Lec 3 & 4 - Hallucinogens, stimulants and sedatives Flashcards
(31 cards)
5 classes of Neurotransmitters
- acetylcholine
- amino acid (glutamate, GABA, glycine)
- monoamines (indolamines, catecholamines)
- purines (adenosines)
- peptides (opiod)
acetylcholine
- found in (3)
- used for
- receptors
Found in:
- brain, motor neuron,
- Autonomic NS
- parasympathetic: ganglion
- sympathetic: both ganglionic and termina
Used for: Alzheimer and dementia
Receptors:
- ionotropic: nicotinic R
- metabotropic: muscarinic R
Fly agaric: uses
compound? what does it do? Which receptor? Risk?
What’s main compound?
uses: entheogenic, expectorant, hallucinogen
muscarine found in traces
- mimics ACh action, non-selective agonist of muscarinic ACh R
- profound activation of parasympathetic NS
- NOT DEGRADED by acetylcholinesterase
Main compound: muscimol
ionotropic receptor
ion-gated channel, simple (ex: nicotinic)
metabotropic receptor
more complex, with G-protein (ex: muscarinic)
muscimol
recepto?
symptoms?
muscimol + predrug IBOTENIC ACID (not metabolized version)
- selective GABA receptor agonist
- responsable for drunkenness, sedative, hallucinogen activity
ibotenic acid
Receptor?
Symptoms?
- muscimol pre-drug, agonist of NMDA metabotropic glutamate receptors
- nausea, cramps, vomiting when eat AManita
glutamate
- found in
- used for
- receptors
- found in CNS everywhere
- used to treat sclerosis (ALS): excites motor, sensory and cognitive neurons
- receptors: (excitory)
- ionotropic: NMDA receptor (ibotenic acid)
- metabotropic: group I, II, III
role of NMDA receptors?
extrasynaptic, synaptic?
–> excitotoxicity
NMDA receptors play crucial role in health and function of neurons
- extrasynaptic NMDA receptos responsible for excitotoxicity and cell death
- synaptic NMDA R contribute to health and logevity of cells
risks links with excitotoxicity: stroke, traumatic brain injury, alzheimer…
Gamma- -aminobutyric Acid (GABA)
found in
- used for
- receptors
(subunits? two types? React to what?)
PAM
- everywhere in CNS used for: - anxiety, rehab - inhibit sensory and cognitive neurons - sedation, muscular/CV relaxation, inhibits pain, reflexes Receptors: (inhibitory) 5 subunits many binding sites for drugs
- ionotropic: GABAa receptor
Chlorine, responsible for sedative effects of GABAa agonists- Metabotropic: GABAb receptors
PAM
PAM: increase proba that agonist will bind (Gaba to GABAa)
GABAa:
Barbituates and benzodiazepines (PAM)
sedative, hypnotic, antxiolytic, muscle relaxant
Glycine
found in
- used for
- receptors
- found in spinal cord: inhibit spinal cord interneurons
- used to treat plasticity
- receptors: ionotropic: Cl- channels
Monoamines (2 types)
enzyme degrading?
- indolamine: serotonin (from tryptophan)
- catecholamines: dopamine, norepinephrine, epinephrine (from tyr)
both degraded by same enzyme: monoamine oxidase
Ayahuasca (2 main components
1st one does 2 things
2nd one: properties, how to take it, receptors?
Harmine:
- MAOI inhibits breakdown of monoamine transmitters (5Ht, DO) + hormones (melatonin, EP, NOR)
- -> more 5HT and DO: anti-depressant
- diabetes: induces proliferation of a-b cells in pancreas (glucagon et insulin)
DMT (dimethyltryptamine)
- hallucinogenic properties
- cannot be eaten bc monoamine oxidase in stomach –> sniffing it
- agonist of 5HT receptors
- DMT can accumulate in crebreal cortex, amygdala,
serotonin
type of monoamine?
found where? (2)
produced by what?
used for
receptors
indolamine
found in
- brain: limbic fct (emotions, mood)
- guts to help with bowel mvts (produced by enterochromaffin cells lining digestive tract) –> brain gut axis! link between depression and gut health (more nerves in gut than spinal cords)
used for depression and sleep (converted to melatonin)
Receptors:
- ionotropic: 5HT 3: excitatory
- matebotropic: 5HT 1-7 excitatory, inhibitory
serotonin receptors
–> neurotransmitters that can influence:
- GABA: leads to inhibition
- Glutamine: excitatory
serotonin levels
low (5)
high (3)
normal (2)
low:
- depression,
- anxiety,
- increased pain sensitivity
- bad sleep
- fatigue
high
- medical emergency
- possibl edeath
- caused by SRIs, OTC supplements (Sero reuptake inhib)
normal:
- happiness
- relaxation
serotonin agonists
DMT, LSD, ergotamine
dopamine
type of monoamine?
where?
used for?
receptors?
catecholamine
found in brain and brainstem
- substantia nigra: reward, addiction
- hypothalamus: inhibits prolactin release
used for: schizophrenia, psychosis, parkinson’s disease
receptors:
- ionotropic: none
- metabotropic: D1 and D2
dopaminic pathways
dopamine = nT used by - reward pathways (mesolimbic and mesocortical one) o memory o motivation and emotions o reward and desire o addiction
- tuberoinfundibular
o hormonal regulation
o maternal behaviour
o pregnancy - nigrostriatial pathways
o motor control
o death of neurons in here: Parkinson
dopamine levels:
low, high for each pathway?
nigrostriatal (mvt)
- low: parkinson, EPS
- high: chorea, TICS, athetosis
mesocorticolimbic (mood, reward)
- anhedonia
- high: psychosis, euphoria, hallucination
tuberoinfundubular
- low: hyperlactinemia
- high: inhibit prolactin
coca and cocaine
what does it do?
how?
- stimulant
- cocaine: mix leaves with solvent, mash it
o loss of contact with reality
o euphoria
o increase dopamine: risk of addiction - blocks reuptake of monoamine nT so DO concentration increases
- leads to increased available synaptic transmitters
- chronic use leads to decreased availability of D2 receptors
norepinephrine
type of monoamine?
where?
used for?
receptors?
catecholamine
found in brain
- locus ceruleus: cortex, arousal, attention
- ANS: sympathetic neurons (effector organs, postganglions neurons)
used for: ADHD, anxiety, cardiac failure
receptors:
- ionotropic: none
- metabotropic: alpha 1 et beta 1 (excitatory), A2 et B2 (inhbitory)
ephedra
effects?
mechanism?
Stimulant:
ephedrine alkaloids cause: - CNS stimulation - cardiac stimulation - tachycardia - elevated blood pressure can also have sleep problems, anxiety, headaches.. banned in US
mechanism: like amphets
- enters presynaptic neuron through NET (norepinephrine transporter)
- enters vesicule through vesicular monoamine transporter (VMAT)
- released into cytoplasm and synaptic cleft with NET
