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Psy 459 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What are the catecholamines?

A

Dopamine
Epinephrine
Norepinephrine

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2
Q

What are the psychoactive drugs that directly affect catecholamine receptors?

A

Methamphetamine/amphetamine
Ritalin(ADHD)
Adderall
Cocaine
Buspar(anti-anxiety)
MAO inhibitors (antidepressants)
L-dopa(Parkinson’s disease)
Some anti psychotic medications

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3
Q

What do the neurotransmitters have in common?

A

All neurotransmitters are directly or indirectly derived from amino acids or are amino acids, and all amino acids share the same core structures(amine group, and carboxyl)

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4
Q

Where are all catecholamines derived from?

A

From the amino acid tyrosine

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5
Q

What is tyrosine?

A

It is a non essential amino acid. It is derived from essential amino acid phenylalanine

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6
Q

What is the synthesis?

A

Tyrosine is synthesized by tyrosine hydroxylase(TH) to make Dopa (addition of hydroxyl group)-this is considered the rate limiting enzyme
Dopa is synthesized by aromatic amino acid decarboxylase(AADC) to make dopamine ( removal of carboxyl group)
dopamine is synthesized by Dopamine Beta-hydroxylase (DBH) to make norepinephrine (addition of hydroxyl group)
Norepinephrine is synthesized by Phenyl-ethanonolamine-N-methyltransferase(PNMT) to make epinephrine( addition of a methyl group)

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7
Q

What happens after synthesis?

A

Catecholamines are packaged into vesicles.

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8
Q

What is the role of active transport?

A

Active transport processes keep high concentrations of catecholamines inside the vesicles

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9
Q

What is the transporter?

A

Vesicular Monoamine Transporter-2 (VMAT-2)

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10
Q

What use a VMAT-2?

A

Catecholaminergic neurons

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11
Q

What is inhibited by autoreceptors on neuron cell bodies, terminals, and dendendrites?

A

Catecholamines release is inhibited by autoreceptors on neuron cell bodies, terminals, and dendrites.

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12
Q

What is the role of this autoreceptors?

A

They enhance the opening voltage-gated K+ channels=outflow
This shortens the duration of action potential and reduces Ca+ influx and vesicle exocytosis

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13
Q

How does catecholamines inactivation occur?

A

Catecholamines inactivation occurs reuptake and degradation in the presynaptic terminal and in the synaptic cleft.

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14
Q

What happens in the Synaptic cleft?

A

Breakdown of the catecholamines by monoamine oxidase (MAO Aand B)

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15
Q

What are MAO?

A

MAO inhibitors are a class of antidepressants medications
Breakdown by COMT in synaptic cleft

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16
Q

Dopamine pathways in the brain:
Dopamine and movement

A

Nigrostriatal tract: axons in the substantia nigra extend to the basal ganglia. Caudate putamen and globes pallidas

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17
Q

Role of the substantia nigra?

A

Facilitates voluntary movement
Loss of neurons in the substantia nigra leads to Parkinson’s disease

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18
Q

Dopamine and Reward

A

Mesolimbic dopamine pathway: from the ventral tegmental area to various structures of the lambic system.
It’s the primary reward pathway.
This pathway is thought to contribute to the development of addiction

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19
Q

Dopamine pathways

A

Mesocortical dopamine pathway from VTA to the prefrontal cerebral cortex, cognition of reward
Also known as a reward pathway
Contribute to the development of addiction

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20
Q

Brain reward center

A

Red: high dopamine normal pleasure and interest
Yellow: medium dopamine difficulty feeling joy or pleasure
Green: low of dopamine, lack of pleasure

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21
Q

What are catecholamines?

A

Adrenal gland: Catecholamines are also hormones

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22
Q

What is epinephrine?

A

Epinephrine is secretory products of the adrenal gland
“Flight-or-fight response”
Short term stress hormone
Prepare the body for strenuous activity

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23
Q

Norepinephrine as a “stress hormone” in the periphery
Stress hormones

A

Breathing rate increases
Blood flow to skeletal muscles increases
Intestinal muscles relax
Pupil dilate
Blood pressure in arteries increases
Blood sugar levels increase
Heart rate increases

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24
Q

What is the role of the epi-pen?

A

Acts locally and reaches general circulation
Relaxes muscles of the airways
Increases vasoconstriction, this reduces swelling
Increases heart rate, this increases O2 in take

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25
Q

What is the norepinephrine synthesis?

A

Locus coeruleus(LC) in the pons: dense collections of NE neurons
These fibers extend to nearly all areas of the brain, cerebellum, and spinal cord

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26
Q

What is the composition of the Acetylcholine?

