Slpa 853 - Neurology - Psychopharmacology

Front 1

Neurotransmitters are either:

Back 1

-simple amino acids (GABA, Glutamate)
-synthesized within neurons (indogenous)

Front 2

What are some assumptions about drugs?

Back 2

-viewed as "exogenous" (from outside) chemicals
-alter neuron activity
-have effects at low doses

Front 3

Most anesthetic drugs affect synaptic action in one of two ways:

Back 3

-blocking the release of transmitter from the pre-synaptic cell
-blocking the receptors on the post-synaptic cell

Front 4

What is pharmacokinetics?

Back 4

study of drug absorption, distribution within body, and elimination

Front 5

What are the different routes of drug administration into the body? (5)

Back 5

-intravenous (IV)
-intraperitoneal (IP- into the gut--lab animals)
-subcutaneous (under the skin)
-intramuscular (IM- into the muscle)
-oral

Front 6

What is the dose-response (DR) curve?

Back 6

depicts the relation between drug dose and magnitude of drug effect

Front 7

Different drugs have different D-R curves. Why?

Back 7

-different sites of action
-different levels of affinity

Front 8

What is affinity?

Back 8

the readiness with which two molecules attach

Front 9

A drug with high affinity will produce effects at _____ concentrations.

Back 9

low

Front 10

A drug with low affinity must be administered in _____ doses.

Back 10

high

Front 11

The effectiveness of two drugs with same sites of action can vary considerably if they can have different ___________ for their binding sites.

Back 11

affinities

Front 12

Ideally, a drug should have high affinity for sites of action that produce ______________.

Back 12

therapeutic effects

Front 13

Ideally, a drug should have a low affinity for sites of action that produce ________________.

Back 13

toxic side effects

Front 14

Why do drug effects diminish with repeated administration?

Back 14

-changes in number of brain receptors for drug
-decrease in affinity of receptors to bind drug

Front 15

_________ is associated with tolerance.

Back 15

Withdrawal

Front 16

What is sensitization?

Back 16

drug effects increase with repeated administration

Front 17

What is tolerance?

Back 17

drug effects diminish with repeated administration

Front 18

What is a placebo?

Back 18

an innocuous substance without a specific physiologic effect
-subject's belief that they receive a medication can trigger real physiological responses that mimic the effect of a drug

Front 19

What are the 4 basic steps of a NT?

Back 19

-synthesized
-stored
-released
-terminated

Front 20

A receptor's affinity for a specific molecular structure, a ligand, is similar to the relationship between what?

Back 20

a "lock and key"

Front 21

A drug molecule with the "best fit" to the receptor will:

Back 21

elicit the greatest response from the cell

Front 22

When a ligand bonds:

Back 22

the electrical properties of that cell changes

Front 23

Drug occupation of a receptor either serves as an....

Back 23

-agonist
-antagonist

Front 24

What is an agonist?

Back 24

-a drug occupation of a receptor
-binds to and activates receptors
-facilitates the NT effects

Front 25

What is an antagonist?

Back 25

-a drug occupation of a receptor
-a receptor blocker that binds but does not activate
-will interfere with the binding of NT

Front 26

Each NT has multiple ________ ________ on the postsynaptic membrane. AND Each receptor has one or more types of _______ ________ allowing different substances to affect the receptors function.

Back 26

-receptor types
-binding sites

Front 27

Describe primary mechanisms of drugs: Affecting release of NT (presynaptic).

Back 27

-affects neurons ability to release NT
-presynaptic heteroreceptor

Front 28

Describe primary mechanisms of drugs: Affecting reception of NT (postsynaptic).

Back 28

-direct agonists
-a drug that binds and activates

Front 29

Describe primary mechanisms of drugs: Affecting synapse (synaptic).

Back 29

-direct antagonists (receptor blocker)
-blocking reuptake
-inactivation NT

Front 30

What happens when drugs occupy receptor's binding cites?

