Psychopharmacology Flashcards
1
Q
DRUGS X THE SYNAPSE
A
- various substances (naturally occurring toxins/psychoactive chemicals) alter synaptic transmission
2
Q
SYNAPTIC SEQUENCE
A
- strong stimulation -> impulse (action potential)
- impulse propagated further down axon (axonal propagation/conduction)
- when axon terminal reached -> synaptic transmission (via neurotransmitter vesicle interaction, pushing toward membrane) initiated -> next neuron
3
Q
SYNAPTIC TRANSMISSION
A
- vesicles containing neurotransmitter reach membrane; open so neurotransmitter released into synaptic cleft
- neurotransmitter binds to receptors in postsynaptic neuron
- if receptors = ion-channels, open when neurotransmitter interacts w/them
- if receptors = non-ion, interact w/specific ion-channels; eventually open them
- consequence = ions enter postsynaptic neuron; leads to Post-Synaptic Potential
4
Q
NEUROTRANSMITTER INACTIVATION X RECYCLING
A
- diffusion = transmitter lost in inter-cellular space
- enzymatic degradation = enzymes break down transmitter
- re-uptake/uptake = transmitter recycled either in pre/post-synaptic neuron; most economical way to inactivate transmitter; saves synthesis resources
5
Q
SUBSTANCE INFLUENCE X SYNAPTIC SEQUENCE PHASES
A
- some act early as propagation of action potential
- others may influence transmitter release
- other modulate how transmitter interacts w/post-synaptic channels (receptors)
- finally some alter neurotransmitter presence in synapse via inactivation/recycling modulation
6
Q
CHEMICAL INTERFERENCE W/AXON SIGNALS
A
- via blocking sodium channels in axon’s membrane (ie. TTX (tetrodotoxin) in some fish species)
- TTX produces diaphragm paralysis/death via respiratory failure (10k+ times deadlier than cyanide)
7
Q
SUBSTANCE INTERFERENCE W/TRANSMITTERS
A
- tetanospasmin toxin interferes w/neurotransmitter GABA vesicles fusing w/cell membrane
- reduces GABA amount released into synapse
- GABA = inhibitory neurotransmitter; results w/excitation/inhibition neural signal imbalance
- results w/v strong uncontrollable muscle contractions (tetanus); can be lethal
8
Q
NEUROTRANSMITTER PATHWAYS
A
- excitatory synapses = glutamate (+ others)
- inhibitory synapses = GABA (+ others)
- mainly excitatory BUT also inhibitory synapses -> acetylcholine/dopamine (+ others)
- monoamines = single amino neurotransmitters (ie. adrenaline; noradrenaline; serotonin; dopamine; histamine; melatonin)
9
Q
SIT: ACETYLCHOLINE X BOTULINUM
A
- acetylcholine = neurotransmitter w/2 receptor types (nicotinic/excitatory OR muscarinic/inhibitory)
- botulinum toxin = used in BOTOX to treat wrinkles via synaptic effectiveness at neuromuscular junction reduction in facial muscles; formed via improperly canned bacteria food); interferes w/acetylcholine release at nicotinic synapses via preventing vesicles from fusing w/cell membrane
10
Q
SIT: AMPHETAMINE
A
- amphetamine = v structurally similar to dopamine so can enter dopamine-releasing neurons directly via membrane/via binding to dopamine transporter (molecule recycling dopamine back into cell via synaptic cleft)
- inside, amphetamine facilitates dopamine release from vesicles when they fuse w/membrane
11
Q
DOPAMINERGIC PATHWAYS
A
- amphetamine/other drugs (ie. cocaine/heroin/marijuana) = profound effect on dopaminergic brain pathways
- 1 pathway = particularly crucial in explaining potent drug effects; VTA (ventral tegmental area) projections -> nucleus accumbens (cell group in basal ganglia)
- VTA/nucleus accumbens = involved in pleasure/reward/motivation
12
Q
SUBSTANCES X RECEPTOR INTERACTIONS
A
- certain substances just bind to receptors (blocking neurotransmitter’s path) w/o opening channel
13
Q
SRI: ANTAGONISTS
A
- antagonist = occupies/blocks channel w/o opening it
CURARE - plant toxin (South America) occupies acetylcholine’s receptors in excitatory/nicotinic synapses blocking them -> paralysis
- above curare = antagonist
- curare used in surgery as anaesthetic agent
14
Q
SRI: AGONISTS
A
- agonist = imitates neurotransmitter beh; ^ effect
HEROIN - artificially modified morphine form (in opium)
- endorphine agonist; natural body chemicals bind to opiate receptors; reduces pain; induces relaxation
MARIJUANA/CANNABIS - contains THC (anandamide (natural body chemical binding to cannabinoid receptors) agonist)
- anandamide = emotion/pain/appetite/memory
TOBACCO - contains nicotine (stimulates nicotinic receptors; acetylcholine agonist)
