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Neuroscience > L5: CNS Neurotransmitters > Flashcards

L5: CNS Neurotransmitters Flashcards

1
Q

There are 2 groups of NTs: Small molecule transmitters and peptide transmitters. Compare & contrast their synthesis and packaging.

A

1) Small molecule NTs (eg. ACH, NE)
- synthesis of ENZYMES in cell body
- slow axonal transport of enzymes
- at pre-synaptic terminal, enzymes synthesize NTs from precursors already there
- packaged into vesicles w/ help of transport proteins

2) peptide NTs (VIP, opiods)
- synthesis of ENZYMES & PRECURSORS in cell body
- fast axonal transport
- at pre-synaptic terminal, enzymes modify NT precursors

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2
Q

Why can’t peptide NTs respond quickly to increased demand?

A

Although the transport down the axon from cell body to pre-synaptic terminal is fast, the fact that the precursors are made at the cell body make it hard for peptide NTs to respond quickly to increased demand. Unlike small molecule NTs, they have precursors at the terminal boutin ready to be synthesized by enzymes.

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3
Q

Compare and contrast the 2 groups of NT receptors

A

1) ionotropic
- fast
- ligand gated ion channels
- formed by 4-5 subunits
- selective for size
* *very complex b/c many combinations of subunits give rise to diff affinity, selectivity of ion channels

2) metabotropic
- slower
- g-protein coupled receptors
- monomeric
* *similar to ionotropic receptors, these receptors vary with different properties

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4
Q

Acetylcholine is synthesized in the pre-synaptic terminal when enzymes catalyze the rxn btw acetyl-coA & choline. How is ach removed from the synpatic cleft?

A

acetylcholinesterase into acetate & choline. Choline is re-taken up again

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5
Q

How does Sarin gas (Organophosphates: insecticides) lead to muscle paralysis?

A

inhibit acetylcholinesterase causing a build up of acetylcholine in the synaptic cleft leading to continued depolarization of post-synaptic cell making it refractory to sub ACH release = muscle paralysis

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6
Q

Describe Ach receptors

A

1) ionotropic/nicotinic Ach receptors

2) Metabotropic/muscarinic Ach receptors
* **mediate most of Ach effects in brain

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7
Q

Atropine

A

sympathomimetic leading to pupil dilation by antagonizing AchR

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8
Q

Scopolamine

A

for motion sickness and is a AchR antagonist

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9
Q

Myasthenia Gravis

A

autoimmune condition when autoantibodies attack ionotropic/nicotinic AcHr in NMJ. Symptoms include fatigue, diplopia, droopy eyelids (ptosis), difficulty in speaking, swallowing, chewing.

Treatment - acetylcholinesterase inhibitors

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10
Q

Glutamate is the major excitatory NT in CNS. Explain the phenomenon of Excitotoxicity

A

high extracellular concentration of glutamate is toxic to neurons. During strokes, O2 deprivation, glutamate re-uptake is slow causing more glutamate to remain in synapse, which can cause neuronal damage. Therefore, drugs are targeting glutamate receptors to prevent neuronal damage in such cases.

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11
Q

What is the precursor to glutamate in the pre-synaptic terminal?

A

glutamine

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12
Q

How is glutamate removed from synaptic cleft?

A

Mainly by glial cells. Once in glial cells, glutamate is converted back to glutamine b/c glutamine is less toxic and then glutamine is transported back into nerve terminal

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13
Q

What are the 3 types of ionotropic glutamate receptors?

A

NMDA, AMDA, Kainate = all excitatory Na+ channels

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14
Q

What makes NMDA receptors unique?

A

Unlike the other ionotropic glutamate receptors (AMDA, Kainate), NMDA receptors are unique:

  • Ca2+ can pass thru
  • mandatory glycine binding
  • Mg2+ blocks receptor which is released by depolarization

Hence, to activate NMDA receptors, you need glutamate, glycine & depolarization to get Mg2+ off

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15
Q

Are there both metabotropic and ionotropic glutamate receptors?

A

yes

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16
Q

GABA is the major inhibitory NTs in CNS. How is GABA removed from cleft?

A

glial cells

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17
Q

Epilepsy is related to increase or decrease GABA levels?

A

decrease GABA

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18
Q

What is the precursor to make glycine in the terminal bouton?

A

serine

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19
Q

How is glycine removed from cleft?

A

Glial cells

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20
Q

Increase glycine can be due to defects in glycine transporter, which can lead to what types of problems?

A

lethargy, mental retardation (neonatal disease)

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21
Q

GABAa, GABAc and glycine receptors are ionotropic receptors. What kind of channels are they?

A

inhibitory Cl- channels

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22
Q

List some drugs that are GABA receptor agonists

A

1 - benzodiazepines (Valium) used as tranquilizer

2 - barbiturates (phenobarbital) used as anesthetics for epilepsy

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23
Q

What is strychnine?

