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PSYC 304 > Neural Communication II > Flashcards

Neural Communication II Flashcards

1
Q

how does neuronal trasmission begin in the axon terminal?

A
  • axon ends in terminal boutons (buttons) that have vesicles filled with neurotransmitters
  • action potential travels to bouton and depolarizes
    1. causes voltage-gated Ca++ channels to open
    2. Ca++ causes vesicles to fuse with membrane
    3. neurotransmitters are released into the synapse
  • dendrite membrane has receptors that fit with neurotransmitters
  • receptors are often just closed channels that open when they bind with neurotransmitters
    • also called ligand-gated ion channels
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2
Q

what are the different types of receptors?

A
  • ionotropic receptors (ligand-gated ion channels)
  • metabotropic receptors (GPCRs)
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3
Q

what are ionotropic receptors?

A
  • let ions cross, ligand-gated ion channels
  • activate EPSPs and IPSPs by allowing ions to cross the membrane
    • excitatory (depolarize) - Ca crossing
    • inhibitory (hyperpolarize) - Ch crossing (Chloride)
  • fast, transient effect - when neurotransmitter is no longer binded, effect is gone
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4
Q

what are metabotropic receptors? what happens when neurotransmitters bind to them?

A
  • signalling proteins: G-protein-coupled receptors (GPCRs)
  • don’t directly change voltage or allow ions to cross, they have a metabolic effect
  • neurotransmitters bind and G proteins break off and activate in the cell
    • activate or inhibit process in the cell
  • they modulate the cell and modulate signals
  • slow, longer lasting effect
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5
Q

what are some examples of modulatory effects of metabotropic receptors?

A
  • can activate signalling molecules
  • can change transcription and translation
  • can open or close other channels
    • cause signal cascades
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6
Q

what are the common receptor locations?

A
  • postsynaptic side - most common (dendrite)
  • presynaptic - on the axon
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7
Q

what are some examples of receptors that are on the pre-synaptic side?

A

autoreceptors and heteroreceptors

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8
Q

what are autoreceptors and what do they do?

A
  • usually GCPRs and have an inhibitory effect
  • accepts it’s own released neurotransmitters (dopamine)
  • uses negative feedback to make sure not too many neurotransmitters are released
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9
Q

what are heteroreceptors and what do they do?

A
  • modify how the synapse works
  • binds to a different neurotransmitter than the one released by the axon
  • also modular, increases or decreases neurotransmitter activity (the amount released)
    • affect lingers for a little
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10
Q

in what ways are neurotransmitters cleaned up?

A

diffusion, enzymatic degradation, re-uptake

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11
Q

how does diffusion work to clean up neurotransmitters?

A
  • neurotransmitters just float away
    • not the best solution because they’ll bind to other receptors
    • only happens when the goal is for the neurotransmitter to bind to other targets
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12
Q

how does enzymatic degradation work to clean up neurotransmitters?

A
  • enzymes break down neurotransmitters into components (COMT, MAO)
    • not the best solution either because we have to use energy to make the neurotransmitter again
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13
Q

how does re-uptake work to clean up neurotransmitters?

A
  • transporters push molecules back into the cell (back in axon) and back into the vesicles
    • DAT - transporters on the membrane pack the neurotransmitter into the axon
    • VMAT2 - transporters on the vesicles pack the neurotransmitter into the vesicles
    • done in both the pre-synaptic side and the astrocytes
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14
Q

what are the two main drug types?

A
  • agonist - increase effects in neurotransmitter system
  • antagonist - decrease effects in neurotransmitter system
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15
Q

what is glutamate?

A
  • the primary excitatory neurotransmitter that is used throughout the brain
  • ionotropic receptors
    • AMPAR - binds to AMPA drug
    • NMDAR - binds to NMDA drug (also allows calcium in, important for learning)
    • kainate receptor
  • metabotropic receptors - some are excitatory, and some are inhibitory
    • mGluR
    • our autoreceptor on the axon is a metabotropic receptor
  • effect depends on what Glutamate binds to, it’s not always excitatory
  • often not a great target for drugs because it’ll affect the whole brain
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16
Q

what are some glutamate antagonists? what does it mean to be a glutamate antagonist?

