psychopharmacology Flashcards
(21 cards)
Psychopharmology=
study of effect of drugs on nervous system
Drug=
substance produced OUTSIDE the body, that in relatively small doses alters the functions of cells within the body
Drug in CNS=
Drugs affect communication between neurons, usually by interfering with chemical transmission across synapses
Agonist vs antagonist drugs
Agonist= INCREASES post-synaptic effect of the NT
Antagonist= DECREASES the post-synaptic effect of the NT
4 main ways drugs can affect transmission across a synapse»
- Direct effect= direct agonist
- Direct effect= direct ANTAgonist (both competitive binding)
- Indirect effect= indirect agonist
- Indirect effect= indirect ANTagonist (both non-competitive binding)
Agonistic drug effects (6)
- drug increases synthesis of NT molecules
- drug increases no of NT molecules by destroying degrading enzymes
- drug increases release of NT molecules from terminal buttons
- drug binds to autoreceptors & blocks their inhibitory effect on NT release
- drugs bind to Post-S receptors & either activate them or increase effect on them by NT molecules
- drugs block deactivation of NT molecules by blocking degradation or reuptake
Glutamate & alcohol> (why does alcohol cause memory blanks)» (4)
- Alcohol in INDIRECT ANTAGONIST of NMDA glutamate receptor
- reduces affinity of g for receptor
- receptor involved in memory
- why alcohol causes ‘‘memory blanks’
Neurotransmitter systems (2)
- glutamate (excitatory) & GABA (inhibitory) are main NT used for specific communication between neurons in the brain
GABA & valium> How is anxiety reduced
- GABA is inhibitory NT
- benzodiazepines (e.g. valium) are INDIRECT AGONISTS for GABA
- increasing affinity of GABA for GABA Cl- channel
- more inibition of neural messaging
- benzodiazepines reduce anxiety but in high does can cause coma & death due to too much neural inhibition)
Dopamine & L-DOPA for parkinson relief» (3)
- dopamine involved in motor function
- loss of dopamine-releasing-neurons from substantia nigra> basal ganglia causes parkinsons (tremors & movement difficulty)
- L-DOPA is precursor to dopamine so increases dopamine levels in remaining neurons, relieving symptons
Dopamine & cocaine»
- dopamine is NT used in “reward” pathway
- cocaine is dopamine re-uptake blocker
- this means there is an accumulation of dopamine in synapses of reward pathway
- this leads to overstimulation & feelings of euphoria
smart drugs (narcolepsy & modafinil)
- modafinil can help brain performance (increase creativity & retention)
- elevates histamine levels in hypothalamus (antihistamines inhibit production of histamine & cause drowsiness)
- by increasing histamine production, modafinil can keep you more awake
- alternatively, mf may affect brain by increasing dopamine like cocaine
Histamines & brain» (2)
- All neurones synthesising histamine are present in tuberomammaliary nucleus (part of hypothalamus)
- these neurons supply with nerves the: cortex, pituitary & thalamic nuclei, the amygdala, hippocampus, spinal cord & cerebellum
concept of addition (4)
- leads to tolerance, in which larger & larger doses are required to produce same effect
- if users tops taking drug, the compensatory mechanisms will dominate & user will suffer from withdrawl
- main factor that causes users to continue taking drug is NOT desire to avoid withdrawal but desire for ‘high’
- addictive drugs reinforce drug taking behaviour
what are the 3 ways long term meth use can damage the brain?
- cause acute NT changes
- rewiring brains reward system
- causing brain cell death
Can you recover from meth addiction>
Yes & no:
- abstience: increase in dopmaine transporters
- but neurological tests didnt FULLY improve]
-increase not sufficent for completel function recovery
- due to heavy meth causing cell death
- recovery from cell death is not always possible
psychiatric symptoms seens in later stage addiction>
- dementia
- psychosis
- schizophrenia
what does recovery from addicition (in terms of brain function) depend on? (3)
-HOW LONG you used the drug
-how regularly used
-how much used
Recovery from addiction- improvements after 6-12 months»
- restoration of NT activity in parts of the brain regulating personality
- normalisation of brain receptors & transporters
- improvement in depression & anxiety
- stabilisation of mood swings
- improvement in focus & attention
- fewer nightmares
- reduction in jitteriness & emotional rages
what is the one thing that may not readily improve after years of abstinence>
drug cravings
Antagonistic drug effects>
- Drug blocks the synthesis of NT molecules (by destroying synthesising enzymes)
- Drug causes the NT molecules to leak from the vesicles & be destroyed by degrading enzymes
- Drug blocks the release of NT molecules from terminal buttons
- Drug activates autoreceptors & inhibits NT release
- Drug is a receptor blocker (binds to Post-SR & blocks effect of NT)