Back 30

-does not open ion channels (just blocks receptor)
-prevents NT from opening the ion channel

Front 31

True of false: Some drugs open ion channels permanently.

Back 31

True (or for a very long time)

Front 32

Describe barbiturates.

Back 32

-make many of inhibitory synapses stick "open"
-thus, barbiturates produce "super-inhibition"

Front 33

What is "super-inhibition" and what does this produce?

Back 33

-the inability to excite neurons
-produces: deep sleep, unconsciousness, and eventually death when all neurons stop firing

Front 34

What is presynaptic heteroceptor?

Back 34

-an axoaxonic synapse
-one axon synapses on another axon

Front 35

What does the first neuron cause?

Back 35

either presynaptic inhibition or facilitation of the second one

Front 36

What is presynaptic inhibition?

Back 36

activation of receptors that inhibit the opening of calcium channels

Front 37

What is presynaptic facilitation?

Back 37

activation of receptors that facilitate the opening of calcium channels

Front 38

What are the 2 types of termination of postsynaptic potential?

Back 38

-reuptake into button
-destruction of transmitter by enzyme

Front 39

Describe prolongation of postsynaptic potential.

Back 39

-acting as agonists, drugs can interfere with any of these processes:

--deactivation of molecules responsible for reuptake
--binding with enzyme that normally destroys transmitter (e.g., acetylcholinesterase can be made ineffective which usually destroys acetycholine)

Front 40

Where are NTs synthesized and released from?

Back 40

presynaptic terminal

Front 41

NTs have brief effects on what? AND what are these effects known as?

Back 41

-postsynaptic membrane
-action potentials (IPSPs and EPSPs)

Front 42

Describe the creation of NTs.

Back 42

most are synthesized in the cytoplasm of the terminal buttons and stored into newly formed synaptic vesicles

Front 43

What are the primary NTs?

Back 43

-Acetylcholine (ACh)
-Monamines
-Amino Acids

Front 44

Name the primary monamines?

Back 44

-Dopamine (DA)
-Norepinephrine (NE)
-Serotonine (5-HT)

Front 45

Name the primary amino acids.

Back 45

-Glutamate
-GABA
-Glycine

Front 46

Which NT is the primary efferent transmitter in the CNS?

Back 46

Acetylcholine (ACh): axons and terminal buttons containing ACh are distributed widely throughout the brain

Front 47

All muscular activity is accomplished by the release of what?

Back 47

ACh

Front 48

In the periphery, ACh neurons are found where? AND what is their function?

Back 48

- found at neuromuscular junction (stored here)
-cause muscles to contract

Front 49

Describe ACh neurons in the brain.

Back 49

are distributed widely and are generally facilitatory in the brain

Front 50

What function do ACh neurons have in the dorsal pons?

Back 50

REM sleep

Front 51

What function do ACh neurons have in the medial septum?

Back 51

control hippocampus for memory functions

Front 52

What function do ACh neurons have in the basal forebrain?

Back 52

-activating cerebral cortex
-facilitating learning, especially perceptual learning

Front 53

What enzyme is ACh deactivated in the synapse by? AND where is this enzyme present?

Back 53

-the enzyme acetylcholinesterase (AChE)
-in the PS membrane

Front 54

What reactivates ACh?

Back 54

choline

Front 55

Describe Botulinum toxin. AND tell how it affects ACh.

Back 55

-Botox: a bacteria that can grow in improperly canned food. A teaspoon could kill the human population. For SLP, inserted into VFs for spasmodic dysphonia.

-an ACh antagonist (prevents presynaptic release of ACh)

Front 56

What are potential symptoms of black widow spider venom? AND tell how it affects ACh.

Back 56

-twitching, trembling, paralyzed breathing, convulsions, and in extreme cases, death
-ACh agonist (triggers the release of ACh)

Front 57

What do insecticides do to insects and to humans? AND tell how they affect ACh.

