exam 2 Flashcards
neurotransmitter
chemical messenger in the brain
neurohormone
messengers through the blood
can also be neurotransmitters depending on location (ex: serotonin is hormone when found in stomach)
neuromodulator
moderate the effects of other neurotransmitters but do not do anything themselves
Acetylcholine (Ach) function
memory, arousal, regulates involuntary functions, muscle contraction
also involved in narcolepsy, ocd, depression
Acetylcholine (Ach) in CNS
alzheimer’s disease: there is a decrease in production of ach
rem sleep: ach levels are high during this
Acetylcholine (Ach) in PNS
in neural muscular junctions
Why do you die if Acetylcholine (Ach) is blocked from receptors in PNS?
leads to paralysis of muscles like the diaphragm —> suffocation
Acetylcholine (Ach) Recpetors
Muscarinic: Ach and specific mushrooms like these receptors
Slow = Metabotropic
Nicotinic: nicotine likes these receptors
fast = ionotropic
Nor epinephrine (NE) functions
NE is a precursor to Epi bc of similar chem structure
usually inhibitory (in quiet environment)
excitatory if startled
arousal and mood
may be more important than serotonin when treating depression
too much NE can lead to mania —> bipolar disoder
Nor epinephrine (NE) enzymes
COMT breaks down NE into O methylated metabolites
MAO breaks down monoamine NE into Deanimated metabolites
Nor epinephrine (NE) Receptors
all of its receptors are slow (metabotropic)
Alpha 1: post synaptic / excitatory
Alpha 2: autoreceptors
Beta 1: inhibitory
Beta 2: autoreceptors
Epinephrine function
aka adrenaline
released from adrenal glands —> sympathetic ns
regulates blood pressure
Dopamine (DA) function
pleasure, mood, arousal
DA is released when pleasure happens, it doesn’t cause it.
constant release of it classically conditions the body which leads to addiction
is a precursor to NE (DA –> NE –> Epi)
Dopamine (DA) Receptors
all are slow (metabotropic)
D1 and D5: couple to G protein and stimulate adenylyl cyclase
D2,3,4: couple to G protein and inhibit adenylyl cyclase
Dopamine (DA) Psychological Relations
working memory: type of short term memory
- holds and manipulates memory (say “silk” —> remove L —> say it again “sik”
reward reinforcement: released
schizophrenia, tourettes, hunington’s disease
Serotonin
mood, arousal, sleep, sex, depression, pain sensitivity
largest group of sub receptors
Amino Acids
amino acids that can act as nt
both are ionotropic but can act as metabotropic
Glutamate: primary excitatory
GABA: primary inhibitory (barbiturates, alc, gen. anesthesia)
Peptides
all peptides are slow (chain of 2-10 amino acids)
receptors are metabotropic
endorphins:
- oxytocin: causes uterus to contract, helps produce milk, orgasms
- vasopressin: makes you pee (like when you drink)
why do food comas happen?
availability of tryptophan (amino acid in food) increases when you eat. tryptophan increases production of serotonin which promotes relaxation and drowsiness
neurotransmitters and diet
you can not predict if what you are eating will fix things / affect neurotransmitters
why are essential amino acids important?
the body does not make them which is why a balanced meal is important
what are the 5 divisions of the brain and where are they?
telencephalon: cerebral cortex (cortical)
myelencephalon: brainstem
metencephalon: brainstem
mesencephalon: brainstem
diencephalon: brainstem
what are the two hemispheres?
left: logic and language
right: creativity (processes info like art and music) and emotion
what are the four lobes of the brain?
occipital: vision
parietal: sensory integration and attention
temporal: memory, hearing, and language
frontal: executive function, higher order processing
limbic system?
pleasure and sensation
basal ganglia?
voluntary movement
parts of diencephalon?
thalamus: sensory relay (center before going to cortex)
hypothalamus: controls pituitary
pituitary: hormone production
parts of mesencephalon?
MIDBRAIN which has..
superior colliculus: visual info & inferior colliculus: auditory (both make up the tectum)
periaqueductal gray: pain control center (manages endorphins), red nucleus, & substantia niagra which make up the tegmentum
parts of metencephalon?
pons: sensory relay center, implications for memory
cerebellum: sensory motor
parts of myencephalon?
medulla: homeostasis
reticular formation: attention, arousal, rem sleep
what is tolerance?
acute and cross tolerance?
tolerance: less sensitivity to drugs
acute: tolerance built up quickly (can happen within same admin)
cross: taking 1 drug can make you tolerant to another (alc & barbs)
tolerance and liver metabolism
more drugs = more p450 enzymes
- the enzymes dont have specific targets, will eliminate any and all drugs
neurotransmitter depletion and tolerance
autoreceptors (feedback loop) –> no more production of those n.t
- hangovers and withdrawal happen as body adjusts itself
down regulation
sucks up receptors limiting chances of action potential due to repeated exposure of n.t
desensitization
receptors die off/ are worn out due to over exposure and are less responsive, not creating action potentials
- G proteins will disconnect from primary messenger
up regulation
creating new receptors due to no action potentials happening bc recepetors are blocked
sensitization
less stimulation needed to create an action potential
neuropeptide synthesis
proteins that attack other drugs to get out of system
- body creates anti opioid peptides to get rid of opioids
habituation
general decrease in response without requiring a specific context to occur
context specific tolerance
reduced response is tied to the environment or context in which the stimulus is presented
new terms for positive & negative reinforcement
reinforcement contingency (pos)
escape contingency (neg)
new terms for negative and positve punishment
punishment contingency (pos)
penalty contingency (neg)
what is instrumental conditioning?