A
  • means we decrease glutamate activity, which decreases overall brain activity
  • barbiturates - lethal injection
  • nitrous oxide - laughing gas
  • ketamine - “horse tranquilizer”
  • ethanol - drinking alcohol
  • at lower levels → relaxation, at higher levels → diminished consciousness, less brain activity
  • agonists don’t work because glutamate already works at a very high level - too much = extreme anxiety and even seizures
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17
Q

what is GABA?

A
  • primary inhibitory neurotransmitter that is used throughout the brain
  • has both ionotropic and metabotropic receptors
    • GABA-A - ionotropic Cl- receptor, which makes cell more negative and inhibits (IPSPs)
    • GABA-B - metabotropic receptor causes inhibition
  • also not a great target for drugs but better than glutamate because it isn’t as universal in the brain
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18
Q

what are some gaba agonists? what does it mean to be a gaba agonist?

A
  • means we increase gaba activity, which decreases overall brain activity
  • benzodiazepines - anti-anxiety medication
  • ethanol - drinking alcohol
  • chloroform - used to make people lose consciousness
  • ether - an anesthetic previously used
  • at lower levels → relaxation, at higher levels → diminished consciousness, less brain activity, death
  • antagonists don’t work very well, would result in anxiety, just like glutamate agonists
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19
Q

what are amines? what are some examples?

A
  • small molecule neurotransmitters that are metabotropic and play a modulatory role
  • released into brain area and hit many neurons
  • dopamine (DA), epinephrine (adrenaline), norepinephrine (noradrenaline), serotonin (5-HT), histamine
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20
Q

where does dopamine originate from?

A
  • originates from two nuclei in the tegmentum
    • substantia nigra pars compacta - axons go to basal ganglia
    • ventral tegmental area - axons go to basal ganglia and other brain areas
  • projects to some (but not all) brain areas
  • DA also made in hypothalamus, where it is a hormone
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21
Q

where do we get dopamine from?

A
  • precursors from diet: tyrosine - in foods with high amino acid content, protein (and phenylalanine)
    • converted from tyrosine and phenylalanine into DA via enzymes
  • overlaps with norepinephrine, they are both catecholamines
22
Q

what are the dopamine receptors like>

A
  • five dopamine receptors: D1R-D5R / D1-D5
    • all metabotropic
    • some positive modulatory, some negative
23
Q

what is the olds and miler experiment? what did it tell us about the role of dopamine?

A
  • Olds and Milner (1954) - meant to target the brainstem, but mistakenly hit a bundle of axons from ventral tegmental area (VTA) to nucleus accumbens (NAcc) in rats brain
  • when a rat hit a lever, it stimulated axons that released neurotransmitters (dopamine)
  • rat would hit the lever until they passed out
  • researchers came to the conclusion that dopamine → pleasure
24
Q

what was the study done in response to the olds and milner study? what did that study tell us?

A
  • same study was done on humans, they self-stimulated dozens of time in a day
    • they said they felt somewhat unpleasant
    • clicking the button made them feel like they were gonna remember something on the tip of their tongue
  • concluded that dopamine does not equal pleasure
25
Q

what relationship does dopamine have with drugs of addiction?

A
  • all addictive drugs directly or indirectly increase dopamine transmission
    • what they all have in common is that using them makes you more likely to seek them in the future
    • levels of pleasure don’t get higher than the first couple hits, but people keep doing it
    • people chase the initial feelings of euphoria
26
Q

what are some drugs that increase dopamine transmission?

A
  • amphetamine and cocaine directly increase dopamine transmission
  • heroin, nicotine, oxycodone, ethanol and cannabinoids indirectly increase dopamine transmission
27
Q

how does Parkinson’s disease relate to dopamine? what does this tell us about dopamine and pleasure?

A
  • Parkinson’s is associated with loss of dopamine in substantia nigra pars compacta (SNc)
    • loss of dopamine results in a loss of voluntary behaviour, but NOT a loss of pleasure
  • there is a relationship between Parkinson’s and levels of pleasure, but is strongly correlated to motor skills
    • think that it may not be from loss of dopamine, but the loss of autonomy
28
Q

what is the treatment for Parkinson’s? what does this tell us about dopamine and pleasure?

