Neurotransmitters Flashcards

1
Q

agonist

A

increases function of Neurotransmitter system

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2
Q

antagonist

A

decreases function of neurotransmitter system

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3
Q

ionotropic receptors

A

receptors that are coupled to ion channels and affect the neuron by causing those channels to open

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4
Q

metabotropic receptors

A

receptors that are associated w/ signal proteins and G proteins

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5
Q

glutamate

A
  • primary exciter NT
  • cuz receptors cause EPSPs
  • bring Na in
  • depends on receptors not NTs
    -metabotropic and ionotropic receptors
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6
Q

glutamate antagonists

A

-decreasing excitation, dampening brain
- sedation, dampen NS
- agonists cause anxiety, seizures

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7
Q

examples of glutamate antagonists

A
  • barbituates
  • nitrous oxide (laughing gas)
  • ketamine
    -ethanol (booze) - hangover = overactivation of glutamate
    (all involved sedation and relaxation)
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8
Q

GABA

A

-primary inhibitory NT
- ionotropic and metabotropic
- ultimate inhibitroy effect

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9
Q

GABA agonist examples

A

-benzos
- ethanol
-G antagonist too, fatal in excess
- chloroform
-ether

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10
Q

gaba agonists

A

increasing inhibition in brain
- sedation, relaxation, relief from anxiety

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11
Q

types of amines

A

-dopamine
-epinephrine
-norepinephrine
-histamine
-serotonin

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12
Q

amines

A
  • all metabotropic
  • modulatory role
  • bigger than amino acid, smaller than protein
  • many receptors
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13
Q

dopamine

A

classic assctn of pleasure
- projects from ventral tegmental area tonucleus accumbens

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14
Q

dopamine drugs

A
  • all addictive drugs directly or indirectly increase dopamine transmission
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15
Q

dopamine in parkinson’s

A
  • 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
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16
Q

L-DOPA as parkinson’s treatment

A
  • L DOPA already in brain
  • extra pill is converted into DA in brain via enzymes
  • replacement therapy
  • restoration in movement
17
Q

dopamine antagonists

A
  • 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
18
Q

norepinephrine

A

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

19
Q

propranolol

A
  • 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
20
Q

serotonin

A

-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

21
Q

SSRIs

A
  • 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
22
Q

SSRI efficacy

A
  • 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
23
Q

hallucinogens

A
  • 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
24
Q

acetylcholine

A

-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
25
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
26
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
27
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
28
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
29
fentanyl and naloxone
naloxone = opiod adonist - blocks opiod