Lecture 10 Flashcards

1
Q

Criteria for neurotransmitters:

A
  1. present in presynaptic terminals
  2. released in response to stimulation
  3. able to interact with postsynaptic receptors
  4. rapidly removed from the synapse
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2
Q

Neurotransmitters need mechanisms for:

A
  1. synthesis and/or storage
  2. release
  3. transmitter action i.e. specific receptors
  4. transmitter removal
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3
Q

It does not count as neurotransmitters if:

A

has continuous stimulation

cannot be removed from the synapse

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4
Q

What are the three main types of transmitters/modulators?

A

ACh
Amino acids
Biogenic amines

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5
Q

Name four amino acid neurotransmitters

A

Glutamate (excitatory)
GABA (inhibitory)
glycine (inhibitory)
aspartic acid

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6
Q

Name biogenic amine neurotransmitters

A

Catecholamines (adrenaline, noradrenaline, dopamine; go through different steps to synthesize specific amine)
Serotonin (also called 5-HT)
Histamine

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7
Q

Name four neuropeptides

A

Enkephalin (natural opiate)
Substance P
Cholecytokinin
beta - endorphin (hugely different in size but works in same system)

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8
Q

Amino acid and amine neurotransmitters are:

A

small molecules
stored and released from synaptic vesicles
capable of many binding to and activating (ligand-gated channel receptors, G-protein coupled receptors)
Can do short-term and long-term signalling

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9
Q

The peptide neurotransmitters are:

A

large molecules
stored in secretory granules
only activate G-protein coupled receptors
made in soma

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10
Q

Glutamate is:

A

Most common, excitatory transmitter in CNS
Amino acid, found in all neurons
3 glutamate receptor subtypes based on the drugs which act as selective agonists
Action is terminated by selective uptake into presynaptic terminals and glia

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11
Q

Glutamate cannoe be used as a what? and why?

A

Marker

- Found everywhere but in neurons which use glutamate as a neurotransmitter, the concentration is much higher

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12
Q

How much more glutamate do glutamatergic neurons have compared to neurons that use glutamate for protein synthesis?

A

2-3 times

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13
Q

Name the three receptor subtypes::

A
  1. AMPA receptor
  2. NMDA receptor
  3. Kainate receptor
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14
Q

Where is AMPA receptor found and how is it activated?

A

Most widely distributed

Only activated by AMPA drug

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15
Q

How is NMDA receptor activated?

A

Only activated by NMDA drug

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16
Q

What are glia?

A

Supporting cells (2 neuron + 1 glia hypothesis formed now)

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17
Q

What do AMPA receptors do?

A

Mediate fast excitatory transmission
Glutamate binding to AMPA receptors trigger Na and K currents resulting in an EPSP
AMPA is not very permeable to Ca

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18
Q

What are NMDA receptors?

A

NMDA receptors often co-exist with AMPA receptors
- AMPA receptors can be on their own but hard to find
NMDA receptors on their own
NMDA receptors have a voltage-dependent Mg block
- Mg pops out during depolarization
- NMDA receptors become more permeable to Ca
- NMDA receptors need to be indirectly activated by
another transmitter
NMDA receptors are permeable to Ca as well as Na and K
- Their activation can have more widespread, lasting changes in the postsynaptic cell
- Involved in strengthening of synapses

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19
Q

What is an enzyme that converts glutamate to gamma-amino butyric acid (GABA)?

A

Glutamic acid decarboxylase (GAD)

GAD 65 and 67 are markers for GABAergic neurons

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20
Q

How does the conversion from glutamate to GABA terminate?

A

There is a transporter protein that finds GABA and selective uptake into presynaptic terminals and glia

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21
Q

What is GABA?

A

Most common inhibitory transmitter in CNS

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22
Q

In what cases can GABA become an excitatory transmitter?

A

During development when other Cl transporters make sure there is more Cl inside at rest, Cl moves out of cell through GABA-gated Cl channels
- causes depolarization

23
Q

Where in the CNS are GABA especially found?