A

Acetylene group and choline

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27
Q

What are the drugs that affect acetylcholine?

A

Nicotine
Drug treatments for nicotine dependence (mecamylamine, nicotine-replacement therapy, chantix)
Most drug therapies for Alzheimer’s disease
Atropine: a drug antidote for nerve gas poisoning
Scopolamine: an antiemetic, hallucinogenic

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28
Q

What is the synthesis of acetylcholine?

A

ACh is formed in a single step from 2 precursors: choline and acetyl coenzyme A
Most choline comes from consumed foods with natural fats (meat, eggs, vegetables…. Actively transported across BBB)
Acetylcholine CoA is produced during metabolism of sugar

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29
Q

How is the synthesis of ACh catalyzed?

A

Choline acetyltransferase(ChAT) catalyzes the synthesis the synthesis of ACh and is found only in neurons that use ACh ad their transmitter.
ChAT transferse the acetyl group from acetyl CoA to choline.

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30
Q

How is the ACh stored?

A

ACh is stored in vesicles at axon terminals
It moves into vesicles via vesicular ACh transporters (VAChT) in the vesicle membrane)

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31
Q

How is ACh inactivated?

A

It is inactivated by acetylcholinesterase (AChE), which breaks it down to choline and acetic acid.

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32
Q

Where can AChE be found?

A

It can be found in presynaptic and postsynaptic cells
Most choline in the cleft after ACh breakdown by AChE is taken back into the cholinergic nerve terminal by a choline transporter.

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33
Q

Some compounds cause irreversible inhibition of AChE

A

Very toxic varieties are “nerve gases” Sarin and Soman
These are derived from pesticides in 1930’s
Weak, reversible AChE inhibitors are used as insecticides
Human made, reversible inhibitors used to treat Alzheimer’s disease

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34
Q

What is the organization and function of the cholinergic system?

A

ACh is found at:
Neuromuscular junctions
The autonomic nervous system
It is also found isolated within the brain
Fibers originate and stay in brain

35
Q

Where ACh can also be found?

A

In three primary areas which include both projecting neurons and interneurons:
Projecting ACh cell bodies:
The basal forebrain
The brainstem
ACh interneurons
The striatum

36
Q

What are interneurons?

A

They are in the striatum.
Regulation of movement depends in part on the balance between ACh and Dopamine (DA)
In Parkinson’s disease, DA is low and the resulting neurotransmitters imbalance contributes to motor symptoms (there is too much ACh)
Anti cholinergic drugs are sometimes prescribed instead of L-dopa in the early stages of Parkinson’s disease

37
Q

What are the ACh receptors?

A

Two families of cholinergic receptors:
Nicotine receptors: respond to the agonist nicotine, an alkaloid found in the tobacco plant
Muscarinic receptors: respond to muscarine, an alkaloid first isolated from fly agaric mushrooms

38
Q

How does the nicotine ACh receptors work?

A

Nicotine receptors are ionotropic(having) an ion channel
When ACh binds, the channel opens and Na+, K+, and Ca+ enter the neurons or muscle cell, which depolarizes the cell membrane
Nicotine receptors mediate fast excitatory responses in both CNS and the PNS

39
Q

What is the neuronal alpha-4-beta-2 receptor?

A

Most abundant subtype of receptor
Permeable to Na+ and Ca2+
Most important for relaxing effects of nicotine in regular smokers. Anti anxiety
Chantix

40
Q

What are the drugs that directly affect NMDA receptors?

A

Alcohol
Benzodiazepines
Ketamine (aka special K)
Phencyclidine(aka PCP)
Dextromethorphan
Nitrous oxide
Some anti-convulsant medications
Many chemicals involved in “huffing”
1 F.D.A- approved treatment for Alzheimer’s disease

41
Q

What are amino acids?

A

Building blocks of proteins, neurotransmitters
Directly actions as neurotransmitters (excitatory, inhibitory )

42
Q

What amino acid are inhibitory ?

A

GABA
Taurine
Beta-alanine

43
Q

What amino acid are excitatory?

A

Glutamate
Aspartame
Cysteine
Homocysteate

44
Q

What do GABA and glutamate have in common?

A

Act at both ionotropic and metabotropic receptors
Fastest effects due to change in resting membrane potential
Most abundant type of neurotransmitter (70% of all neurons in CNS utilize AANT’s)

45
Q

What do all neuron contain and why?

A

All neuron contain amounts of glutamate.
Glutamatergic neurons use glutamate as transmitter, and have higher concentrations of
These neurons are thought to segregate the glutamate used for transmission from the glutamate used for other functions

46
Q

Where is glutamate synthesized from?