Back 57

-kill insects by deactivating AChE; may have little effect on humans as our blood contains enzymes that destroys them
-ACh agonist

Front 58

Describe Myasthenia Gravis. AND describe what drugs can do for this.

Back 58

-caused by an attack of a person's immune system against ACh receptors located in skeletal muscles
-person becomes weaker as muscle becomes less responsive to ACh

-drugs such as neostigmine (ACh agonist) can return some strength-- produce a more prolonged effect of ACh by inhibiting AChE

Front 59

Describe curare as it relates to ACh.

Back 59

-ACh antagonists
-blocks ACh receptors found in muscle
-produces paralysis
-used for poisoned darts for hunting causing animals to collapse and cease breathing (extracted from several different species of plants in South America)
-used medically to relax a muscle undergoing surgical procedure

Front 60

True or false: Monoamines are produced by several systems of neurons in the brain.

Back 60

True

Front 61

Why is Dopamine (DA) a double duty transmitter?

Back 61

produces both excitatory and inhibitory PSPs depending on the postsynaptic receptor

Front 62

What is Dopamine (DA) important for?

Back 62

-movement
-attention
-learning
-reinforcing effects of drugs that people abuse

Front 63

Describe Parkinson's.

Back 63

a movement disorder that is characterized by: resting tremors, rigidity of limbs, poor balance, difficulty in initiating movements, hypokinetic dysarthria
-caused by degeneration of the dopaminergic neurons that connect the substantia nigra with the caudate nucleus

Front 64

Where does the substantia nigra get its black color from?

Back 64

-melanin which is a natural by-product that is produced by the breakdown of DA
-dissection of this region in individuals with Parkinson's reveals only a pale color

Front 65

Name AND describe the drug that alleviates some symptoms associated with Parkinson's.

Back 65

L-DOPA
-a precursor of DA that, unlike DA, can pass the blood-brain barrier
-causes more DA to be synthesized and released by surviving dopaminergic neurons

Front 66

What is Norepinephrine (NE)?

Back 66

-a hormone produced by the adrenal glands that serves as a NT in the brain
-most regions of the brain receive input from NE neurons

Front 67

Where are the cell bodies of NE located in?

Back 67

-pons
-medulla
-thalamus

Front 68

What is the activation of NE transmitters important for?

Back 68

vigilance--attentiveness to events in the environment

Front 69

What effect does the NE transmitter have on the postsynaptic neuron?

Back 69

generally excitatory

Front 70

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

Back 70

-mood
-eating
-sleep
-arousal
-pain
-dreaming

Front 71

What is a 5-HT precursor?

Back 71

tryptophane ("turkey effect")--produces more serotonin in the brain

Front 72

Where are 5-HT neurons found?

Back 72

in the pons and medulla

Front 73

What effect does LSD have on 5-HT?

Back 73

agonist that stimulates 5-HT receptors

Front 74

What effect does Fenfluramine have on 5-HT?

Back 74

-agonist that facilitates the release of 5-HT and inhibits its reuptake
-suppresses appetite

Front 75

Why do drugs such as LSD and Fenfluramine, which are both agonists for 5-HT, produce different effects?

Back 75

they have different receptors so they cause different effects on the neuron

Front 76

What effect does Fluoxetine (Prozac) have on 5-HT?

Back 76

agonist that inhibits reuptake of 5-HT

Front 77

What are the most common transmitter substances?

Back 77

amino acid NTs

Front 78

True or false: Amino acid NTs are found in only complex nervous systems and were likely late to evolve.

Back 78

False: found in very primitive nervous systems, perhaps first to evolve

Front 79

What is the general modulating role of amino acid NTs?

Back 79

-effect is to raise and lower the threshold of excitation (bias), thus affecting the rate at which APs can occur

Front 80

What effect does the amino acid NT GABA have?

