Final Flashcards
Fast pain fibers
Adelta
Slow pain fibers
C fibers
why does rubbing an injured site reduce pain? What is this called?
Gate control theory. C fiber inhibits inhibitory interneuron, causing projection neuron to tell brain that youre in pain. If you rub pain site, c fibers will still be activated but a beta fibers will also be activated, stimulating inhibitory interneuron causing it to inhibit projection neuron. ppt 10 slide 11
endogenous opioid that inhibits substance P (Pain) release. what type of inhibition?
enkephalin through presynaptic inhibition. opiate receptors are on presynaptic terminals of primary afferent axons with SP. probably how morphine works
what neurotransmitters coming from descending brain pain pathway seem to control enkephalin to inhibit release of substance P
5HT and NE
ppt 10 slide 20
yes
first peptides discovered linked to endogenous analgesia? what is the other major opioid peptide product?
Met-enkephalin and Leu-enkephalin were first to be discovered endogenous opioid peptides, another one is Beta endorphin
cell bodies for beta-endorphine, enkephalin, and dynorpin and their receptors are highly concentrated in what brain region? associated with experience of pain
LIMBIC SYSTEM
opioid analgesics exert their effects through (agonist or antagonist) actions on families of receptors
agonist- similar structure to endogenous opiates
hallmark sign of opiate use
pinpoint pupils- MIOSIS
major opioid antagonist
naloxone
what opioid receptor type do morphine and fentanyl act HARD on? Why do we try to shy away from these guys because of it, beginning the development of drugs that bind to other opioid receptor types
morphine and fentanyl fuck with mu receptors hard. mu receptor is implicated with respiratory depression symptoms and the development of physical dependence. We are developing mixed opioids to avoid the mu receptor activation and focus on kappa and delta activation
major opioid antagonists- which has longer half life (is more involved in opioid-dependence maintenance)programs)
naloxone (fast action antagonist) and naltrexone (LONGER half life. blocks effect of injected heroin for up to 48 hours
three main NON-SELECTIVE COX inhibitors (a branch of NSAIDs)
main selective COX-2 inhibitor (Branch of NSAIDs)
aspirin, ibuprofen, indomethacin
Celecoxib (Celebrex)
t or f acetaminophen is not an NSAID
t, it has relatively little anti-inflammatory activity
why should COX-2 inhibitors be used with caution
COX is made endogenously, a bunch of COX-2 selective inhibitors would cause CV events
two cholinergic hallucinogens. which is agonist which is antagonist
muscarine- agonist at muscarinic receptors
scopolamine- antagonist
four catecholamine (NE) like hallucinogens that he wanted us to memorize
Mescaline- peyote,
MDA/MDMA- synthetic, mix of catecholamine and 5-HT effects,
Myristin and Elemicin (in nutmeg and mace)
t or f- MDMA works by building up serotonin nerve terminals
F- MDMA DESTROYS serotonin nerve terminals
most important indolamine in our body and its most important receptor
serotonin,
5-HT 1A
can increase amount of 5-HT in somebody’s body by putting them on what kind of diet
high tryptophan diet
important 5-HT1A receptor agonist, reduces 5-HT release
8-OH-DPAT
5-HT antagonist
methysergide
5-HT storage inhibitor used as a tranquilizer
reserpine
5-HT pump inhibitors used as an antidepressant
chlorimipramine
5-HT synthesis inhibitor, antisleep, mild aphrodisiac
p-Chlorphenylalanine (PCPA)
5-HT MAOI, antidepressant
iproniazid
5-HT toxin
5,6-Dihydroxytryptamine (5,6DHT)
what nt does this drug act like- psilocybin and psilocin, LAA, DMT
5-HT
what nucleus does LSD potentially work on, how
raphe nuclei, it inhibits it. raphe nuclei releases its own 5ht, and has 5ht1a receptors. It inhibits itself with too much 5ht so LSD acts as 5ht to inhibit it
Dissociative anaesthetics (2). what kind of trips do they give you bitch
PCP- Phencyclidine (Sernyl)
bad trips
Ketamine
less bad trips
where is the PCP binding site? what receptor? does it make it an antagonist or an agonist or what
located inside NMDA cation channel, below magnesium binding site, making it an antagonist
