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10
Q

What déterminâtes the effect of a specific chemical messenger on the postsynaptic cell?c

A

The action of the messenger depends on the properties of the receptor with which the transmitter binds.

It DOES NOT depend on the chemical nature of the neurotransmitter.

Ex : there is nicotonic ACh and muscarinic ACh. The difference is the type of receptor

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11
Q

What do the agonist and antagonist do respectively?

A

Agonist : mimics the effect of the neurotransmitter

Antagonist : blocks the effect of the neurotransmitter

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12
Q

What is the motor unit?

A

The motor neuron and muscle cell it inervates

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13
Q

Explain the neuromuscular junction ( how the neurotransmitter actually reaches the other side and everything…)

A

The synaptic vesicles lead the neurotransmitter to synaptic cleft.
Then the nt reach the postsynaptic receptors.
This leads to the channels opening and releasing potassium and intaking sodium ions.
This leads to depolarization of postsynaptic.

The depolarization opens voltage-gated sodium channels.
This leads to Na+ inflow (positive feedback after)
This all embodies the AP

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14
Q

Explain the 9 steps of chemical transmission

A

1) transmitter is synthesized and stored in vesicles
2) An action potential invades the presynaptic terminal
3) Depolarization of the presynaptic terminal causes opening of voltage-gated Ca2+ channels
4) Influx of Calcium causes vesicles to bind with presynaptic membrane
5) Transmitter is released in synaptic cleft via exocytosis
6) Transmitter binds to receptor molecule in postsynaptic membrane
7) This causes opening or closing of postsynaptic channels
8) Postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of postsynaptic cell
9) Retrieval of vesicular membrane from plasma membrane (Reuptake)

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15
Q

What are the two types of proteins involved with the binding of vesicles to membrane? What are their roles?

A
  • SNARE proteins : bring two membrane close together
    —> synaptobrevin (vesicle membrane)
    —> syntaxin and SNAP-25 (in plasma membrane)
  • Calcium binding protein :
    —> synaptotagmin (in vesicles membrane, binds calcium)
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16
Q

The reversal potential for the GABA-A receptor is -65mV. When patch clamping a
GABA-A receptor, which way will ions flow through the ion channel if the
membrane potential is -60mV when GABA is applied to the bath?

A

Cl- will grow in.

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17
Q

What are the mechanisms involved in the recovery and degradation of the neurotransmitter?

A
  • Reuptake: neurotransmitter re-renters the pre-synaptic axon terminal.
  • diffusion: away from the synapse
  • enzymatic destruction (inside cytosol, or in synaptic cleft)
    ex: AChE cleaves ACh to inactive state
18
Q

What are the two gating mechanisms at chemical synapses?

A

1) Direct gating (or Ligand-gated ion channels):
- receptor = effector
- Ionotropic receptors

2) Indirect gating (G-protein-coupled receptors):
- receptor protein that binds transmitter is distinct from the ion channel
- effects of transmitter binding receptor are coupled to an effector protein by a set of G-proteins
- receptor =/ effector
- Metabotropic receptors

19
Q

On what does the effect of opening an ionotropic channel depend?

A

It depends on the type of ion.
ex: flow of Chloride would be into the cell, as this ion is negatively charged and would want to bring the Vm down to the E(Cl)
This would make it less likely for the cell to fire an AP (as it is further from threshold potential)

20
Q

What is an inhibitory synapse?

A

IPSP —> flow of ions makes it harder to reach threshold

21
Q

REVIEW REVERSAL POTENTIAL!

A

Review

22
Q

What are the forms that the effector of the metabotropic receptor can take?

A
  • G-gated ion channel

- enzyme (créâtes second messenger)

23
Q

What are the characteristics of metabotropic receptors?

A
  • metabotropic receptors that use second messengers act too slowly to fire an AP
  • they influence the efficacy of direct gating channels (ionotropic channels)
  • these channels are called neuromodulatory
  • neurotransmitters that hind metabotropic receptors are called neuromodulators
24
Q

What are a receptor’s two major functions?

A

1) recognize and bind transmitter

2) activate effector proteins

25
Q

What are the 3 types of glutamatergic receptors?

A

AMPA receptor

NMDA receptor

Kainate receptor

26
Q

What is important to know about NMDA receptor?

A
  • is a glutamate receptor that is both a ligand gated (glutamate must be bound) and voltage gated (at rest, the channel is blocked by Mg++)
27
Q

Why is it said that NMDA receptor is a coincidence receptor?

A
  • channel opens only when both pre and post synaptic elements are active
  • Pre synaptic cell is active - it’s releasing glutamate
  • post synaptic cell is active - it’s depolarized (AMPA receptors) and therefore Mg++ block in NMDA is removed)
28
Q

What happens once the Mg++ block is removed from NNDA channel?

A
  • Sodium and Ca++ enter postsynaptic cell
  • the increased intracellular Ca++ initiates a cascade of events :

) activates enzymes
) regulates opening of ion channels
) affects gene expression

29
Q

Cite 2 inhibitory neurotransmitters?

A

Glycine and GABA —> lead to influx of Cl- into postsynaptic cell

30
Q

What are 4 neurotransmitters that use ionotropic receptors?

A
  • ACh
  • Amino acids : ) glutamate
    )GABA
    )Glycine
31
Q

What are 4 neurotransmitters that use metabotropic receptors?

A

The same as for ionotropic

32
Q

What constitutes a G-proteins?

A

3 subunits : delta, beta and gamma

33
Q

In a GPCR, what happens when the transmitter binds the GPCR?

A
  • GDP is replaced by GTP and the trimer splits apart into active delta and gamma x beta subunits
  • delta and gammabeta subunits interact with ion channels or enzymes that activate second messenger systems
34
Q

What is phosphorylation?

A

Protein kinases transfer phosphate from ATP in cytosol to proteins.

35
Q

What is the effect of phosphorylation on channels?

A

Changes conformation of protein and determines whether a channel is open or closed.

36
Q

What is dephosphorylation?

A

Protein phosphatases remove the phosphate groups.

37
Q

How do GPCRs amplify the signal?

A

1) neurotransmitter binds receptor
2) receptor activated G-protein
3) G-protein stimulâtes adenylyl Cyclades (enzyme) to convert ATP to cAMP
4) cAMP activates protein kinase A
5) Protein kinase A phosphorylates potassium channels

38
Q

What is synaptic integration?

A

Synapses add together the inputs from different presynaptic cells.

39
Q

What are the two mechanisms for synaptic integration?

Define them

A

Spatial summation: several spatially distinct inputs fire simultaneously such that their postsynaptic effects cause sufficient depolarization to reach threshold

Temporal summation: the summation of sequential postsynaptic effects of an individual presynaptic input leads to a depolarization that reaches threshold.

40
Q

What happens to a sub threshold potential?

A

It decreases exponentially with distance as it travels down the dendrite

41
Q

What are the effects of the location of inhibitory inputs?

A

Presynaptic inhibition:

  • decreases depolarization in presynaptic terminal. Less quanta is released.
  • specific, aimed at particular excitatory inputs

Postsynaptic inhibition:
- affects all inputs therefore not specific.

Brain And behaviour (BIBB109) (28 decks)

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