Back 80

inhibitory (IPSP - hyperpolarizing effects--makes cell more negative--cell less likely to fire)

Front 81

What effect does the amino acid NT Glutamate have?

Back 81

excitatory (EPSP - depolarizing effects)

Front 82

What does GABA stand for?

Back 82

Gamma-aminobutyric-acid

Front 83

What two receptors have been identified for GABA?

Back 83

GABAa and GABAb

Front 84

What is the primary inhibitory transmitter substance for GABA? AND what does it do?

Back 84

GABAb receptors: open K+ channels, producing hyperpolarizing postsynaptic potentials

Front 85

What would happen to the brain without the inhibitory effects of GABA?

Back 85

-brain would become unstable (seizures)
-Epilepsy: may be caused by decline of GABA-secreting neurons

Front 86

What is the principle excitatory transmitter substance in the brain and spinal cord?

Back 86

glutamate (almost all neurons in the brain are influenced by glutamate)

Front 87

What is the function of glutamate?

Back 87

-depolarizes neurons and increases cell excitability
-activates postsynaptic neurons by glutamate receptor-linked Na+/Ca++ channel

Front 88

True or false: Glutamate is produced in abundance by the cell's metabolic processes.

Back 88

True

Front 89

What receptors mediate synaptic plasticity?

Back 89

AMPA receptors

Front 90

What is synaptic plasticity?

Back 90

means that the brain's pathways are capable of changing

Front 91

What will the lack of AMPA receptors do?

Back 91

make it difficult to learn/re-learn new information

Front 92

What happens with glutamate after a brain injury?

Back 92

-neurons release glutamate onto nearby neurons which become excited, overloaded with calcium and die
-destruction of the cell is caused by excessive CA++ activating enzymes within the postsynaptic cell
-damage may be stopped by drugs that block these receptors

Front 93

Describe Glycine.

Back 93

-an inhibitory NT in spinal cord and lower portions of the brain
-ionotropic receptor that controls chloride channel

Front 94

What does the removal of inhibitory effect (caused by glycine NT) cause the muscle to do?

Back 94

to contract continuously (Tetanus, Strychnine)

Front 95

What is tetanus?

Back 95

-lockjaw
-bacteria releases chemical that prevents the release of glycine

Front 96

What is strychnine?

Back 96

-serves as a glycine antagonist causing convulsions and death
-found in seeds of a tree found in India

Front 97

What effects do narcotics have? AND give some examples.

Back 97

-effects ranging from mild dulling of the senses, pain relief, and sleep, to stupor coma, and convulsions
-egs: morphine, codeine, heroin, opium, OxyContin

Front 98

Define general depressants. AND give some examples.

Back 98

-a drug or agent that has the effect of slowing the rate of the body's vital functions
-egs: alcohol, diazepam (Valium), chlordiazepoxide (librium), barbituates, methaqualone (Quaalude), "glue"

Front 99

What are barbituates? AND give some examples.

Back 99

-prescription sedatives
-egs: amobarbital (Amytal), pentobarbital (Nembutal), secobarbital (Seconal)

Front 100

Give examples of stimulants.

Back 100

cocaine, caffeine, amphetamine

Front 101

Give examples of hallucinogens.

Back 101

LSD, Mescaline, Psilocybin, Peyote, marijuana

Front 102

What drugs typically cause decreased salivation?

Back 102

-Oxybutin (Ditropan)
-Diphenhydramine (Benadryl)

Front 103

What is GERD? AND what drugs often cause this?

Back 103

-gastroesophageal reflux
-Nifedipine (Procardia) and Albuteral

Front 104

What drugs often cause impaired motor function?

Back 104

-Haldol
-Thorazine
-Risperidone

Front 105

What drugs typically cause impaired cognition and attention?

Back 105

-Diazepam (Valium)
-Lorazepam (Ativan)

Front 106

What drugs typically distort taste?

Back 106

-Chemotherapy
-Tetracycline