A

Cortex and striatum

24
Q

What happens when there is too much or too little inhibition via GABA?

A

Too much: Coma or loss of consciousness

Too little: Seizures

25
What is autoinhibition?
When the GABAergic neuron inhibits itself | - keeps signal specific to that timing
26
What is disinhibition?
inhibitory synapses can act as a shunt and make membrane potential more negative at one point.
27
When there is disinhibition, how much change in voltage is there at the soma?
none
28
What is double inhibition?
If the neuron is GABAergic, it can be inhibited by another GABAergic neuron, causing excitation
29
How are GABA-A receptors modulated?
Other chemicals can bind to the GABA-A receptor and modulate the response to GABA binding These chemicals have no effect without GABA binding
30
Name the chemicals needed for GABA-A receptor modulation and their effects.
Ethanol - behavioral effects (is addictive) Benzodiazepines (e.g. diazepan) - used to treat anxiety by increasing frequency of channel opening Barbiturates - sedatives and anti-depressants - increases duration of channel opening Neurosteroids (metabolites of steroid hormones) - e.g. Progesterone - Can break down into two neurotransmitters - metabolites of progesterone can affect GABA-A receptors (PMT...)
31
What difference can be found between normal people and people suffering from anxiety attacks when it comes to GABA-A receptor distribution?
PET scan from a patient suffering anxiety attacks - Labelled with a benzodiazepine (engn diazepam) - Shows loss of GABA-A receptors
32
What are opiates?
Drugs derived from the opioid poppy
33
What are examples of opiates?
Heroin, morphine
34
What are opioids?
A broad class of natural and synthetic compounds
35
What are examples of opioids?
Endorphins
36
What do opioids and opiates do?
Elicit effect by activating opioid receptors
37
What are endorphins?
Naturally occurring small proteins or peptides | ENDogenous proteins with mORPHINE like properties
38
Name a few examples of endorphins?
Endorphin, enkephalin, dynorphin
39
How are endorphins synthesized?
Formed in the RER | Packaged into secretory granules by Golgi apparatus
40
How are opioid receptors distributed?
Widely distributed in the CNS but concentrated in nociceptive areas
41
How many types of opioid receptors are there?
three ; mu, kappa, sigma
42
What do opioid receptors in the spine contribute to?
Blocks pain signal (analgaesia)
43
What do opioid receptors in the periaqueductal grey do?
Regulates sensation of "pain"
44
What do opioid receptors in the amygdala do?
Regulates emotional component
45
What do opioid receptors in the frontal cortex do?
Cognitive aspects
46
What do opioid receptors in the brain stem (medulla oblongata) do?
Depress respiration and cough reflex (may induce vomiting)
47
What do opiate receptors do?
Can prevent voltage-gated Ca channels Opening or increase opening of K channels, both hyperpolarize the cell Decreases cAMP production via Galphai
48
What are the three types of G-proteins?
1. Gs: Stimulatory G-proteins 2. Gi: Inhibitory G-proteins 3. Gq: Phosphorylatory G-proteins
49
Name three therapeutic uses of opiates:
1. Analgesia - reduces perception of and emotional response to pain (perception - receptors, emotional - amygdala) 2. Intestinal disorders: reduces diarrhea (decreases dehydration) 3. Antitussine - cough suppressant (codeine - less addictive than heroin)
50
What are the four problems that restrict therapeutic use?
1. Serious side effects 2. Tolerance 3. Dependence 4. Relieve dull visceral pain bettern than sharp pain
51
What are the serious side effects from the use of opiates?
Respiratory depression - breathing rate decreases when opiates are too high Sedation Constipation
52
What happens when tolerance develops?
Reduced clinical effect | Higher dosage needed for same effect
53
What happens when dependence develops?
Leads to withdrawal symptoms An emotional need to take drugs Depends on dosage and time period