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Biological Psychology > Psychopharmacology > Flashcards

Psychopharmacology Flashcards

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1
Q

DRUGS X THE SYNAPSE

A
  • various substances (naturally occurring toxins/psychoactive chemicals) alter synaptic transmission
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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
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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
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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
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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
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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)
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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
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8
Q

NEUROTRANSMITTER PATHWAYS

A
  1. excitatory synapses = glutamate (+ others)
  2. inhibitory synapses = GABA (+ others)
  3. mainly excitatory BUT also inhibitory synapses -> acetylcholine/dopamine (+ others)
    - monoamines = single amino neurotransmitters (ie. adrenaline; noradrenaline; serotonin; dopamine; histamine; melatonin)
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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
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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
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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
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12
Q

SUBSTANCES X RECEPTOR INTERACTIONS

A
  • certain substances just bind to receptors (blocking neurotransmitter’s path) w/o opening channel
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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
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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
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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
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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

Biological Psychology (21 decks)

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