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Neuro Exam III > CNS Neurotransmitter Systems - SRS > Flashcards

CNS Neurotransmitter Systems - SRS Flashcards

1
Q

What are the major amino acid NT’s?

Which are excitatory and which are inhibitory?

A

-Excitatory

  • Glutamate
  • Aspartate

-Inhibitory

  • GABA (gamma amino butyric acid)
  • Glycine
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2
Q

What are the small molecule NT’s we use?

A

Acetylcholine
Monoamines

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3
Q

What are the monoamine NT’s?

A

Catecholamines

  • Dopamine
  • Norepinephrine

Serotonin (5-hydroxytryptamine, 5-HT)

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4
Q

Describe steps 1-8.

A

(1) Synaptic vesicles synthesized in the cell body are transported down the axon
(2) Small molecule neurotransmitters are synthesized in the nerve terminals and loaded into synaptic vesicles. This is often an ATP-dependent process requiring transport proteins. (In contrast, peptides are synthesized and packaged into vesicles in the cell body.)
(3) Depolarization of the presynaptic nerve terminal by an arriving action potential causes opening of voltage-dependent Ca++ channels and influx of Ca++
(4) Fusion of vesicles with plasma membrane and release of vesicle contents into synaptic cleft
(5) Binding and activation of postsynaptic receptors
(6) Postsynaptic membrane response
(7) Elimination of transmitter from synapse by reuptake transporter or
(8) Elimination of transmitter from synapse by enzymatic breakdown

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5
Q

Is there retrograde synaptic signaling? If so what does it do?

If not, why is there not?

A

There is.

Modulates NT release

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6
Q

How do virtually all drugs that act in the CNS produce their effects?

A

Modification of some step in the chemical synaptic transmission

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7
Q

What are some presynaptic sites of drug action?

A
  1. Neurotransmitter synthesis
  2. storage
  3. metabolism
  4. release
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8
Q

The primary postsynaptic site of drug action is what?

A

The neurotransmitter receptor

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9
Q

How do drugs that target the NT receptor work? (2 ways)

A
  1. Direct receptor interaction (agonist or antagonist)
  2. Indirect action by modulating second messengers (see metabotropic receptors below)
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10
Q

Describe the synthesis, release and storage of glutamate.

A
  1. Synthesis occurs in the brain from glucose and other precursors. Glutamate is a nonessential amino acid that does not cross the blood-brain barrier.
  2. Storage: Glutamate is taken up into synaptic vesicles by an ATP-dependent transporter
  3. Release occurs in response to nerve impulses
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11
Q

How is glutamate inactivated?

A

Released glutamate is initially taken up by glial cells, where it is converted into glutamine, then transported out of the glia, taken up by glutamatergic nerve cells, and converted back into glutamate.

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12
Q

What are pathophysiological aspects of glutamate?

A
  • Synaptic plasticity; learning and memory
  • Migraine – excessive glutamate release contributes to the cortical spreading depression implicated in the aura of migraine headache
  • Excitotoxicity and Cell Death
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13
Q

Detail the synthesis, storage and release of GABA (Gamma-amino butyric acid)

A
  1. Synthesis occurs locally from glucose, pyruvate, or occasionally other amino acid precursors
  2. Storage: GABA is loaded into synaptic vesicles by a vesicular transporter
  3. Release occurs in response to nerve impulses
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14
Q

How is GABA inactivated?

A

GABA signal is terminated by rapid reuptake by several types of plasma membrane transporters; GABA is also taken up by glial cells

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15
Q

What does a GABA dysfunction lead to?

A

Hyperexcited states, since it balances glutamates excitatory action.

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16
Q

GABAA recptors have binding sites for other molecules, what are some of these to be aware of?

What is their impact when bound?

A
  1. benzodiazepines
  2. barbituates
  3. alcohol

Enhance the inhibitory effects of GABA

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17
Q

What are benzodiazepines used for therapuetically?

A
  1. generalized anxiety disorder,
  2. panic disorders,
  3. sedation,
  4. sleep disorders
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18
Q

What are barbituates used therapeutically for?

A
  1. sedative-hypotonics
  2. antiepileptics
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19
Q

What type of channel does glycine utilize?

A

ligand-gated Cl- channel

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20
Q

What does glycine act as a coagonist with? At what receptors?

A
  1. Glutamate
  2. NMDA
21
Q

What impact does Tetanus toxin have on the body?

A

Inhibits glycine release

22
Q

Describe the synthesis, storage and release of ACh.

