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PSYC 211 > CHAPTER 4: NEUROTRANSMITTERS AND NEUROMODULATORS > Flashcards

CHAPTER 4: NEUROTRANSMITTERS AND NEUROMODULATORS Flashcards

1
Q

What is the excitatory amino acid NT in the brain?

A

glutamate

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2
Q

What is the inhibitory amino acid neurotransmitter in the brain?

A

-Gamma-aminobutyric acid or GABA

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3
Q

What is the inhibitory amino acid NT in the spinal cord and lower brain stem?

A

glycine

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4
Q

What is glutamate?

A
  • amino acid

- most important excitatory neurotransmitter in the brain

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5
Q

What is a vesicle glutamate transporter?

A

-proteins in the vesicle membrane that pump glutamate into a vesicle

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6
Q

How is glutamate produced, stored and released?

A
  • PRODUCTION: Synthesized from a precursor (glutamine) by an enzyme (glutaminase).
  • STORAGE: vesicle glutamate transporters package glutamate into vesicles.
  • RELEASE: action potential, glutamate released from presynaptic terminal.
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7
Q

What are the 4 major types of glutamate receptors?

3 ionotropic receptors, 1 metabotropic receptor

A
  • ionotropic: NMDA receptor, AMPA receptor, kainate receptor.
  • metabotropic: metabotropic glutamate receptor
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8
Q

What is the main function of metabotropic glutamate receptors?

A

-presynaptic autoreceptors

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9
Q

What is the main function of AMPA and NMDA receptors?

A

-important roles in the cellular basis of learning and memory.

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10
Q

How can glutamate open a calcium channel on an NMDA receptor?

A
  • a glycine molecule must be attached.
  • a magnesium ion must be removed from the magnesium binding site (this happens if the post synaptic membrane is partially depolarized.
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11
Q

What are the two conditions for an NMDA receptor to open?

A
  • glutamate is present
  • postsynaptic membrane is depolarized.
  • NMDA receptor= voltage and neurotransmitter dependent ion channel
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12
Q

How does PCP (phencyclidine) act on the calcium ion channel?

A
  • binds to its site which is located deep within the ion channel, next to the magnesium binding site.
  • Prevents the calcium ions from passing through the ion channel.
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13
Q

Which other drug has similar effects as PCP?

A

Ketamine, thought to bind on the same site as PCP.

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14
Q

How is glutamate reuptaken and deactivated?

A
  • Removed from synapse by excitatory amino acid transporters

- Broken down into it’s precursor (glutamine) by the enzyme glutamine synthase

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15
Q

What is PCP?

A

-Phencyclidine a drug that binds with the PCP binding site of the NMDA receptor and serves as an indirect antagonist

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16
Q

What are excitatory amino acid transporters?

A

proteins that remove glutamate from the synapse

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17
Q

What is glutamine synthase?

A

Enzyme that breaks down glutamate into its precursor glutamine.

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18
Q

What is GABA?

A
  • Amino acid

- Most important inhibitory NT in the brain

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19
Q

Where is GABA distributed?

A

widespread distribution throughout brain and spinal cord

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20
Q

How is GABA produced?

A
  • from a precursor: glutamic acid

- by the action of enzyme GAD

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21
Q

What is a vesicle GABA transporter?

A

-Proteins in the vesicle membrane that pump GABA into a vesicle

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22
Q

What is the main function of GABA-secreting neurons?

A

-exhibit inhibitory influence to keep brain stable

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23
Q

What are seizures are result of?

A
  • lacking or poorly functioning GABA-secreting neurons or receptors
  • During a seizure interconnected excitatory neurons all fire uncontrollably
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24
Q

Are GABAa receptors ionotropic or metabotropic?

A

ionotropic

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25
Q

What channels do GABA a receptors control?

A

-chloride channels

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26
Q

How do some drugs produce their effects with GABA receptors?

A
  • barbiturates, alcohol, and benzodiazepines

- they bind at various GABAa binding sites

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27
Q

How is GABA reuptaken and deactivated?

A
  • removed from synapse by GABA transporters

- broken down by enzyme GABA aminotransferase.

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28
Q

What is glycine?

A

-Inhibitory neurotransmitter in spinal cord and lower portions of the brain

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29
Q

What are the effects of tetanus on glycine?

A

-The bacteria that causes tetanus releases a chemical that prevent the release of glycine (and GABA as well)

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30
Q

What would the removal of the inhibitory effects of glycine synapses cause?

A

-continuous contraction of muscles

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31
Q

What is a direct antagonist for glycine receptor?

A

Strychnine

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32
Q

Where does Acetylcholine (ACh) function?

A

Both in CNS and PNS

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33
Q

What is ACh’s primary role in the PNS?

A

Primary NT to control muscle contraction

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34
Q

In the CNS, what are the 3 specific location sand pathways where ACh is found?

A
  • Dorsolateral pons
  • Basal forebrain or nucleus basalis
  • Medial septum
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35
Q

What is the function of ACh in dorsolateral pons?

A

-role in REM sleep

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36
Q

What is the function of ACh in the basal forebrain or nucleus basalis?

