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Neuropharmacology > What other ways can a drug affect neuronal transmission? > Flashcards

What other ways can a drug affect neuronal transmission? Flashcards

1
Q

What is neurotransmission?

A

An umbrella term that refers to anything affecting 1) neuron firing, 2) neurotransmitter release, or 3) receptor actions
- it refers to all actions at the synapse

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2
Q

What happened in 1952?

A

Fatt and Katz placed electrodes at the neuromuscular junction to record the muscle activity with no stimulation

  • they discovered that the voltage change of the electrode always increased/decreased quantally (by a factor of the minimum voltage)
  • thus, they concluded that neurotransmitter release must also be quantal, in discrete packages
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3
Q

What does quantal mean?

A

By a factor of something, and not anything in between

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4
Q

What neurotransmitter do most neurons at the neuromuscular junction release?

A

Acetylcholine

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5
Q

Which protein plays an important role in ACh release?

A

Syntaxin

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6
Q

What is the neuromuscular junction?

A

The point where neurons and muscles meet

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7
Q

What effect does clostridium botulinum have on the body?

A

This bacteria can paralyze the body and even arrest respiration

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8
Q

How does clostridium botulinum effect neurotransmission?

A

It releases a toxin into the post-synaptic neuron that halts the ability of syntaxin from aiding the vesicle containing ACh to get to the cleft, so that the vesicle cannot dock on the cleft

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9
Q

What is syntaxin? What does syntaxin do?

A

Syntaxin is a protein found in the synapse of a neuron; this protein guides the vesicle towards the synaptic cleft to release its neurotransmitter

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10
Q

What are vesicles?

A

The phospholipid bilayer packet within the synapse that contains the neurotransmitter

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11
Q

Which compound is NECESSARY for the synthesis of ACh?

A

choline

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12
Q

Why do we need a diet that contains a minimal amount of choline?

A

Because our body cannot produce choline on its own, but only minimal amounts are needed to synthesize ACh

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13
Q

What are some foods containing choline?

A

Eggs, brains, kidneys, beans

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14
Q

What is the reaction to synthesize ACh?

A

choline + acetyl coenzyme A together react to form ACh (via choline acetyltransferase)

OR

acetylcholine + co-enzyme A react to get back to choline

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15
Q

Which compound is RESPONSIBLE for the synthesis of ACh?

A

choline acetyltransferase (ChAT)

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16
Q

In what two ways would one need a choline supplement?

A
  1. If one has a very poor diet

2. If one is pregnant

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17
Q

What are docking proteins?

A

Proteins that sit on the vesicles

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18
Q

What is one example of a docking protein?

A

Syntaxin

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19
Q

What is Dale’s Law?

A

The law that states that one neuron only releases one type of neurotransmitter (although today we know that this law isn’t 100% accurate)

20
Q

What neurotransmitter would a cholinergic neuron release?

A

ACh

21
Q

Where does the synthesis of ACh take place?

A

In the mitochondria of the cholinergic cell

22
Q

How does the neurotransmitter get inside the vesicle?

A

Via the vesicular ACh transporter (for ACh)

23
Q

Describe the process of the vesicular ACh transporter bringing ACh into the cell?

A

The transporter swaps one hydrogen proton out for every one NT particle in
- uses indirect energy to swap out H+ for ACh, due to the concentration gradient of H+ being higher inside the cell vesicle compared to the outside

24
Q

How is hydrogen kept at a higher concentration inside the vesicle compared to the outside?

A

Via the proton antiporter (which pumps H+ into the cell using ATP)

25
Q

What are AChEIs (acetylcholine esterase inhibitors)?

A

A family of drugs that blocks the effect of the enzyme that breaks ACh down (AChE)

26
Q

How is ACh cleared from the synapse? Why does this have to be a quick process?

A

ACh is cleared by reuptake via one of two processes

  1. LACU (low affinity choline uptake) - this has the same effect as if the choline particles were simply diffused back into the pre-synaptic neuron
  2. HACU (high affinity choline uptake) - uses active transport to bring the choline up into the pre-synapse
27
Q

How is ACh primarily deactivated?