A

Glutamate is synthesized from glutamine using glutaminase

47
Q

What do EAAT and Vglut mean?

A

Vglut: Vesicular glutamate transporter
EAAT: excitatory amino acid transporter

48
Q

What are the 3 types of ionotropic glutamate receptors?

A

AMPA receptor: named for the selective agonist AMPA, a synthetic amino acid analog
NMDA receptor: named for the agonist NMDA, a synthetic amino acid.
Kainate receptor: named for the selective agonist Kainic acid.

49
Q

What is the of the ionotropic glutamate receptors?

A

It depolarize the postsynaptic cell membrane, which leads to an excitatory response

50
Q

What is the role of the AMPA and kainate receptors?

A

AMPA and Kainate receptors ——flow of Na+ depolarizes

51
Q

What is the role of the NMDA receptors?

A

NMDA receptors allow both Na+ and Ca2+ to pass, Ca2+ also activates a second messenger

52
Q

What are the unique characteristics of NMDA receptors?

A

Flow of both Ca2+ and Na+
Steps in NMDA receptors activation:
1. Glutamate binds to AMPA receptors
2. Na+ flows into neuron through AMPA receptor
3. This causes Mg2+ to “pop out” of the channel in NMDA receptors
4. Glutamate and co-agonist binds to NMDA receptor- it opens

53
Q

What happens with the influx of Ca+ ions through NMDA channels?

A

The influx of Ca2+ ions through NMDA channels activates several protein kinases
The end result is long term potentiation (memory formation)

54
Q

What linked NMDA receptors with learning?

A

3 other lines of evidence have linked NMDA receptors with learning:
Treatment with NMDA receptor antagonist leads to impaired learning.
1. Alcohol
2. Benzodiazepines
3. Ketamine
4. Phencyclidine

55
Q

How many metabotropic receptors does glutamate have?

A

Glutamate has 8 metabotropic receptors designated mGluR1 to mGluR8
mGluR1 “Family”: mGluR1 and mGluR5 (q-linked )
mGluR 2 “Family”: Gi-linked, presynaptic
mGluR 3 “Family”: Gi linked, presynaptic

56
Q

How are metabotropic receptors?

A

They are widely distributed throughout the brain

57
Q

The role of the metabotropic receptors?

A

They participate in locomotor activity, motor coordination, cognition, mood, and pain perception.
mGluR drugs are being developed for treatment of many neuropsychiatric disorders

58
Q

What are the major inhibitory amino acid transmitters?

A

GABA and Glycine

59
Q

How important is inhibitory transmission?

A

Inhibitory transmission is just as important as excitatory, if GABA-A receptors are blocked, convulsions and death can result.

60
Q

How is GABA synthesized?

A

GABA is synthesized only by GABAergic neurons. It is made from glutamate and catalyzed by glutamic acid decarboxylase

61
Q

What are the actions with GABA?

A

GABA moves into vesicles via vesicular GABA vesicular transporters VGAT
GABA is removed from the synaptic cleft by 3 different transporters GAT-1, GAT-2 , and GAT-3

62
Q

Textual description of GABA synthesis

A

Glutamate from astrocytes is taken up by glutamine transporter
Glutamine is converted to glutamate by glutaminase
Glutamate is converted to GABA by glutamic acid decarboxylase
GABA is transported into neuron and astrocyte by GABA transporter
Astrocyte GABA is reverse metabolized to glutamate by GABA transminase
Glutamate is metabolized to glutamine synthetase, which is pumped out of astrocyte

63
Q

How many receptors do GABA receptors?

A

GABA A receptor- ionotropic
GABA B receptor- metabotropic

64
Q

The role of GABA A receptor?

A

GABA A receptor channels allow Cl- to move from outside to inside the cell
This causes hyper polarization and inhibition of the postsynaptic cell
Each receptor consists of five subunits, of various combinations of four types
Drugs affecting GABA A receptors bind to different subunits

65
Q

What are the GABA A receptors in clinical pharmacology?

A

Diazepam: classic benzodiazepines used to treat anxiety and alcohol withdrawal
Agonist at GABA A receptors
Antagonist of AMPA receptors (Topamax)
Inhibit GABA transminase
Also affects Na+ channels (Depakote)

66
Q

What are the psychoactive substances that interact with serotonin systems?

A

Selective serotonin reuptake inhibitors(SSRIs)
Methamphetamine
Methylenedioxymethamphetamine(ecstasy)
Lysergic acid diethylamide(LSD)
Psylocybin(magic mushrooms)
Mescaline(cactus)
Canthinones(khat shrub)

67
Q

What is serotonin?

