Neurotransmitters Flashcards
agonist
increases function of Neurotransmitter system
antagonist
decreases function of neurotransmitter system
ionotropic receptors
receptors that are coupled to ion channels and affect the neuron by causing those channels to open
metabotropic receptors
receptors that are associated w/ signal proteins and G proteins
glutamate
- primary exciter NT
- cuz receptors cause EPSPs
- bring Na in
- depends on receptors not NTs
-metabotropic and ionotropic receptors
glutamate antagonists
-decreasing excitation, dampening brain
- sedation, dampen NS
- agonists cause anxiety, seizures
examples of glutamate antagonists
- barbituates
- nitrous oxide (laughing gas)
- ketamine
-ethanol (booze) - hangover = overactivation of glutamate
(all involved sedation and relaxation)
GABA
-primary inhibitory NT
- ionotropic and metabotropic
- ultimate inhibitroy effect
GABA agonist examples
-benzos
- ethanol
-G antagonist too, fatal in excess
- chloroform
-ether
gaba agonists
increasing inhibition in brain
- sedation, relaxation, relief from anxiety
types of amines
-dopamine
-epinephrine
-norepinephrine
-histamine
-serotonin
amines
- all metabotropic
- modulatory role
- bigger than amino acid, smaller than protein
- many receptors
dopamine
classic assctn of pleasure
- projects from ventral tegmental area tonucleus accumbens
dopamine drugs
- all addictive drugs directly or indirectly increase dopamine transmission
dopamine in parkinson’s
- loss of substantia nigra in tegmentum
- 1/2 major DA producing region
- loss of voluntary movement, facial expressions
-loss of D, loss of movement - not necesarily loss of pleasure
L-DOPA as parkinson’s treatment
- L DOPA already in brain
- extra pill is converted into DA in brain via enzymes
- replacement therapy
- restoration in movement
dopamine antagonists
- schizo medication all dopamine antagonists
- ppl w/ S have higher baseline pleasure? = hyperactive DA systems –> not increase in pleasure, increase in loss of touch w/ reality (hallucinations)
- decrease motivation, but not pleasure
- can be systematic or directly injected into VTA or Nacc
- decreasing DA motivation to seek larger rewards - salamone 90s
norepinephrine
originates in brain stem - locus coeruleus
- gun shot heard, makes you more alert
- causes heterosynaptic facilitations
- via heteroreceptors
- causes bigger EPSPs
- sensitizes system, more awake
- enhancement of memory by stress/emotion
- PTSD
- overactivation of memory
- little req’d to recall event
propranolol
- norep receptor antagonist
- feel calm during stressful situation
- take advantage of during reconsolidation - PTSD
- intensity of recollectoin decreased, next recollection is less painful
- neuromodulator - metabotropic receptors
serotonin
-primarily from raphy nucelli
- brain stem
-raphe = seam
-precursor for: tryptophan –> amino acid foods (glutamate, GABA)
- don’t cross into brain well unless carbs also present
- serotonin depletion = struggle w/ stroop task, aggressive
- no immed change in mood
- modd decrease in those w/ familial depression
SSRIs
- prozac –> depression
- chem imbalance
- blocks serotonin from being removed from the synapse
- effect of SSRIs quick, improvements are slow
0 targets monoamines - transports work similarly
- only kinda selective
SSRI efficacy
- no better than placebo for mild to mod depression
- helpful in MDD BUT can’t differentiate between drug effects or regression to the mean (get better on their own)
- most data wasn’t published
hallucinogens
- serotonin agonists
- psylocibin, DMT, LSD,
- activate serotonin receptors
- radical changes to our conscious perception and thoughts, minimal effects on mood
- serotonin helps organize sensation and reception
-therapeutic value
acetylcholine
-neuromuscular junction - where axons in motor neuron meet muscle
-tell to contract
-use acetylcholine to send msg
in basal forebrain too
- wakefulness and attention
- 1st NT discovered
-nicotine - acetylcholine receptor agonist
endocannabinoid system
- 2 NTs, 2 receptors
- GPCRs
- THC and CBT
NTs cant sit around in vesicle, really good at crossing membranes
- small, fatyy
-can’t keep them in vesicle, so we make them when need on the dendrites
- post synaptic side
- float away receptors on axons
- retrograde transmission
-weaken connection between 2 cells at a synapse
- memory = change in function or shape of synapse
- less NT release = axon smaller, less rom for NT to exit
-criteria for addiction being met through DA increase
- not fatal because receptors are not dense in myencephalon
- cannabis is a cannibinoid receptor agonist
adenosine
atp = cellular energy
-adenosine is atp byproduct
- ADP, AMP, A group and P group
-A builds throughout day, acting as singlaling molecule
caffein blocks adenosine receptors, but the body makes more so we get mroe tired when needing coffee
adenosine receptors
A binds, causes inhibition of overall levels of firing in cells
- signalling responsible for daytime sleepiness
-block A receptors via coffee
-more are then inserted = tolerance
endogenous opiods
-endorphins
-giant peptide NTs
-receptors area ll GPCRs
-many NT and receptor types/subtypes
- the neurotransmitter system that exogenous opiods mimic
- heroin - opiod agonist
-system for minimizng, dampenign pain - in crisis, pain not registered
- receptors found in SC, periacqueductal gray, nucleus accumbens
-lots of receptors in myelencephalon = why overdoses fatal
fentanyl and naloxone
naloxone = opiod adonist
- blocks opiod