happens while you’re doing A TASK
- does not transcend to other tasks
- tolerance is related to difficulty of task
- cravings happen: body will try to maintain homeostasis when it sees trigger
- tolerance can transfer to similar drugs
drug dependence vs abuse
dependence: needed to be able to function
abuse: using at HIGH levels
drug psychological dependence primary
primary: anticipated pleasure not actual
- cravings
secondary psychological and physical dependence
secondary: continued use bc fear of withdrawal
physical: stop taking=withdrawal
physical dependence theory
people feel crappy so they take drugs
- does not explain relapse and why we go back
incentive sensitization theory
anticipated pleasure
- explains relapse, cocaine, purging and binging
what drugs are equally psychological and physically addictive
alcohol and barbiturates
what drugs are highly psychologically addictive and low physically
psycho stimulants
what drugs are low psychological and high physical addictive
caffeine
prescription drugs
what drugs are not considered addictive
lsd and shrooms
how to treat drug dependence
recognition of problem (usually rock bottom)
incentive to change
underlying causes
break cue dependent cravings
drug treatment
what does drug treatment do for drug dependence?
reduces cravings
blocks drug effects
long lasting
less toxic
why are drugs hard to classify?
small differences in chem structure causes different effects
different effects at different levels
why we take them (recreational vs medicinal)
how are drugs named?
code
chemical
generic
brand
street
neurotransmission and drugs
can impact different stages of neurotransmission and action potential
- epilepsy medication or SSRI (block re uptake of serotonin)
what are psycho stimulants
they increase neurological activity
- caffeine: most widely used (200-300mg avg)
- nicotine
- amphetamines: uppers like adderall
- cocaine
what are opioids
narcotics
made from poppy plant
opium (made from dried up internal juices)
- morphine
- heroin (semi synthetic morphine: turns back into morphine after it passes BBB)
codeine (made from latex paste)
- vicodin
- oxycodone
- hydrocodone
what are atypical/ second generation drugs?
they’re not supposed to cause bad side effects / they produce fewer side effects
sedative hypnotics & anxiolytics
alcohol
barbiturates
benzodiazepines
inhalants
anticonvulsants
alcohol
cns depressant
reduce excitability of neurons (works in gaba)
low does (chill) high dose (sleep)
slows down intake of sodium and potassium which makes it harder for action potentials to occur
why does alcohol act as stimulant toward beginning?
alc suppresses frontal lobe (exec function) but limbic system continues to fire which is why we do things we would not do sober
- lower inhibitions
what is bac?
blood alcohol content
legal limit: .08% which means for every 100ML of blood there is .08% alcohol in it
alcohol dehydrogenase
enzyme that breaks down alcohol into acetaldehyde
psychological effects of alcohol
increase social integration
poor judgement
violence / aggression
memory loss
no impulse control
physiological effects of alcohol
lowers body temp: causes pores to dilate, blood rushes to skin, body releases liquid & evaporates
heart rate increases
increases stomach acid: why you shouldn’t drink on empty stomach
dehydration: increases urination
breakdown of alcohol
alcohol
acetaldehyde (poison, makes you sick)
acetic acid
carbon monoxide
water
alcohol receptors
gaba : increases activity
nmda: activity reduced (glutamate)
effects of alcohol (liver)
liver metabolism: reduces way in which liver processes glucose and production of certain fats
- fatty liver: accumulation of fat
alcohol hepatitis: inflammation of liver (stage 1 of liver disease)
- jaundice
- fluid in abdomen
- fatigue
cirrhosis is building up of scar tissue from burst cells in liver
cognitive effects of alcohol
visual spatial skills
brain shrinkage (hippocampus specifically, but overall)
wernicke’s (short term / confusion) korsakoff (long term memory loss) syndrome
benefits of alcohol
increases TPA production: decreases blood clots and increases HDL (good cholesterol)
reduces susceptibility of getting sick
stress reduction
mood enhancer
disease model vs compulsive drug use disorder
disease model: cont control use, have to get sober by yourself, all or nothing
compulsive: flexible theory in terms of treatment
type 1 vs 2 alcoholism
1: binge/purge
more female
no thrill
guilt
2: starts earlier
just drinking, no binge
thrill seek
no guilt
violent
criminal activity
more genetic than 1
stages of alc withdrawal
1: 5-6 hrs
tremors
nausea
sweating
2: 15-30 hrs
seizures and convulsion risk
3: 48 hours
DT
bizarre delusions
hypothermia
tachycardia
potentially death
johnson intervention vs motivational interviewing
J.I: typical intervention
does not work
attacks people and makes denial worse
M.I: therapist mindset
have to know where people are in addiction mindset to properly treat them
alcoholism treatments
coercion (interventions)
physical dependence: anticonvulsants
naltrexone: most effective chem treatment to control cravings
cue exposure therapy
antabuse is used but does not work: it is poison makes u sick
fetal alcohol syndrome
first trimester most sig. risk
severe intellectual disability / low iq
smaller than avg brains (basil g)
heart issues
smooth cleft
extra eye fold
poor muscle coordination
bad behavior no guilt
impulsive
barbiturates
alcohol in pill form
used for sedation in surgery
inhibitory effects: gaba and k (potassium)
shortens rem sleep bc it increases deep sleep (delta) and shortens high level sleep (alpha waves)
anxiolytics
treat anxiety
phobia
panic disorder
generalized anxiety disorder
ptsd
ocd
benzodiazepines
indirect agonist for gaba receptors
not addictive, but tolerance built up fast
muscle relaxers
aggression reducer
anticonvulsant
high physical dependence
risk of seizures (during withdrawal)
long term side effects: headaches, violence, nausea
buspirone
anticonvulsant but not a benzo
used as add on bc too many side effects in high dosages
emotional symptoms
atypical anxiolytic: does not affect motor control, make you sleep
serotonin agonist