PCP like drugs stimulate firing of what neurons
VTA dopaminergic neurons
THC receptors CB1 and CB2 are GPCRs or ionotropic, what part of neuron are they located, how do they mostly act
GPCRS, CB 1 are located on terminals and axons, act to inhibit release of NT, CB2 are on surface of WBCs
Ring structures that interact with a receptor and mimic the action of an endogenous ligand on CB receptors
cannabinoids
most effective brain structure to yield self stimulation in rats? What is the main nt type in this area
Medial forebrain bundle MFB. catecholamines. rewarding stimulation causes release of NE into amygdala and hypothalamus (ascending pathway- caudal-rostral). Its stimulation causes dopaminergic neurotrans to be stimulated in the ventral tegmental area to release dopamine in the nucleus accumbens
3 long length dopaminergic systems
nigrostriatal mesolimbic mesocortical
stimulation of MFB leads to increased stimulation of _____ which causes increased release of DA nts into ______
VTA, nucleus accumbens
Drugs of abuse either act to activate system through cell bodies in VTA or to act directly on receptors in nucleus accumbens for reinforcement
Dopamine acting on the nucleus accumbens does what for GABA’s action on globus pallidus
DA inhibits neurons in the nucleus accumbens, producing locomotion by inhibiting the release of GABA onto globus pallidus
slides 50-56 ppt 12
yes
what would you do in order to avoid death from delirium tremens in alcohol withdrawal if you were trying to wean somebodyoff
substitute alcohol with pentobarbital. mild intoxication maintained for 1 to 1.5 days and then you can start withdrawal. immediate withdrawal of a neurodepressant can lead to death
most consistent pharmacotherapy to treat amphetamine and cocaine dependence
tricyclic antidepressants (desipramine)
there is a relationship between behavioral performance and level of arousal. Highly or lowly aroused you perform worse than if you were moderately aroused. what law is this
Yerkes-Dodson Law
three components of emotion
(1) overt behavior, (2) physiological changes (autonomic, endocrine, cardiovascular, respiratory, GI, immune), and (3) subjective (personal) cognitive feelings.
Long-term exposure to one stressor or the exposure to a new stressor in the presence of an existing stressor produced exhaustion of resources in dealing with stressors and leads to morbidity/death. what is this called
General adaptation syndrome GAS
stress: repeated activation of _______ predisposes one toward developing chronic hypertension
defense response
slide 39-42 ppt 13
yes
_____ is synthesized in the hypothalamus and secreted to control ACTH release from anterior pituitary, causing glucocorticoid release from adrenal cortex.
In addition, it is also present in brain pathways and activates nuclei with the CNS as a neurotransmitter.
corticotropin releasing factor CRF. enhances startle response by interacting with amygdala
plasma cortisol concentrations in depressed patients higher or lower than controls on average
higher. cortisol peaks in the morning, dips while you sleep. remains pretty high for people who are depressed though
what can be administered to lower plasma cortisol concentrations? does it work in people with depression?
Dexamethasone (DEX) lowers plasma cortisol. can work with people with depression for a little bit but only for a little bit then the levels skyrocket again
does REM sleep start early or late for depressed patient? how about sleep latency (time before they actually fall asleep)? how about deep sleep levels
REM starts super early
sleep begins super early. Reduced REM latency and reduced sleep latency. no sleep levels 3 & 4
how does sleep deprivation affect some depressed patients the next day
their mood increases crazy
when is best time to do light box therapy with people who have SAD
morning
what does the monoamine theory say about neurotransmitters and depression. Is this theory correct? how about the popularity of the treatment used?
functionally deficient monoaminergic (NE and 5-HT) transmission in the CNS causes depression.
