Psychopharmacology Flashcards Preview

Biological and Cognitive Foundations > Psychopharmacology > Flashcards

Flashcards in Psychopharmacology Deck (36):
1

sites of action

points at which molecules of drugs interact with molecules located on or in cells of the body
 

2

pharmokinetics

the process by which drugs are absorbed, distributed, metabolized, and excreted in the body

3

routes of drug administration (11)

intravenous
intraperitoneal
intramuscular
subcutaneous
oral
intrarectal
inhalation
topical
insufflation
intracerebral

4

efficacy of a drug

relationship between receptor occupancy and ability to initiate a response

5

direct agonist

when a drug influences a receptor the same way as a neurotransmitter and opens a channel immediately

6

direct antagonist

when a drug blocks the site of a neurotransmitter, thereby directly blocking reaction

7

lipid solubility

the most important determinant of drugs reaching the bloodstream because teh BBB blocks only water-soluble molecules

8

dose response curves

tell the amount of drug and magnitude of effect per side effect. the margin of safety between the two effects determines the usability and safety

9

therapeutic index

a number that represents how many times a safe dose of the drug must be taken to produce toxic effects

10

affinity

the ease of two molecules joining together. high affinity=effects at low concentration. low affinity=effects at high consentration

11

compensatory mechanism of withdrawl

decrease in effectiveness of binding with receptors (decreased affinity)

and coupling receptors to ion channels (decreased efficacy)

12

How do drugs effect the production of neurotransmitters?

neurotransmittes are synthesized from precursors (the precursor is the agonist)
synthesis of the neurotransmitter is controlled by enzymes. if a drug inactivates an enzyme, it will prevent the neurotransmitter from being prduced (making it an antagonist)

13

How do drugs effect the storage and release of neurotransmitters?

 

transporter molecules that fill the synaptic vesicles with neurotransmitters can be blocked by a drug (making it an antagonist)
drugs can deactivate the protein that fuses synaptic vesicles with presynaptic membrane (making it an antagonist)

others can bind with proteins and trigger release of neurotransmitters (making it an agonist)

prevent the release of NT at a terminal bouton (antagonist)

14

indirect antagonist

drug binds to an alternative binding site on receptor (does not interfere with binding site for principal ligand) 

noncompetitive binding

 prevents ion channel from opening

15

indirect agonist

drug attaches to an alternative binding site on receptor (does not interfere with binding site for principal ligand) 

opens ion channel/facilitates action of receptor

16

presynaptic heteroreceptor

located in membrane of terminal button and receives info from the other button
 

17

How do drugs effect autoreceptors

stimulation of autoreceptor will cause less neurotransmitter to be released (making it an antagonist)
blocking an autoreceptor will increase the neurotransmitter (making it an agonist)
durgs can bind with autoreceptors at the dendrites an activate them (making it an antagonist)
drugs can bind with autoreceptors at the dendrites and block them (making it an agonist)

18

How do drugs effect reuptake or destruction of neurotransmitters?

drugs can block transport molecules from reputaking into the synapse (making it an agonist)
drugs can bind with enzymes that would kill the neurotransmitter and prevent it from doing so (making it an agonist)

19

glutamate

neurotransmitter with transmitting effects
most excitatory neurotransmitter
raise and lowers teh threshold of excitation.
NDMA controls sodium and calcium ions and causes a depolarization 
AMPA receptor that controls sodium channels to produce EPSP
communicates with GABA

20

GABA

Has transmitting effects
inhibatory neurotransmitter
produced from glutamaic acid
GABAis ionotropic to control chloride channel
GABAis metabotropic and controls potassium channel
communicates with glutamate

21

glycine

main inhibitory neurotransmitter in the CNS
receptor is ionotropic and controls chlorine channel
spinal cord and lower parts of the brain

22

neurotransmitters with modulating effects

(they activate or inhibit neuronal circuits)

acetylcholine
norepinephrine
serotonin
dopamine

23

acetylcholine

responsible for all muscular movement
found in ganglia of ANS and at organs in parasympathetic branch of ANS
synapses are acetylcholinergic
deactivated by the enzyme acetylcholinesterase after being released from terminal button

24

ACh in dorsolateral pons

REM sleep

25

ACh in basal forebrain

activate cerebral cortex and facilitate learning

26

ACh in medial septum

electrical rhythms of hippocampus and modulate formation of memories

27

types of ACh receptors

nicotinic receptor: fast, ionotropic, stimulated by nicotine, blocked by curare
muscarinic receptor: slow, metabotropic, stimulated by muscarine, blocked by atropine

28

dopamine

excitatory and inhibitory potentials. affects movement, attention, learning, reinforcment

29

3 systems of dopaminergic neurons

nigrostriatal system: from substantia nigra to basal ganglia; involved in movement
mesolimbic system: in ventral tegmental area to limbic region; involved in reinforcing effects
mesocortical system: from VTA to PFC; involved in formation of short term memories, planning, strategy preparation

30

norepinephrine

found in ANS
dopamine is converted into norepinephrine through dopamine B-hydroxylase enzyme
neurons that release norepinephrine are noradrenergic
increase vigilance 

cell bodies that release NE located in medulla & pons 

31

serotonin

plays role in regulation of mood, sleep, arousal, and regulation of pain
cell bodies in raphe nuclei of midbrain, pons and medula
 

32

peptides

2 or more amino acids linked by a peptide bond
produced from larger polypeptides that are broken down 
released from all parts of the terminal button

act on receptors belonging to other cells close by
once released, they are destroyed by enzymes

(example: endorphins)

33

lipids

can transmit messages between cells
endocannabinoids are best known for analgesia, sedation, appetite, and reduction of nausea
not as many receptors in the brain stem 
 

34

nucleosides

compund that consists of a sugar molecule bound with a purine or pyramidine base
adenosine: a nucleoside that is released by astrocytes when neurons are short on fuel and oxygen and activates receptors that dialate blood vessels. accumulates while awake, decreases during sleep. 

35

soluble gases

nitric oxide and carbon monoxide are used to help neurons communicate
nitric oxide controls muscles in intestines, dialates blood vessels in brain, and changes blood vessels in erections
carbon monoxide controls muscles in intestines and dialates blood vessels in the brain

36

Why do drugs differ in their effectiveness?

1.  Different sites of action 

e.g. morphine & aspirin -both analgesics

morphine site-neurons involved in pain perception

aspirin site- reduces chemical messenger of pain 

2. Affinity of drug to site of action and efficacy