Carlson Ch 4

Front 1

Pharmacokinetics

Back 1

– the process by which drugs can be administered

Front 2

Sites of action

Back 2

the points at which molecules of drugs interact with molecules located on or in cells of the body, thus affecting some biochemical processes of these cells

Front 3

Drug effects

Back 3

the changes we can observe in an animal’s physiological processes and behavior

Front 4

Drug

Back 4

an exogenous chemical not necessary for normal cellular functioning that significantly alters the functions of certain cells of the body when taken in relatively low doses

Front 5

Psychopharmacology

Back 5

study of the effects of drugs on the NS and on behavior

Front 6

Routes of Administration

Back 6

Injection:drug is dissolved and suspended in a liquid, and injected via hypodermic needle
Intravenous, intraperitoneal, intramuscular, subcutaneous, intracerebral, intracerebroventricular
--Oral: into the mouth; swallowed
--Sublingual:placing substance beneath the tongue
--Intrarectal:into the rectum
--Inhalation: vaporous substance into the lungs
--Topical:directly onto the skin or mucous membrane

Front 7

Best way to look at drug effectiveness

Back 7

Dose response curve
--effect of drug versus dose

Front 8

Maximum effect

Back 8

point when increasing dose does not produce stronger effect

Front 9

Margin of safety

Back 9

the difference between dose-response curves; desirable effect and toxic effect

Front 10

most desirable drug

Back 10

= LARGE margin of safety

Front 11

Therapeutic index

Back 11

measure of a drug’s margin of safety

Front 12

lower therapeutic index =

Back 12

more care taken in prescribing the drug

Front 13

Therapeutic Index Ratio

Back 13

RATIO = desired effects dose (50%)/ toxic effects dose (50%)

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Most desirable Drugs

Back 14

High affinity for therapeutic effects
Low affinity for toxic effects

Front 15

Affinity

Back 15

the readiness with which 2 molecules join together

Front 16

High affinity

Back 16

theraputic affects

Front 17

low affinity

Back 17

toxic effect

Front 18

Sites of Drug Action

Back 18

Agonist (AGO)
Antagonists (ANT)

Front 19

Agonist (AGO)

Back 19

facilitates or mimics NT
---DIRECT AGO: binds to receptor site --> opens ion channel
---INDIRECT AGO: attaches to alternative site--> facilitates opening of channel

Front 20

Antagonist (ANT)

Back 20

blocks or inhibits NT
---DIRECT ANT: binds to receptor site--> prevents ion channel from opening
---INDIRECT ANT: attaches to receptor site-->prevents opening of ion channel

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ACh (Acetylcholrine) roles

Back 21

---Movement
---Activation of the cerebral cortex-
learning and memory
---REM sleep and dreaming

Front 22

ACh has 2 components

Back 22

1. Choline – derived from breakdown of lipids
2. Acetate – anion found in vinegar

Front 23

Production of ACh

Back 23

1. in presence of the enzyme choline acetyltransferase (ChAT)
2. the acetate ion is transferred from Acetyl-CoA to the choline molecule, yielding a molecule of ACh and CoA

Front 24

Too much ACh in cleft

Back 24

then it opens too many channels causing either
1. Inhibitory would be paralysis 2. excite it and get spaticity

Front 25

Botulinim Toxin

Back 25

ANT); prevents release of ACh

Front 26

Black Widow Spider Venom

Back 26

(AGO); stimulates release of ACh

Front 27

Curare:

Back 27

(ANT) blocks ACh receptors (temporary paralysis but brain still works)

Front 28

Neostigmine:

Back 28

(AGO); AChE inhibitor (used in persons with myasthenia gravis)
Defends the enzyme from destroying Ach,

Front 29

Location of ACh

Back 29

---Dorsolateral Pons: REM sleep
----Basal Forebrain:
Cortical activation; facilitates learning
---Medial Septum: controls electrical rhythms of hippocampus and modulates it s functions (including formation of memories

Front 30

Destruction of Acetylcholine

Back 30

ACh released from terminal button-->deactivated by acetycholinesterase (AChE)-->produces choline and acetate-->reuptake returns choline to terminal button-->choline converted back to ACh

Front 31

Monoamines 2 catergories

Back 31

1. Catecholamines
2. Indolamines

Front 32

Catecholamines

Back 32

1. Dopamine (DA)
2. Epinephrine (minor importance in the brain compared to NE)
3. Norepinephrine (NE)

Front 33

Indolamines

Back 33

Serotonin (5-HT)

