Neurotransmitters Flashcards

1
Q

What is a feature of the metabotropic Neurotransmitter Receptor

A

It uses 2nd messengers to relay a signal intracellularly (Enzymatic reaction)

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2
Q

What are the two functions of 2nd messengers?

A
  1. To amplify a signal

2. To alter a signal

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3
Q

Give three examples of 2nd Messengers

A
  1. cAMP (nucleotide-based)
  2. diacylglycerol (lipid-based)
  3. Ions (Calcium)
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4
Q

What enzyme produces cAMP?

A

Adenylyl cyclase

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5
Q

Where can Acetylcholine be found?

A

It can be found at the neuromuscular junction - where a synapse meets the muscle cell

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6
Q

What different functions can Acetylcholine have?

A
  1. Relaxation of heart muscle cells
  2. Contraction of skeletal muscles
  3. Release of saliva from salivary glands
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7
Q

What two molecules is Acetylcholine made of?

A

Acetyl-CoA and Choline catalyzed by AchTransferae

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8
Q

What does VAChT (Vesicular ACh Transporter) do?

A

VAChT exchanges one molecule of Ach with 2H+ ions. The H+ ions are actively being loaded into the vesicle (ATP), so VAChT can exchange H+ for Ach

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9
Q

How is the signal neurotransmission of Ach terminated?

A

Ach is being broken down in the synaptic cleft by an enzyme called Ach-esterase

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10
Q

What part of ACh is being recycled after its breakdown?

A

The Choline part is being recycled

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11
Q

What are the names of the two types of ACh receptors?

A
  1. Nicotinic (ionotropic)

2. Muscarinic (metabotropic)

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12
Q

What ions flow through the Nicotinic ACh receptors?

A

Positive ions (mainly Na+)

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13
Q

What affects the differences between Nicotinic receptors in different parts of the body?

A

The subunit composition of those receptors affects many of its functions.

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14
Q

When is a G-protein active?

A

When its receptor is activated, bound GDP is being released and GTP binds to the site. The protein is then cleaved into an active alpha-subunit and beta/gamma-complex

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15
Q

What ACh receptors are found on the heart, skeletal muscles, and salivary glands?

A
  1. Muscarine 2 receptor on the heart (metabotropic)
  2. Nicotinic receptor on the skeletal muscle
  3. Muscarine 1 receptor on the salivary glands.
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16
Q

Name a few examples of toxins for ACh receptors

A
  1. Muscarine (Muscarinic receptor agonist)
  2. Nicotine (Nicotinic receptor agonist)
  3. alpha-bungarotoxin (Nicotinic antagonist)
  4. Curare (Nicotinic antagonist)
  5. Atropine (Muscarinic antagonist)
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17
Q

What is Glutamate made of?

A

Glutamate is made of Glutamine, catalyzed by Glutaminase

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18
Q

How is Glutamate being transported inside a vesicle?

A

It works in a similar way to ACh, where H+ ions are actively pumped inside the cell using ATP, and Glutamate is then exchanged by VGLUT (vesicular Glutamate Transporter) with the H+ ions inside the cell.

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19
Q

Why can’t glutamate be broken down in the synaptic cleft?

A

Because there is no enzyme to break down glutamate

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20
Q

How is Glutamate removed from the synaptic cleft?

A

Glutamate is being pumped out by Glial cells, then transformed into Glutamine, and transported back to the cell to be reused

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21
Q

What does EAAT stand for?

A

Excitatory Amino Acid Transporter (found on Glial cells - transports glutamate inside)

22
Q

Why does glutamate have to be transported back to the presynaptic cell as glutamine?

A

Because if the unmetabolized glutamate is being released by the glial cell into the environment, it has the chance to excite the neurons needlessly - this is why it must be metabolized first

23
Q

What are the names of Glutamate ionotropic receptors?

A
  1. AMPA
  2. NMDA
  3. Kainate
24
Q

What is the name for the metabotropic Glutamate receptors?

A

mGluR (metabotropic glutamte receptor)

25
Q

What is the function of Glutamate?

