Hallucinogens: PCP and Ketamine 15th Flashcards
in what sense are dissociative a Hal
it decouples perceptual from sensory; can’t make sense of sensory signals
how are dissociative stimulants
induce euphoria and numbing= can turn into panic= stimulant
what causes the amnesia in dissociative
if brain can’t make sense of sensory signals it won’t encode it
T: muscle flaccidity
catalepsy
what schedule is ketamine
1
ketamine is being used in … research
schizophrenia due to glutamate connection
T: a synthetic analog of a legally restricted or prohibited drug, devised to circumvent drug laws. (dissociates fall under this)
designer drugs
what is the full name for dissociative
dissociative anesthetic hallucinogen
what 3 drug classes do dissociates fall under
depressants, stimulants and hallucinogens
2 things that make them depressant
sedative, pain
dissociative separate … from …
perception from sensation
3 general effects of dissociative
amnesia, analgesic, catalepsy
what were dissociates destined for
surgery (didn’t know side effects)
what schedule are these drugs in US?
2 for vet use
PCP and ketamine are the same kind of dissociative Hal but have Dif effect
f opposite
what was the similar effect of PCP and ketamine
anesthesia
street name for ketamine
special K, vitamin K (very dangerous have other meanings) bump, green, super acid
how is ketamine in took 4
insufflation, inhalation, injection (medical), oral (assault)
how long does onset take for ingestion vs insufflation, inhalation, injection
ingestion: 2 hour
others 10-60 min
full name for PCP
phencyclidine
why is PCP less common
pricer
street names for PCP
Angel Dust, ozone, rocket fuel
what is the ironic thing about the street names of PCP
refer to methods of preparation
2 intake methods for PCP how long for onset for each 2
insufflation (1min) or inhalation (5 min)
how long does PCP last
30 min onset to 18 hours
T: a yellowish “oil” solution that cigarettes or joints are dipped in PCP
embalming fluid
T: PCP mixed with Marijuana
killer joints (sherms)= rocket fuel best
T: PCP crystals ground and sprinkled on oregano, parsley, alfalfa and smoked
angel dust (the oregano doesn’t do anything)
why does dosage influence the MOA on the dissociatives
binding affinity of chemical at Dif doses
what NT disrupted in low doses
seretonin and dopamine
any permissive hypothesis with dissociative
no because it has to do with binding affinity
what do dissociatives do to dopamine of seretonin
repuptake inhibitor
what does it do as a reuptake inhibitor
disengages the mechanism (messing with metatropic function not just blocking= LT effects)
low doses act as a partial agonist for …2
5-HT2A, D2 receptors (reward potential and Hal components)
high doses influence what NT
Ach
what do high doses do to ach
antagonist
what are the act receptors called 2
muscurininc and nicotinic
… NT is responsible for memory
ACH
what does antag of nicotinic receptors do
muscle contractions
what does antag of muscarinic receptors do 3
memory deficits, analgesia and arousal
what is an NT effected at both low and high doses
NMDA (glutamate) receptor
what does it do at NMDA
antagonize
T: lasting strengthening of synaptic connections due to repeated firing
LT potentiation
what happens to LT potentiation on dissociative
disrupts it with stopper signal due to lack of NMDA = fire apart wire apart= decouple
what is the behaviour effect of LT potentiation disruption
results in disordered learning from not being able to remember
the Moa depends on dose but do the effects?
yes Dose dependant effects
how much is a low dose
under 5 mg
effects of low dose of PCP and ketamine ? 2
drunk-like state, numbness in extremities
at what dose does it work like an anesthetic
low
what is a moderate dose
5-10 mg
effects at moderate dose
disconnectedness from environment, dissociativeness from body/body distortion (feels like being low in iron)
high dose effects?
sympathomimetic, hallucinations (distortions)
is it true sympathy mimetic?
no its panic in response to reaction to what’s happening to your body
for people who use high doses what are the lingering effects
up to 2 moths of Lingering schizophrenic-like symptoms
T: looking at something and can only see one part of picture e.g persons eye
microscopia
what is macroscopia
can’t focus on anything see everything (attention)
delusions, paranoia, disordered thinking, catalepsies and catatonia, sparse/garbled speech, micro/macroscopia occur from high doses of PCP or ketamine what do these resemble
schizophrenia
what does this tell us about schiz
support glutamate hypothesis (instead of dopamine)
Ketamine: “…” perceive experience simulating near-death (heading toward light) or only being able to see apart of setting
keyhole
what dose causes depressant effects
moderate
Analgesia means less exertion
f allows for excessive exertion
problem with Analgesia allows for excessive exertion
injury to self
what does it feel like to be on ketamine or PCP: why?
“Superhuman” strength and “invulnerability” because not feeling pain= not getting feedback from body
T: Delusional fantasies of omnipotence, power, perception
and the belief in a “god-like” status effect of ketamine
megalomania
how does ketamine change fear of death
pathological decreased fear of death
illogical fear of death with megalomania in ketamine or PCP
no for PCP (say god but won’t follow through e.g. flying)
ketamine will follow through
what happens to megalomania LT
perception stays LT from chronic prolonged use
PCP and ketamine results in depressive symptoms
depressive- like symptoms (drug induced Dif course)
is the depression caused long term?
morphs into schizo like psychosis
what causes the depressive symptoms from PCP and ketamine
Chronic antagonism of glutamate receptors leads to deficits in memory, speech, logic
is there tolerance with PCP and ketamine?
accrued tolerance
what does LT depression mean
neurons not connected dendrites pulling back= strictly physiological not emotional
what is accrued tolerance
increasing amounts over time as you keep taking more
why do they separate animal surgeries using dissociates
to avoid accrued tolerance= Separation of administration by days prevents tolerance
how does tolerance influence drug behaviour for users
Prolonged regular intake requires higher doses to achieve effect
is there tolerance to psychedelic effects?
Chronic ketamine injection results in permanent tolerance to psychedelic effects (NMDA receptors so down regulated)
is there physical dependance with dissociatives
only for PCP
does PCP cause brain damage
hard to say because its associated with a lifestyle
what causes the dependance in PCP
effects on dopaminergic centers
is the withdrawl of PCP the result of brain damage
maybe
is there psychological dpeednace in dissociatives
yes
what psycholigcal depednace symptoms
cravings have been observed, related to euphoria
how has ketamine been used therepudically
to treat depression
T: ketamine used to treat depression
ketamine psychedelic therapy
there is a close relationship between glutamate and … in brain
glucocorticoids (glutamate activating cortisol in brain= too much surpasses seretonin)
what is the logic behind using ketamine for treating depression
target antagonize glutamate receptors on glucocorticoid receptors
target antagonize glutamate receptors on glucocorticoid receptors did studies find this to be true with MDD?
one dose of Ketmaine resulted in alleviation of depressive symptoms within hours
how long did the effects of ketamine on dep last
lasted a week
what happened to suicidal ideation after ketamine
Suicidal ideation diminished in 40 min (better than antidepressants in this way)
T: Inhibition of glutamate at NMDA allows for glutamate to bind elsewhere, and facilitate BDNF
glucocorticoid theory
what happens if brain is saturated in cortisol
LT fight flight changes = anxiety
what does cortisol do to seretonin system
antagonists it
what does cortisol do to seretonin system
antagonists it
MDD has higher levels of glucocorticoids
t
free floating cortisol will cause worse MDD
f no whee to sit in NMDA remove self from glucocorticoid= seretonin back into play on receptors
ketamine provides support for what theory of depression brain chemistry
Glucocoritcoid theory not BDNF