Front 34

Dopamine (DA) Roles

Back 34

1. Movement
2. Attention
3. Learning
4. Higher cortical problem solving
5. Pleasure

Front 35

Locations of Dopamine Neurons

Back 35

1. Nigrostriatal:
Control of movement
2. Mesolimbic:
Nucleus accumbens reinforces drug use
3. Mesocortical:
Excitatory effect on frontal cortex; formation of STM; planning; problem solving strategy

Front 36

Dopamine precursors

Back 36

Tyrosine-->L-Dopa-->Dopamine

Front 37

Amphetamine:

Back 37

(AGO); blocks reuptake

Front 38

Cocaine:

Back 38

(AGO); blocks reuptake

Front 39

Ritalin:

Back 39

(AGO); blocks reuptake

Front 40

Clozapine:

Back 40

Antipsychotic

(ANT); blocks D4 receptor

Front 41

Chlorpromazine:

Back 41

(ANT); blocks D2 receptor
Antipsychotic

Front 42

Levels of Dopamine

Back 42

Too much=schizophrenia--so you want to take an ANT
to little= Parkinson-- want to give AGO

Front 43

Tyosine

Back 43

essential amino acid

Front 44

Blocking Receptor effect on NT

Back 44

decreases the productivity

Front 45

Blocking the uptake

Back 45

increases the effectiveness

Front 46

Parkinson treatment

Back 46

Caused by degeneration of the nigrostriatal system
---L-Dopa
Increases dopamine (Agonist)

Front 47

Depression

Back 47

not enough dopamine
give MAO-I (because the MAO is the enzyme that kills dopamine)

Front 48

Norepinephrine (NE) Precursor

Back 48

tyrosine --> L-DOPA -->dopamine --> norepinephrine

Front 49

Norepinephrine (NE) System

Back 49

cell bodies located in locus coeruleus (dorsal pons)
---Increase in vigilance

Front 50

Norepinephrine (NE) Role

Back 50

increased vigilance, attention, sexual behaviors, control of appetite

Front 51

Serotonin (5-HT) Roles

Back 51

1. Regulation of mood
2. Control of eating
3. Sleep/dreaming and arousal
4. Regulation of pain
5. Regulating impulsivity

Front 52

Serotonin (5-HT) Precursors

Back 52

Tryptophan --> 5-HTP --> Serotonin (5-HT)

Front 53

Serotonin (5-HT) location

Back 53

Cell bodies in the Raphe nuclei

Front 54

LSD:

Back 54

(AGO); stimulates 5-HT release
(presynaptic) causes more synaptic vesicles to fuse

Front 55

MDMA (Ecstasy)

Back 55

(AGO); stimulates 5-HT release

Front 56

Fenfluramine:

Back 56

(AGO); stimulates 5-HT release and inhibits reuptake

Front 57

Fluoxetine (Prozac):

Back 57

(AGO); inhibits reuptake

Front 58

3 Most Common Amino Acids in the Brain

Back 58

1. Glutamate
2. GABA
3. Glycine

Front 59

Glutamate

Back 59

principle excitatory NT in the CNS
---Direct excitatory and inhibitory effects on axons
---They raise or lower the threshold of excitation, thus affecting the rate at which action potentials can occur

Front 60

GABA

Back 60

principle inhibitory NT in the brain
----Stabilizes brain activity from uncontrollable neuron firing (i.e. seizures)

Front 61

Glycine

Back 61

inhibitory effect over muscles
---Located in spinal cord and lower brain

Front 62

ACh Receptors

Back 62

1. Nicotinic receptors (Ionotropic)
2. Muscarinic receptors (Metabotropic)

Front 63

Nicotinic receptors (Ionotropic)

Back 63

stimulated by nicotine
---Rapid actions – ion channels directly controlled
---Some found at axoaxonic synapses in brain where they produce presynaptic facilitation
----Curare (ANT) – drug that blocks nicotinic receptors; causes temporary paralysis but the brain still works

Front 64

Muscarinic receptors (Metabotropic)

Back 64

stimulated by muscarine (found in poisonous mushroom)
----Slower action – ion channels indirectly controlled by second messengers
---Predominate in CNS
----Atropine – drug that blocks muscarinic receptors

Front 65

Myasthenia gravis

Back 65

a hereditary disorder caused by an attack of a person’s immune system against acetylcholine receptors located on skeletal muscles
the person becomes weaker as the muscles become less responsive to the NT (ACh)

Front 66

Neostigmine

Back 66

(AGO) is used in persons with myasthenia gravis
----AChE inhibitor
---The person regains some strength because the ACh that is released has a more prolonged effect on the remaining receptors
----This drug cannot cross the blood-brain barrier (no effect on AChE found in CNS)

Front 67

Can choline attach directly to Acetate?

Back 67

NO: (it is transferred from a molecule of acetyl-CoA)