A
  • L-DOPA is a Parkinson’s Disorder treatment
    • DOPA is already created in the brain
    • when we insert L-DOPA into brain, the brain will create dopamine
  • L-DOPA treatment improves motor function but doesn’t necessarily increase pleasure
  • D1 agonists have been used in the past, but too much of them and too much L-DOPA have negative side effects (impulse problems)
    • shopping and shoplifting compulsivity, severe gambling, hyper-sexuality
  • when you give L-DOPA to healthy participants, it has no impact on positive mood
29
Q

how does schizophrenia relate to dopamine? what does this tell us about dopamine and pleasure?

A
  • dopamine theory of schizophrenia → unusually high levels of dopamine
  • individuals with schizophrenia do not have higher baseline pleasure
  • dopamine receptor (D2R) antagonists treat schizophrenia (block dopamine)
    • the more effective D2R antagonists were in the brain, the better they treated schizophrenia by blocking D2R
30
Q

what did Salamone’s T-maze task tell us about dopamine, pleasure, and motivation?

A
  • had a maze that was designed so that low effort = low reward and high effort = high reward
  • control - rats usually go for high effort and high reward option
  • dopamine antagonist - rats go for low effort and low reward instead
  • if DA was pleasure, they would be at a deficit for pleasure and would want to get the higher reward
  • in reality, DA antagonist made them less motivated to go for the high effort, high reward
  • giving a dopamine antagonist = decreased motivation but not pleasure
31
Q

how do we know that dopamine release is related to reward prediction error?

A

Schultz et al. (1990s) - study on Pavlovian learning, classical conditioning
- at first, DA neurons fire for unexpected rewards
- then, they start associating the light with grape juice (reward)
- then, DA neurons only fire to the stimuli that predicts the reward (light)
- another condition where the light goes up but no reward is given: the neurons still go off when the light turns on, but they go silent when the predicted reward is not delivered
- dopamine goes up when something unexpectedly good happens, and goes down when something unexpectedly bad happens

32
Q

what is the reward prediction error and how is dopamine release related?

A

reward prediction error - when an outcome is better or worse than expected
- dopamine release is related to reward prediction error
- when something better than what we expect happens, dopamine rises
- when something worse than what we expect happens, dopamine decreases

33
Q

what does dopamine actually do?

A
  • important for movement, especially motivated movement
  • important for learning as related to movement and motivation
  • important for levels of arousal, attention, executive function
  • it is NOT the pleasure molecule
34
Q

what is norepinephrine? how does it impact memory?

A
  • works very similarly to epinephrine, both are hormones and a neurotransmitters
  • originates in brain stem region called the locus coeruleus
  • norepinephrine projects all over the brain
  • affects baseline levels in wakefulness and arousal and also fluctuate according to stress
  • enhances memory based on stress/emotion, arouses brain areas and gets the system ready to better remember things
    • affects flashbulb memories, vivid memories of a time that was emotionally charge
  • evolutionarily useful, things that are stressful or emotional are the most valuable
35
Q

what are norepinephrine receptors like?

A
  • has two main receptor types (⍺1-2, β1-3 - alpha and beta) with subtypes & sub-subtypes
    • all metabotropic (GPCRs)
  • causes heterosynaptic facilitations via heteroreceptors
36
Q

how has propranolol been used in relation to PTSD? explain why it works.

A
  • PTSD is a result of the strong emotions and strong memories caused by norepinephrine
  • propranolol (beta blockers) is a norepinephrine receptor antagonist, originally used for heart conditions
    • take propranolol and recount traumatic event while body is relaxed, memory is supposed to be reconsolidated differently (can treat PTSD)
  • the reason this might work is that memories are fragile and malleable when they are recounted over and over again
    • talking about the memory again brings it into working memory, put it into long term memory differently
37
Q

in what other context was propranolol used as treatment?

A
  • also tried this treatment of people who recently had a breakup
    • made them think of how their significant other was a jerk
    • resulted in less heartbreak
38
Q

what is serotonin? what are its receptors like?

A
  • primarily released from the raphe nuclei (brain stem)
    • projects all over the brain, especially the cortex, thalamus, cerebellum
  • precursor: tryptophan in amino acid rich foods (protein)
    • can’t get across blood brain barrier without carbs, which means serotonin decreases
  • serotonin depleted when tryptophan is taken away or prevented from absorption
  • there are 15 receptor types, almost all are metabotropic (modulatory)
39
Q

what happens when serotonin from diet is depleted?