Theory has no pharmalogical evidence, however monoamine transmission manipulations are still the most successful treatment approaches
what drug can you use to cause depression
reserpine. inhibits NE and 5-HT storage.
how do tricyclic antidepressants work. what theory of depression do they belong tow
block reuptake of NE and 5-HT. a part of the monoamine approach
what is alpha methyltyrosine used for. what theory of depression does it belong to
calming of manic patients by inhibiting synthesis of norepinephrine
how does ECT increase mood? what nts are involved
increases CNS response to NE and 5-HT
What does methyldopa do
inhibits NE synthesis, decreases mood
slide 27 ppt 14
yes
does depression increase or decrease your heart rate? how does it affect your heart rate variability
increases heart rate, decreases heart rate variability
Irreversible MAOI inhibitor? Reversible MAOI inhibitor? if you were prescribing it to test out on a new patient, which one would you use and why
Irreversible- Tranlcypromine
Reversible- Moclobemide
you would give them moclobemide because you want to use a reversible inhibitor so you don’t have to wait for new MAO’s to be made in case the medication doesnt work
what do MAOI’s do
inhibit monoamine oxidase which is an enzyme that regulates the amount of NE and 5-HT in the presynaptic terminal. Inhibiting MAO increases the amount of NE and 5-HT in the presynaptic terminal
what kind of people aren’t able to be prescribed tricyclic antidepressants (TCA)
people with heart issues
how do Tricyclic antidepressants work (TCA)
inhibit neuronal reuptake in NE, 5-HT and DA neurons
what is an effective treatment drug for bipolar disorder
Lithium
how does lithium work to treat bipolar disorder
increases time between manic episodes, depressive episodes. has a calming effect during manic episodes. proposed to inhibit release of NE
postmortem studies of schizophrenia show lower neuron count, larger ventricles, and also an absence of ______
gliosis- normally when we lose brain mass, gliosis is a typical response (proliferation of glial cells)
schizophrenics show what kind of activity in the frontal cortex
hypofrontality
schizophrenics show a disorganized (what brain region)
hippocampus
current theory of schizophrenia with neurons and shit
schizophrenia is thought to be produced by excessive activity at D2 receptors. Therapeutic dose for neuroleptics correlates with their affinity for the D2 receptor
D1-like receptors are (excitatory or inhibitory) D2-like receptors are (excitatory or inhibitory)
D1- excitatory
D2- inhibitory
what tract inhibits secretion of prolactin? how?
Tuberohypophyseal tract inhibits secretion of prolactin- it is an intermediate length DA tract
schizophrenia may develop as an insult to the fetus occurs during the ____ trimester
second
slide 21 ppt 15 very important
yes
first drug used to treat schizophrenia in 1950s hint it was a tranquilizer
chlorpromazine
how do neuroleptics produce an antipsychotic action
decrease DA activity by blocking DA receptors
also increase prolactin release (side note)
are neuroleptics hydro or lipophilic
highly lipophilic
what type of drug causes tardive dyskinesia,what do we do to avoid it
neuroleptic, use atypical antipsychotics like CLOZAPINE
what toxin can be used to model parkinsons in primates after some dumb kids took it cuz they thought it was acid
Toxin = N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can be used to model parkinsons in primates boy
physiology of parkinsons NTs
reduction in inhibitory DA neurons in basal ganglia
slide 38-41 ppt 15
yes
what drugs do we use for parkinsons treatment
L-DOPA because it crosses blood brain barrier and is a precursor to DA which does not cross BBB. We can supplement that with carbidopa which doesnt cross BBB- it is an antagonist of the enzyme that converts L-DOPA to DA so that way DA isn’t made before crossing BBB
Knowing thyself: what is this effect called- people remember words from a list well that they previously thought described themselves
self-reference effect
parts of brain that are more active when you are resting- what is this called and where are they at
(this also includes an area that changes signal when thinking about the self)
default network- medial pfc, inferior parietal lobule.
vACC changes signal when we are thinking about ourselves
what part of brain is active when we are making positive judgments about OURSELVES
vACC ventral anterior cingulate cortex- part of default network. When we are making highly self relevant positive judgments, there is little signal change. When we are making highly self relevant negative judgments, there is a large decrease in signal- default network is deactivated
what part of brain is active while you are taking the point of view of others
right temporoparietal junction
brain area important for interpreting eye gaze- active when we are thinking about the intentions behind someone’s eye movements
superior temporal sulcus
brain area related to interpretation of the eye gaze of others and how it is affected in autism
superior temporal sulcus is smaller in autism
While a person is acting, they may have no insight into their behavior at the time of action, but can look back on it later and be like yeah what the fuck that was stupid- this is indicative of damage where
orbitofrontal cortex
when a person is bad at judging behavior of others in negative social scenarios, this is indicative of damage where
frontotemporal lobe