A

facilitate learning

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37
Q

What is the function of ACh in the medial septum ?

A

memory formation

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38
Q

How is ACh produced?

A
  • synthesized from precursors choline and acetylcoenzyme A,

- by the enzyme choline acetyltransferase (ChAT)

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39
Q

What is choline acetyltransferase (ChAT)?

A

The enzyme that transfers the acetate ion from acetyl coenzyme A to choline, producing the neurotransmitter acetylcholine.

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40
Q

What is vesicle ACh transporter?

A

Proteins in the vesicle membrane that pump acetylcholine into a vesicle

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41
Q

What is Botulinum toxin (Botox) and how does it act on ACh?

A
  • produced by the bacteria: clostridium botulinum
  • acetylcholine antagonist
  • prevents release of ACh by terminal buttons.
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42
Q

What is the ionotropic ACh receptor stimulated by?

A

nicotine (found in tobacco leaves)

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43
Q

What is the metabotropic ACh receptor stimulated by ?

A

muscarine (found in the mushroom amanita muscaria)

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44
Q

Which type of ACh receptor is mostly contained in the PNS and why?

A
  • ionotropic nicotinic receptors

- because muscle fiber shave to contract quickly , and nicotinic receptors are rapid-acting

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45
Q

Which type of ACh receptor is mostly contained in the CNS and why?

A
  • metabotropic muscarinic receptors

- they control ion channels and production of second messengers so they are slower

46
Q

What is ACh deactivated by ?

A

enzyme acetylcholinesterase (AChE) which is present in the post synaptic membrane.

47
Q

What are AChe inhibitors used for?

A

to treat myasthenia gravis.

48
Q

What are monoamine NT produced by?

A

Several regions of the brain

49
Q

What is the general function of monoamine NT?

A

Modulate functions of widespread regions of the brain either increasing or decreasing brain functions

50
Q

What are the four types of monoamine? ( also included as indolamines)

A
  • dopamine
  • norepinephrine
  • epinephrine
  • serotonin
51
Q

What are the 3 that belong to the subclass of monoamines called catecholamines?

A
  • dopamine
  • norepinephrine
  • epinephrine
52
Q

What types of post synaptic potentials does dopamine (DA) produce? (excitatory or inhibitory)

A

both excitatory and inhibitory

53
Q

What functions of the body does dopamine affect?

A
  • movement
  • attention
  • learning
  • reinforcing effect of drugs
54
Q

Where do the three most important dopamine pathways originate?

A

in midbrain structures: subtantia nigra and ventral tegmental area

55
Q

What is the
-origin
-location of terminal buttons
of the nigrostriatal system?

A
  • ORIGIN: substantia nigra

- TERMINAL BUTTONS: neostriatum (caudate nucleus and putamen)

56
Q

What is the
-origin
-location of terminal buttons
of the mesolimbic system?

A
  • ORIGIN: ventral tegmental area

- TERMINAL BUTTONS: nucleus accumbens, amygdala and hippocampus

57
Q

What is the
-origin
-location of terminal buttons
of the mesocortical system?

A
  • ORIGIN: ventral tegmental area

- TERMINAL BUTTONS: prefrontal cortex

58
Q

What are the behavioural effects of the nigrostriatal system?

A

control of movement

59
Q

What are the behavioural effects of the mesolimbic system?

A

Reinforcement effects of addictive drugs

60
Q

What are the behavioural effects of the mesocortical system?

A

short-term memory, planning, strategies for problem solving

61
Q

What does the degeneration of dopaminergic neurons that connect the substantia nigra with the caudate nucleus cause?

A

Parkinson’s disease

62
Q

What is the precursor for the two major catecholamines (dopamine and norepinephrine)?

A

tyrosine, which is an essential amino acid that we must obtain from our diet.

63
Q

How is tyrosine modified to become dopamine?

A
  • modified by enzyme tyrosine hydroxylase do become L-DOPA

- L-DOPA modified by enzyme decarboxylase to become dopamine

64
Q

How does dopamine become norepinephrine?

A

-converted by enzyme dopamine B-hydroxylase.

65
Q

What are vesicle monoamine transporters?

A

Proteins in the vesicle membrane that pump monoamine NT into a vesicle.

66
Q

What drug are people with Parkinson’s disease often given?

A
  • L-DOPA

- because it can cross the blood-brain barrier for conversion to DA

67
Q

What are the metabotropic types of dopamine receptors?

A

-D1, D2, D3, D4, D5.

68
Q

How is DA reuptaken and deactivated?

diagram

A
  • DA transporters remove DA from synapse

- Deactivation of catecholamines is regulated by an enzyme called monoamine oxidase (MAO)

69
Q

What drugs serve as agonists for DA?

A
  • amphetamine, methamphetamine (for dopamine and norepinephrine)
  • cocaine, methylphenidate (Ritalin). only dopamine
70
Q

What is cocaine used for?

A

-topical anesthetia

71
Q

What is methylphenidate used for?

A

enhance attention and impulse control in ADHD

72
Q

Where is NE found?

A

both CNS and PNS

73
Q

What is epinephrine a synonym of ?

