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Neuroscience > Lecture 10 > Flashcards

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
Q

What is autoinhibition?

A

When the GABAergic neuron inhibits itself

- keeps signal specific to that timing

26
Q

What is disinhibition?

A

inhibitory synapses can act as a shunt and make membrane potential more negative at one point.

27
Q

When there is disinhibition, how much change in voltage is there at the soma?

A

none

28
Q

What is double inhibition?

A

If the neuron is GABAergic, it can be inhibited by another GABAergic neuron, causing excitation

29
Q

How are GABA-A receptors modulated?

A

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
Q

Name the chemicals needed for GABA-A receptor modulation and their effects.

A

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
Q

What difference can be found between normal people and people suffering from anxiety attacks when it comes to GABA-A receptor distribution?

A

PET scan from a patient suffering anxiety attacks

  • Labelled with a benzodiazepine (engn diazepam)
  • Shows loss of GABA-A receptors
32
Q

What are opiates?

A

Drugs derived from the opioid poppy

33
Q

What are examples of opiates?

A

Heroin, morphine

34
Q

What are opioids?

A

A broad class of natural and synthetic compounds

35
Q

What are examples of opioids?

A

Endorphins

36
Q

What do opioids and opiates do?

A

Elicit effect by activating opioid receptors

37
Q

What are endorphins?

A

Naturally occurring small proteins or peptides

ENDogenous proteins with mORPHINE like properties

38
Q

Name a few examples of endorphins?

A

Endorphin, enkephalin, dynorphin

39
Q

How are endorphins synthesized?

A

Formed in the RER

Packaged into secretory granules by Golgi apparatus

40
Q

How are opioid receptors distributed?

A

Widely distributed in the CNS but concentrated in nociceptive areas

41
Q

How many types of opioid receptors are there?

A

three ; mu, kappa, sigma

42
Q

What do opioid receptors in the spine contribute to?

A

Blocks pain signal (analgaesia)

43
Q

What do opioid receptors in the periaqueductal grey do?

A

Regulates sensation of “pain”

44
Q

What do opioid receptors in the amygdala do?

A

Regulates emotional component

45
Q

What do opioid receptors in the frontal cortex do?

A

Cognitive aspects

46
Q

What do opioid receptors in the brain stem (medulla oblongata) do?

A

Depress respiration and cough reflex (may induce vomiting)

47
Q

What do opiate receptors do?

A

Can prevent voltage-gated Ca channels
Opening or increase opening of K channels, both hyperpolarize the cell
Decreases cAMP production via Galphai

48
Q

What are the three types of G-proteins?

A
  1. Gs: Stimulatory G-proteins
  2. Gi: Inhibitory G-proteins
  3. Gq: Phosphorylatory G-proteins
49
Q

Name three therapeutic uses of opiates:

A
  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
Q

What are the four problems that restrict therapeutic use?

A
  1. Serious side effects
  2. Tolerance
  3. Dependence
  4. Relieve dull visceral pain bettern than sharp pain
51
Q

What are the serious side effects from the use of opiates?

A

Respiratory depression - breathing rate decreases when opiates are too high
Sedation
Constipation

52
Q

What happens when tolerance develops?

A

Reduced clinical effect

Higher dosage needed for same effect

53
Q

What happens when dependence develops?

A

Leads to withdrawal symptoms
An emotional need to take drugs
Depends on dosage and time period

Neuroscience (28 decks)

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