A

Via the enzyme acetylcholinesterase (which is located in the cleft of the neuron)

28
Q

What are the two classes of ACh receptors?

A
  1. Nicotinic ACh receptors (nAChRs)

2. Muscarinic ACh receptors (mAChRs)

29
Q

What kind of receptor type are nAChRs? Where are they primarily found?

A

They are ligand-gated ion channels; found primarily in the PNS (autonomic NS responsible for breathing, heart rate, smooth muscle contraction, digestion, etc)

30
Q

Which ions of the central pore of the nAChRs permeable to?

A

Na+, K+ and Ca2+

- therefore, the binding of ACh on a nAChR is excitatory

31
Q

How many different subunits does a nAChR have? What is the implication of this?

A

there are 17 different types, each with a specific number of receptors within that type (ex. Alpha type has 10 different receptor types)
- this means that nAChRs have an incredible amount of variability (10 to the 17th power)

32
Q

What are the health implications of nicotinic ACh?

A

it reduces Parkinson’s tremors and improves memory in Alzheimer’s

33
Q

What is curare?

A

It is a reversible (competitive) antagonist of nAChR that paralyzes

  • it removes the ability of ACh to act on the nAChR
  • the antidote for curare poisoning is an AChEI (which outcompetes the toxin)
34
Q

What kind of receptor type are mAChRs? Where are they primarily located?

A

They are G-Protein Coupled receptors; located primarily in the CNS

35
Q

How many subtypes of receptors are there?

A

5 subtypes of mAChRs:

  • M1
  • M2
  • M3
  • M4
  • M5
36
Q

Of the different subtypes of mAChRs, which are Gq type receptors? What second messenger pathway does this lead to?

A

M1, M3 and M5 are all GqPCRs

- this means that they activate the PIP2 pathway

37
Q

Of the different subtypes of mAChRs, which are Gi type receptors? What second messenger pathway does this lead to?

A

M2, M4

- leads to inhibitory adenylyl cyclase pathway

38
Q

How are the mAChRs modulatory in their effects?

A

Because the pore is permeable to K+, Ca2+ and Cl-
- it either opens or closes these channels, depending on the post-synaptic receptor (if it’s an Modd receptor to activate PIP2 pathway, or Meven to activate inhibitory adenylyl cyclase pathway)

39
Q

Which mAChRs are most implicated in cognition?

A

M1 and M4

40
Q

Why is it so difficult for pharmacologists to treat Alzheimer’s if we know that ACh is very important in the formation of memories?

A

The search for selective cholinergic agonists is very difficult, because the active site is highly conserved (meaning it is nearly identical across subtypes)
- therefore, it is difficult to develop a drug for a mAChR implicated in memory without affecting a mAChR implicated in autonomic muscle control

41
Q

What are the two main anatomical abnormalities surrounding Alzheimer’s patients?

A
  1. plaques in the brain
  2. tangles of nerves
    - excessive tau proteins cause the failure of the neurons in these two ways
42
Q

How can one attempt to treat Alzheimer’s?

A

With AChEIs

  1. Tachrine (but has a short half life)
  2. Donepezil (longer half life but more severe side effects)
  3. Memantine (a non-competitive antagonist)
43
Q

How do nerve agents work?

A

They phosphorylate AChE (deactivating it) therefore ACh floods the synapse, but the signal is not carried out due to the receptors already being activated with some ACh
- this leads to muscle spasms alongside paralysis

44
Q

What are G-agents? What are some of the examples of G-agents?

A

G-agents were nerve agents developed by the Germans in the 20s and 30s (causes its effect due to inhalation)

  • some G-agents are:
    1. Tabun
    2. Sarin Gas
    3. Soman Gas
45
Q

What are V-agents? What is one example of a V-agent?

A

V-agents were nerve agents developed by the Americans

- one V-agent developed was VX, which is the most toxic and most stable nerve agent (causes its effect topically)

46
Q

What is the antidote to nerve agents? Who was primarily responsible for its development?

A

The antidote is an autoinjector, with two compounds:

  • H16 (which reactivates AChE)
  • atropine (which is a muscarinic antagonist, blocking the effects of ACh while the AChE works to get rid of all the excess ACh)

Neuropharmacology (18 decks)

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