A

Glutamate mediates the excitatory input inside the brain

26
Q

Describe some characteristics of the ionotropic Glutamate receptors

A
  1. AMPA has a very sharp and short action potential. It acts fast and closes fast
  2. NMDA is slower to react but closes slower as well. This gate lets in Ca2+ ions
  3. Kainate is not usually found in the brain
27
Q

How can a Glutamate leak lead to toxicity and eventually death?

A

If glutamate spills in the environment, it will excite the receptors. Ca2+ will flow into the cell and prolonged calcium influx leads to cell death. (snowball effect)

28
Q

What ion is important for blocking the NMDA ion channel?

A

Mg2+ blocks the entrance of NMDA. Because it is positively charged, it repels other positive ions like Ca2+, Na+, and K+ from passing through

29
Q

What is the basic concept of Long-Term Potentiation?

A

By stimulating an NMDA receptor (in the hippocampus), the starting potential of a synapse will be higher so it will be excited more easily

30
Q

Where the metabotropic receptors for Glutamate found and why?

A

They are found on the edge of the synapse and serve as a sensor for when “too much” Glutamate is released.

31
Q

How does the negative feedback loop for Glutamate work?

A

There are metabotropic Glutamate receptors on the edges of both pre and post-synaptic cells. The receptors on the presynaptic cells tell the cell itself to not release more Glutamate if enough is already present in the synaptic cleft

32
Q

What is the function of GABA?

A

GABA is driving all the inhibitory signals in the brain

33
Q

How is GABA transported inside vesicles?

A

In a similar way like ACh and Glu - A vesicle is pumped with H+ and then VIAAT (GABA Transporter) is exchanging H+ with GABA molecules

34
Q

How does GABA get pumped out of the synaptic cleft?

A

GABA does not have any enzymes that break it down, so it gets removed by the Glial cells and the presynaptic cell itself, with the transporter GAT

35
Q

What are the names of the ionotropic GABA receptors?

A

GABA-A

36
Q

What are the names of the metabotropic GABA receptors?

A

GABA-B

37
Q

What anesthetics are used on GABA-A?

A
  1. Benzodiazepines (Valium)
  2. Barbiturates
  3. Alcohol
    First three cause prolonged opening of GABA-A
  4. Picrotoxin - This toxin blocks GABA-A and treats an overdose of the other anesthetics
38
Q

What ions go through the GABA-A receptor?

A

Cl- ions

39
Q

What does GABA-B do?

A

GABA-B suppresses the activity of other ion channels, so no signal can occur. This is done through several pathways (prevents depolarization)

40
Q

What are the five Catecholamines?

A
  1. Dopamine
  2. Norepinephrine
  3. Epinephrine
  4. Serotonin
  5. Histamine
41
Q

What is the metabolic pathway of (all) Catecholamines?

A

Tyrosine -> DOPA -> Dopamine -> NADR -> ADR

42
Q

Where are catecholamines made?

A

They are made in special neurons in the brain. For example, Dopamine is made in the Substantia Nigra.

43
Q

What does Prozac do?

A

Prozac prevents the reuptake of serotonin (unsure, more research neded)

44
Q

Are there ionotropic and metabotropic receptors for Catecholamines?

A

No, there are only metabotropic receptors for catecholamines - however, only Serotonine has a ionotropic receptor

45
Q

Where are Neuropeptides made?

A

In the ER of the neuron

46
Q

Roughly explain the way of Neuropeptides from the nucleus to the synapse

A

The peptide is made in the ER through gene transcription and translation. The Pre-propeptide is then transported to the Golgi, where it is cleaved into a propeptide and packaged in a vesicle. There are also enzymes present in the vesicle that transform the propeptide into active peptides as it travels along the axon, to the synapse

47
Q

What is an example of Neuropeptides?

A

Endorphins (opioid peptides)

48
Q

What do endorphins do?

A

They block pain signals

49
Q

What are examples of unconventional neurotransmitters?

A
  1. NO gas
  2. Endocannabinoids
    They cannot be stored in a vesicle because they go easily through the membrane.
50
Q

Why do endocannabinoids give a pleasurable feeling?

A

Many receptors for this compound are expressed in the substantia nigra, which in turn activates a reward feeling