- short-lived generalised excitatory effect ie. ^ blood adrenaline level
15
Q
NEUROTRANSMITTER INACTIVATION & RECYCLING
A
- diffusion = transmitter “lost” in inter-cellular space
- enzymic degradation = enzymes break down transmitter
- re-uptake/uptake = transmitter recycled either in pre/post synaptic neuron; most economical way to inactivate transmitter; saves synthesis resources; done via transporters (specialised proteins)
- ie. cocaine blocks noradrenaline/dopamine transporter; interferes w/re-uptake; boosts effect
16
Q
CHOCOLATE
A
- contains several psychoactive compounds
- ie. anandamide: neurotransmitter produces naturally in brain; agonist = THC (contained in cannabis)
- ie. phenylethylamine: compound closely related w/amphetamine
- BUT chocolate contains them in tiny amounts; wouldn’t cause noticeable effect (ie. to obtain effect similar to weed, one would have to consume half body weight in chocolate)
17
Q
CAFFEINE
A
- many neurons releasing substances ie. dopamine/adrenaline (catecholamines) also release self-inhibiting transmitter: adenosine
- adenosine binds to receptors in pre-synaptic neuron; inhibits catecholamine release
- caffeine = antagonist; competes w/adenosine for receptors; blocks adenosine; reduces inhibitory effect
- caffeine = non-synaptic effect in neurons; acts on cAMP (cyclic adenosine monophosphate)
- cAMP controls cell energy levels via glucose metabolism regulation
- caffeine inhibits enzyme that breaks cAMP down; ^ cell glucose metabolism
18
Q
LOW ALCOHOL DOSES
A
- alcohol = GABA agonist
- GABA gen in inhibitory synapses; alcohol ^ effectiveness of synapses -> relaxation
- alcohol indirectly stimulates dopamine release; dopaminergic synapses in certain brain parts associated w/reward pleasure/positive motivation (nucleus accumbens/other basal ganglia structures)
- hence small-moderate alcohol euphoria
19
Q
ALCOHOL PSYCHOACTIVITY
A
- moderate = indirectly increases endorphine release
- high = binds to GABA channels -> strong inhibition/sedation
- very high = cell membrane destruction -> brain cell death
20
Q
ANXIETY X GABA
A
- all anxiety disorders partly characterised by GABA-ergic transmission deficits
- bezodiazepines (valium) = GABA agonists; treat anxiety disorders
- effect similar to alcohol BUT bind to dif receptor sites
- DON’T bind to same receptor suites (ie. GABA) aka. non-competitive agonist
21
Q
DEPRESSION
A
- associated w/reduced monoamine (serotonin/dopamine/noradrenaline) transmission
- MAO inhibitors = interfere w/MAO enzyme which breaks down monoamine
- tricyclic anti-depressants = inhibit monoamine transporter; prevent re-uptake
- BUT serotonin = closely linked w/depression (>dopamine/noradrenaline)
- SSRI (selective serotonin re-uptake inhibitors ie. prozac/citalopram) = inhibit serotonin transporter w/o affecting other neurotransmitters
22
Q
SIDE-EFFECTS
A
- drugs affect lots of systems as neurotransmitters involved in lots of functions
- may have unwanted effects
23
Q
SCHIZOPHRENIA X DOPAMINE
A
- schizophrenia associated w/dopamine surplus
- symptoms = paranoia/hallucinations
- neuroleptics (ie. Haldol) = dopamine antagonists; anti-psychotic drugs blocking dopamine transmission via binding to dopamine receptors w/o opening ion channels
24
Q
COCAINE
A
- blocks noradrenaline/dopamine transporter; interferes w/re-uptake/effect boost
- methamphetamine (speed)/amphetamine derivates (ie. ‘ecstasy’) = reduce monoamine transport; attach to enzymes that break monoamines down; overall effect = neurotransmitter transmission boost
- ^ dopaminergic transmission = schizophrenia-esque symptoms in high doses
25
Q
PARKINSON’S X SCHIZOPHRENIA
A
- Parkinson’s/schizophrenia’s medication push dopamine in opposite direction; cause each other’s symptoms in high doses
26
Q
SUMMARY
A
- psychoactive substances act at dis synapse stages
- can affect pre-synaptic processes
1. axonal conduction (TTX)
2. release (botulinum/tetanospasmin) - OR post-synaptic:
1. receptor binding (nicotine)
2. transmitter break down (MAO inhibitors)
3. transmitter re-uptake (cocaine) - psychoactive substances bind to receptors; imitate molecular structure of some endogenous substances in order to fit receptor like a key to a lock
27
Q
NEW CONCEPTS
A
AGONIST VS ANTAGONIST
- substances that bind to receptors
- either imitate/enhance OR preclude transmitter action
COMPETITIVE VS NON-COMPETITIVE
- agonists/antagonists bind to same (competitive)/dif (non-competitive) ion channel/receptor sites as transmitter