A
  1. Synthesis occurs in the presynaptic terminal from choline and acetyl-CoA by the enzyme choline acetyltransferase
  2. Storage: ACh is loaded into vesicles by the vesicle-associated transporter (VAT)
  3. Release occurs in response to nerve impulses
23
Q

Describe the inactivation of ACh?

A

Enzymatic degradation by acetylcholinesterase

24
Q

ACh is utilised in the CNS as well as the peripheral autonomic nervous system and primary motor neurons. What are the roles of ACh in the CNS?

A
  1. midbrain reticular formation (level of wakefulness),
  2. basal ganglia (motor control),
  3. basal forebrain (connections to hippocampus and cortex involved in memory and motor skills)
  4. reciprocal relationship with dopamine in motor control
25
Q

Patients with Alzheimer’s disease have reduced cerebral production of what?

A

choline acetyl transferase

26
Q

What does the decreased production of choline acetyl transferase led to in Alzheimer’s patients?

A
  1. Decreased ACh synthesis
  2. Impaired cortical cholinergic function
27
Q

AChE inhibitors are commonly used to treat AD, describe the outcomes.

A

Benefit is modest and may not impact long-term outcomes

28
Q

What are some diseases of the neuromuscular junction?

A
  1. myasthenia gravis
  2. Eaton-Lambert Syndrome
  3. Botulism
29
Q

What are some sideffects of CNS ACh receptor blockade?

A
  1. drowsiness
  2. memory loss
  3. sedation
30
Q

Describe the synthesis, storage and release of dopamine

A
  1. Synthesis occurs in the presynaptic terminal from tyrosine by the enzymes tyrosine hydroxylase and dopa decarboxylase
  2. Storage: Dopamine is loaded into vesicles by the vesicular monoamine transporter (VMAT)
  3. Release occurs in response to nerve impulses
31
Q

How is dopamine inactivated?

A

Reuptake into the presynaptic cell is mediated by the high affinity dopamine transporter (DAT) or the low affinity plasma membrane monoamine transporter (PMAT)

32
Q

What degenerates in Parkinson’s disease?

A

dopamine neurons in the striatum

33
Q

What is an example of a disease that involves increased dopaminergic activity?

A

Psychosis (Schizophrenia)

34
Q

What types of drugs are used classically to treat psychosis?

A

dopamine D2 receptor antagonists

35
Q

What impact does cocaine abuse have on DA?

A

Produces a DA uptake blockade

36
Q

What do amphetamines do with regard to dopamine?

A

increase dopamine release

37
Q

What is the so-called “reward pathway”?

A

ventral tegmental DA pathways mediate the subjective effects of drugs of abuse

38
Q

Describe synthesis, storage and release of Norepinephrine (NE)

A
  1. Synthesis occurs inside NE granules from dopamine by the enzyme dopamine β-hydroxylase
  2. Storage: NE is stored in the granules where it was produced
  3. Release occurs in response to nerve impulses; co-transmitters and dopamine β-hydroxylase are also released
39
Q

How is NE inactivated?

A

Reuptake into the presynaptic cell is mediated by the norepinephrine transporter (NET)

40
Q

What does NE modulate behvior wise?

A
  1. sleep
  2. wakefulness
  3. attention
  4. feeding behaviors
41
Q

In what disorders does NE play a role?

A

Mood disorders such as depression

42
Q

Describe the synthesis, storage and release of serotonin (5-Hydroxytrytamine, 5-HT)

A
  1. Synthesis occurs in the presynaptic terminal from tryptophan by the enzyme tryptophan hydroxylase
  2. Storage: Serotonin is loaded into vesicles by a vesicular transporter
  3. Release occurs in response to nerve impulses
43
Q

Describe inactivation of serotonin

A

The serotonin uptake transporter (SERT, inhibited by many antidepressant drugs) terminates the neurotransmitter signal by rapidly pumping 5-HT back into the nerve terminal.

44
Q

Decreased 5-HT function is associated with what?

A

Depression

45
Q

What is one way we can treat depression?

A

SSRIs (Selective Serotonin Reuptake Inhibitors) are used to treat depression

46
Q

What behaviors are mediated by 5-HT?

A
  1. agressive behavior
  2. arousal
47
Q

How do ecstasy, LSD and other hallucinogens act?

A

PRobably in part by interacting with 5-HT receptors

48
Q

What is an example of a 5-HT3 antagonist?

A

Ondansetron (and other antiemetics)

49
Q

Atypical antipsychotics are partial agonists at what receptors?

A

5-HT2A receptors

Neuro Exam III (9 decks)

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