A

rat poison

-glycine receptor antagonist will lead to overreactivity in spinal cord & brainstem leading to seizures

24
Q

There are both ionotropic and metabotropic GABA receptors. List them

A 
Ionotropic = GABAa and GABAc
metabotropic = GABAb -widely distributed in brain
25
Q

Within the small molecule NT group, there are amino acids and biogenic amines. Biogenic amines (e.g. dopamine) not used by a lot of neurons in brain, but impt in maintaining

A

mental health

26
Q

Which transporter is used to package biogenic amines (e.g. dopamine)?

A

vesicular monoamine transporter

27
Q

How are biogenic amines removed from cleft?

A

nerve terminals

28
Q

Do biogenic amines have both ionotropic and metabotropic receptors?

A

No, only metabotropic receptors

29
Q

In Parkinsons disease (an example of hypokinesia, a basal ganglia d/o), why are patients treated with L-Dopa?

A

b/c the dopamine containing neurons degenerate leading to motor dysfunction.

30
Q

Briefly describe dopamine’s actions/effects in CNS

A
  • coordination of body movements (in corpus striatum: caudate & putamen)
  • motivation, reward & reinforcement (midbrain)
  • addiction pathway
  • emotional behavior
31
Q

In the CNS, the biogenic amine, NE works to do what?

A

NE projects from Locus Coerulus to forebrain & brainstem, influencing sleep & wakefulness, attention, and feeding behavior

32
Q

What can be used to treat nausea & vomiting

“anti-emetic”

A

dopamine receptor antagonists

33
Q

What is the effect of cocaine on dopamine re-uptake?

A

Dopamine is taken up into nerve terminals and glial cells. Cocaine inhibits this re-uptake, causing more dopamine to stay in the cleft.

34
Q

Amphetamine (used to treat ADHD & narcolepsy) works by

A

inhibiting both dopamine and NE transporters leading to increased dopamine & NE.

35
Q

Serotonin (5-HT) is in which nuclei in brain?

A

Raphe Nuclei in upper brainstem

36
Q

What does serotonin do?

A

regulation of sleep, eating, arousal & wakefulness

37
Q

What are SSRIs?

A

Selective Serotonin Reuptake Inhibitors -used to treat depression & anxiety increasing serotonin in cleft

38
Q

Are there both ionotropic & metabotropic serotonin receptors?

A

Yes, majority are metabotropic; some ionotropic (5-HT3 clss).

39
Q

impairment with serotonin metabotropic receptors disorders is implicated in causing what types of diseases?

A

psychiatric d/os

40
Q

activation of serotonin metabotropic receptors will result in

A

satiety and decreased food consumption

41
Q

Anti-psychotic drugs block which receptors? What are the implications?

A

-block dopamine receptors

this implies that maybe higher levels of dopamine result in certain psychoses

42
Q

anti-anxiety drugs

A
  • selective serotoninin reuptake inhibitors (SSRIs to increase serotonin helps with anxiety)
  • MAO inhibitors = block breakdown of biogenic amines
43
Q

Anti-depressants

A
  • MAO inhibitors

- SSRI

44
Q

Generally describe what peptide NTs do?

A

-modulate emotions, perception of pain, response to stress

45
Q

What determines peptide NTs’ activity?

A
  • biological activity dependent on amino acid sequence

* **due to differences in a.a. sequences, there are 5 catergories of peptide NTs.

46
Q

How are peptide neurotransmitters synthesized?

A

1 - pre-propeptides made in cell body
2 - in ER, pre-propetides are cleaved into propeptides
**individual propeptides can become MANY active peptides w/in a single vesicle
3 - final processing to active peptides occurs in vesicles AFTER they bud

47
Q

What are the 5 categories of peptide NTs?

A 
1 - Brain-gut peptides
2 - Opioid peptides
3 - Pituitary peptides
4 - Hypothalamic-releasing peptides
5 - Miscellaneous peptides
48
Q

How are peptide NTs dealt with in the synaptic cleft?

A

broken down by peptidases

49
Q

T/F: Peptide NTs are often co-released with small molecules

A

True

50
Q

Are there both ionotropic and metabotropic peptide NT receptors?

A

No, just metabotropic

51
Q

What enzyme is used to further activate some peptide NTs in the cleft?

A

endopeptidases

52
Q

What are 3 examples of opioid peptides?

A

endorphins
enkephalins
dynorphins
***all differ in a.a. sequences

53
Q

morphine is an opiod and is used for?

A

used as an analgesic

54
Q

Opioid peptides are widely distributed in the brain and act as ______ & ________.

A

depressants and analgesics

55
Q

Which neurotransmitters only use metabotropic receptors?

A

Dopamine
Norepinephrine
Neuro peptides

Neuroscience (36 decks)

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