A

adrenaline

74
Q

What regions of the brain receive input from noradrenergic neurons?

A

almost every region

75
Q

Where are the cell bodies of the most important noradrenergic system located?

A

in the locus coeruleus (nucleus located in the dorsal pons)

76
Q

What are the primary effects of an activation of NE neurons?

A

increase of vigilance and attentiveness.

77
Q

How is NE produced, stored and released?

A
  • As seen earlier, it is transformed from DA so same thing:
  • synthesized from DA by enzyme dopamine B-hydroxylase
  • since dopamine is already in vesicle, the storage of NE happens in vesicles themselves.
  • Released through axonal varicosities.
78
Q

What is an axonal varicosity?

A

An enlarged region along the length of an axon that contains synaptic vesicles and releases a NT and neuromodulator.

79
Q

How many types of adrenergic receptors are sensitive to both NE and epinephrine and where are they found?

A
  • Four types called alpha a and 2 and beta 1 and 2
  • All metabotropic
  • Found in neurons in the CNS and various organs of body.
80
Q

How is NE reuptaken and deactivated?

A
  • NE transporter removes excess NE from the synapse

- Excess NE in the terminal buttons is deactivated by MAO type A.

81
Q

What are MAO inhibiting drugs (MAOIs) sometimes used for?

A
  • to treat depression, but have side effects

- newer drugs such as selective serotonin, Ne and DA reuptake inhibitors have replaced them.

82
Q

What does serotonin (5-HT) play a role in?

A
  • regulation of mood
  • control of eating
  • sleep
  • arousal
  • pain regulation
  • dreaming
83
Q

Where is 5-HT found?

A
  • found in 9 clusters
  • most is located in the raphe nuclei of the midbrain, pons and medulla
  • 2 most important clusters: dorsal and median raphe nuclei
84
Q

What is 5-HT released from

A

from varicosities, like NE

85
Q

What is the precursor for serotonin?

A

-the amino acid tryptophan.

85
Q

What is the precursor for serotonin?

A

-the amino acid tryptophan.

86
Q

What do 5-HT receptors serve as?

A
  • some types of receptors serves as autoreceptors

- other types serve as postsynaptic receptors

87
Q

How is 5-HT reuptaken ?

A

serotonin transporter removes it from the synapse

88
Q

What drugs that inhibit the reuptake of serotonin play an important role in treatment of mental illness?

A
  • Fluoxetine (Prozac): treatment of depression, anxiety, OCD.
  • MDMA (ecstasy): excitatory and hallucinogenic effects
89
Q

Where is histamine found?

A

In the tuberomammillary nucleus, locate din the posterior hypothalamus

90
Q

What is the important role of histamine?

A

wakefulness

91
Q

What is the effect of drugs that block histamines ?

A

drowsiness

92
Q

How is histamine produced?

A

-Produced from the amino acid precursor histidine by the action of the enzyme histidine decarboxylase

93
Q

What are the histamine receptors and where are they contained?

A
  • H1, H2, H3, H4

- contained in CNS

94
Q

What drugs are antagonist to histamine receptors?

A

-antihistamines like diphenhydramine

95
Q

What are peptides?

A

-two or more amino acids linked together by peptide bonds

96
Q

How are peptides produced?

A

-from precursor molecules which are large polypeptides broken into smaller neurotransmitter molecules by special enzymes

97
Q

Where are peptides released from?

A
  • all parts of terminal button

- no reuptake or recycling

98
Q

What is one of the best known family of peptides?

A

-endogenous opioid: class of peptides secreted by the brain that act as opiates.

99
Q

How do opioids reduce pain?

A

-They mimic some of the effects of endogenous opioid and bind to peptide receptors.

100
Q

When were the receptors for opiate drugs discovered?

A

In the 70s

101
Q

What are the natural ligands for receptors called?

A

enkephalins

102
Q

What are the three different types of opioid receptors?

A

mu, delta, kappa.

103
Q

What are the three neural systems that are activated when opioid receptors are stimulated?

A
  • analgesia
  • inhibition of defensive responses such as fleeing or hiding
  • reinforcement (reward): can lead to abuse
104
Q

What can substances derived from lipids do?

A

transmit messages within or between cells.

105
Q

How do lipid NT produce, store and release?

A
  • appear to be synthesized on demand, produced or released as needed.
  • they are not stored in synaptic vesicles.
106
Q

What are the best known lipid NT?

A

-endocannabinoids: responsible for the effects of THC

107
Q

What are the two types of cannabinoid receptors?

A

-CB1 and CB2.

108
Q

What did scientist Agarwal find about THC?

A
  • THC exerts analgesic effects by stimulating CB1

- acetaminophen also acts on these receptors.

109
Q

How are lipids reuptaken and deactivated?

A
  • anandamide deactivated by the enzyme FAAH

- anandamide transporters are responsible for the reuptake of anandamide to the presynaptic cell

110
Q

What are nucleosides?

A

compound that consists of a sugar molecule bound with a purine or pyrimidine base.

111
Q

What are examples of nucleosides?

A

adenosine and caffeine

PSYC 211 (45 decks)

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