A

Serotonin is also known as 5-HT (5-hydroxytryptamine)
Known as an indoleamine
It is a neurotransmitter that has a wide range of behavioral and physiological functions including regulation of mood, sleep, hunger, anxiety, pain, and learning memory

68
Q

How is 5-HT in the brain?

A

90% exists in the GI tract
Regulates intestinal movement
Only 2% is actually found in the central nervous system
Neurons must make their own 5-HT as it does not cross the BBB

69
Q

Where does serotonin come from?

A

It is derived from tryptophan

70
Q

What is tryptophan?

A

Tryptophan is an essential amino. It therefore must be part of an organisms diet. Availability of tryptophan affects the rate of 5-HT synthesis.
Tryptophan can’t cross BBB by diffusion, must be actively transported by large amino acid transporter(LAT)
Competes with amino acids for transport into brain

71
Q

What is the role of the insulin?

A
  1. When large amounts of carbohydrates (sugars, starches) are eaten, insulin release is triggered
  2. One of the things insulin does is activate the LAT
    Increases uptake of essential amino acids
  3. Consumption of foods rich in tryptophan (meats) equal more tryptophan gets in brain via LAT
    Some of this gets converted to melatonin
72
Q

5-HT in the brain (Raphe Nuclei)

A

In the CNS, neurons that produce 5-HT are found in clusters- in the raphe nuclei of the midbrain, pons, and medulla (brainstem)
These clusters project to broadly and are most inhibitory

73
Q

What does raphe mean?

A

It means “seam”
Rostral raphe group
Dorsal
Linear
Median
Caudal raphe group
Magnus
Obscurus
Pallidus

74
Q

What is the synthesis of serotonin?

A

L-tryptophan to L-5-Hydroxytryptophan by (tryptophan hydroxylase)
L-5-hydroxytryptophan (5-HTP) to 5-Hydroxytryptamine by aromatic l-amino acid decarboxylase

75
Q

The storage, release, and inactivation of serotonin

A

Vesicular monoamine transporter 2 (VMAT2)
Transported into presynaptic vesicles just like catecholamines
Autoreceptors control release (negative feedback)
Mechanism of signaling inactivation is reuptake by SERT (the 5-HT transporter)— SSRIs
Monoamine oxidase (MAO)
MAO breakdown in pre-synaptic terminal after reuptake

76
Q

Concentration of 5-HIAA in the CSF

A

Concentration of 5-HIAA in the CSF is often used to determine the association between 5-HT and psychiatric disorders

77
Q

The 5-HT receptors

A

There are at least 14 receptors for 5-HT
All are metabotropic/ G-coupled, but one
Classified into 7 groups (5-HT 1-7) based on their pharmacological profiles

78
Q

What is the receptors 5-HT1A?

A

5-HT 1A: Gi- the autoreceptor
Reduce cAMP synthesis by inhibiting adenylyl cyclase; or increase opening of K+ channels and membrane hyperpolarization

79
Q

What is the receptors 5-HT2A?

A

5-HT-2A: Gq
Activate the IP3 second messenger system. This results in increases Ca2+ levels in postsynaptic cells and also activates protein kinase C (PKC)

80
Q

Modulation of 5-HT 2A receptors?

A

Agonists at this receptor can be hallucinogenic in humans (LSD)
Antagonist of this receptor (clozapine and risperidone) have been used as antipsychotics

81
Q

What is the 5-HT3 receptor?

A

It is a ligand gated ion channel that is permeable to Na+, K+, and Ca2+

82
Q

Modulation of 5-HT3 receptors?

A
  1. Toxins/irritants in the stomach such as:
    Cancer chemotherapy , HIV medications
    Other nasty things ingested
    Stimulate release of 5-HT in the gut, which stimulates gut 5-HT3 receptors and induces nausea
  2. Toxins in blood such as:
    Medications, poisons, industrial chemics
    Stimulate serotonin release in Area Postrema (5-HT3 receptors)
    5-HT3 antagonists such as ondansetron (zofran and granisetron (Kytril) are used to treat the nausea
83
Q

What are the serotonin syndrome?

A

Too much serotonin is bad and can be deadly
Causes: usually by taking a combination of serotonergic drugs
Very important to be aware of medications you are taking
Symptoms: confusion, agitation, headaches, blood pressure changes, accelerated heart rate, loss of muscle
coordination, nausea, vomiting, diarrhea, shivering, heavy sweating
Treatment: IV fluids, cease medication, drugs that block 5-HT production

Psy 459 (2 decks)

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