A
  • serotonin depleted when tryptophan is taken away or prevented from absorption
    • don’t necessarily see mood go down, but we lose cognitive flexibility
    • increases impulsivity and aggression
  • found that for people who had no family history with depression, serotonin depletion did not result in mood change
    • people with a family history of depression experienced decrease in mood when serotonin was depleted
40
Q

what are SSRIs and how do they work?

A

Selective Serotonin Reuptake Inhibitors
- medication used for depression that makes serotonin floats in synapse for longer, acts as serotonin agonist
- prozac/fluoxetine
- SSRIs are selective, but also affect DA and NE systems
- effects of SSRIs in the brain are quick (45min-1 hour), but improvements are slow (2 weeks)

41
Q

how effective are SSRIs?

A
  • producers of fluoxetine didn’t publish studies on it’s usefulness
    • there was a significant publication bias
  • original meta-analyses determined that SSRIs are no better than placebo for mild to moderate depression
  • may help with major depression but effect size is relatively small
  • 80% of doctors said they’d prescribe it to a patient but only 40% said they’d take it themselves
42
Q

what are hallucinogens? what do they tell us about serotonin and mood?

A

psychedelic drugs that act on serotonin receptors (agonists)
- LSD, DMT, psilocybin
- radical changes to our conscious perceptions and thoughts, minimal effects on mood
- 1/3 of people on psilocybin said it’s the most eye-opening, amazing experience
- 1/3 of people also said it was extremely anxiety provoking
- have been useful in end of life care, PTSD, addictions, and more
- serotonin is not simply a mood molecule
- serotonin organizes cortical networks that see and feel patterns in the sensory world
- serotonin agonists cause the brain to find patterns that don’t exist

43
Q

what is acetylcholine?

A
  • first discovered neurotransmitter
  • seen at the neuromuscular junction - used for muscle contraction
  • also in the basal forebrain
    • related to wakefulness and attention
44
Q

how is nicotine related to acetylcholine?

A
  • nicotine is a acetylcholine receptor agonist
  • lots of acetylcholine receptors in the gut, too much nicotine causes lots of activation in that muscle and causes discomfort
45
Q

what are endocannabinoids?

A
  • two neurotransmitters that bind to two different receptors (GPCRs)
    • bind to metabotropic receptors and are inhibitory
  • weaken the connection between two cells at a synapses
    • same system that is used when we are trying to forget things
46
Q

where are the endocannabinoid neurotransmitters stored, and why?

A
  • neurotransmitters are produced in the dendrite
    • retrograde transmission - move from dendrite to axon
  • aren’t stored in the vesicles because the molecules are good at getting across membrane
    • instead, enzymes make and release neurotransmitter from the dendrite when the drug enters
  • cannabis (THC, CBD) is a cannabinoid receptor agonist
    • there is a relationship between cannabis use and problems with long-term memory retention
47
Q

what is adenosine?

A
  • byproduct of metabolic activity (ATP), not necessarily a neurotransmitter
    • phosphate groups break off of ATP until there are none left, and it’s just adenosine
  • brain is covered in adenosine receptors, they are metabotropic and inhibitory
    • adenosine receptors bind (inhibitory) and makes us tired during the day
  • may be the reason for daytime sleepiness
48
Q

how does caffeine interact with the adenosine system?

A
  • caffeine/theophylline - molecules bind to adenosine receptors, are antagonists
    • block the inhibition, make us feel more awake
    • tolerance builds up as cells adapt and add more adenosine receptors
    • need more caffeine to keep us awake
  • experience caffeine withdrawals in the mornings
    • after about a month of no coffee, body will recognize that there is too much adenosine
    • extra receptors will be removed
49
Q

what are endogenous opioids?

A
  • giant peptide neurotransmitters that are also called endorphins (endogenous-morphine)
  • are used as pain killers
  • receptors are all GPCRs (inhibitory and metabotropic)
    • Mu and Delta receptors
  • receptors found in spinal cord, periacqueductal grey (PAG), nucleus accumbens, more
  • we have a release of endogenous opioids when body is trying to avoid pain in stressful situations
    • ex. mom in a car accident with a broken leg saves their child before passing out
50
Q

what exogenous opioids mimic the endogenous opioid neurotransmitter system?

A
  • heroin - opioid agonist
  • fentanyl - even stronger opioid agonist
    • can be fatal if dosing is wrong
  • naloxone - opioid antagonist
    • used to treat people

PSYC 304 (10 decks)

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