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PSYC 301 > Neural Communication > Flashcards

Neural Communication Flashcards

1
Q

how do cells communicate?

A

via synaptic impulses within the cell

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2
Q

how does communication happen within a single neuron?

A

voltage potential energy!!

- used needles/electrodes inside and outside of cells to measure the membrane potential

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3
Q

what is the easiest way to measure the membrane potential and why?

A

in invertabrates becasue they have HUGE axons/neurosn by comparison
they also have no myelin
OG is the squid boy

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4
Q

what is the chemical gradient?

A

the concentration gradient of ions wanting to flow from high to low

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5
Q

what is the electrical gradient?

A

positively/negatively charged ions move around and change the membrane potential (MP)
- absense of a positive charge is negative!

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6
Q

what is the phospholipid bilayer?

A

hyrophilic heads on one side and hydrophobic tails on the other, so water and lipids etc will not make it through because of both those components
- only way to get through is through channels (passive) and pumps (active)

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7
Q

what is neuron resting MP

A

-65 is inside the cell

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8
Q

why is neural communication chemical?

A

there are two ions that result in a lot of the change (na and K)
they move into the cell/out of the cell (not freely!)

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9
Q

how is neural communication electrical?

A

k and na have positive charges and as they move through the membrane it changes!!

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10
Q

what is the difference between channels and pumps?

A

channels: passive along gradient
pumps: require ATP and push against gradient

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11
Q

what is the Sodium Potassium Pump

A
  • in the cell
  • pushes 3 NA OUT
  • pushes 2 K IN

membrane
- consumes 2/3 of neuronal energy

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12
Q

how does the na k pump effect chemical and elecritcal gradient?

A

chemical: more sodium on the outside: will want to flow into the cell
potassium wants to flow out

electrical: outside the cell will be more positive, net positive flow of charge outside, cell inside is negative, only bumps it like 10mV, not enough for the full potential

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13
Q

how does the SPP use ATP?

A

breaking the atp bond releases energy and causes the pump protein to change shape and molecules are released into the environment (phosphate is released and goes back to its main confirmation)

  • slow compared to other processes
  • **
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14
Q

what are leaky channels?

A

Potassium channels that allow K+ to flow freely through the membrane
Na+ cannot! (channels are usually closed)

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15
Q

what is the effect of the leaky channel?

A

the two gradient forces push on each other to reach an equilibrium with net exchange zero and a membrane potential of -65/70

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16
Q

when a NT binds to a postsynaptic receptor, what are the two effects it could have?

A
  1. depolarize (move closer to zero) EPSP
  2. Hyperpolarize (move further from zero, making more negatve) IPSP

EPSP: increase liklihood of AP
ISPS: decrease “

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17
Q

what is the transmission of PSPs? how is it like electric signals on an uninsulated wire?

A

graded
decremental (decrease with time/length)
rapid

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18
Q

how can EPSPs and IPSPs sum?

A

spatially: more than one terminal on a body
termporally: same terminal on a body firing within the same window of time

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19
Q

how do you generate an action potential?

A

you must hit the trigger “threshold of exitation” - or else it just fizzles out

Sum of EPSPs and IPSPs reach the depolarization threshold

AP: massive reverasl of MP for a bit

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20
Q

what is the main method of brain communication?

whats its story?

A

the action potential!

  • all or none
  • not graded (always the same in size/shape)

glias cannot do this

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21
Q

how do neurons convey magnitude?

A

firing rate and length of firing

***

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22
Q

what are voltage gated Na + channels?

A

depending on voltage (-55/65ish mV), protein takes on a different shape, the sodium pore opens and lets sodium into the cell

once its reached the peak, it inactivates

both forces are pushing sodium IN (electrical and chemical)

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23
Q

how do the voltage gated channels turn off (inactivate)

A

automatically after 1 ms a ball and chain type thing that plugs the channel flips up and plugs it! (inactivated NOT closed)
- it will only reopen once RMP is reached again

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24
Q

how does repolarization happen?

A

voltage gated k channels open!! since the MP is now positive, both forces/gradients are pushing k + out of the cell
nak pump restores the ion balance over time!

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25
Q

when do the voltage gated k channels activate?

A

when the na ones inactivate. late to show up and late to leave
-late to leave meaning they are still open during hyperpolariazation phase

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26
Q

what is the relative refractory period and absolute refractory period?

A

relative: harder to generate an AP but its possible (during hyperpolarization)
absolute: impossible to generate an AP (during repolarization)

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27
Q

what are the 2 proteins responsible for RMP and the 2 responsible for AP?

A
  • ask becca
    RMP: pump and leaky channels
    AP: voltage gated channels
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28
Q

subthreshold and suprathreshold stimulaion of an axon?

A

sub: exitatory potential produced but doesn’t go all the way down the axon: it diminishes
supra: exceeds the threshold and produces an AP that continues down the axon undiminished

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29
Q

how does conduction in an unmyelinated axon work?

A
  • na channels are EVERYWHERE: LOADED with voltage gated channels
  • constant regeneration over and over
  • activate their neighbouring channels
  • slower than myelination because of the constant regeneration (even tho channels are faster than pumps)
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30
Q

why does an AP only move in one direction if the channels are everywhere?

A

because the channels previously are in the absolute refractory period!

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31
Q

how does conduction in myelinated axon work?

A

saltatory conduction: the signal ‘jumps’ from node to node at the speed of light

wrapped in schwann/oligodendros

na channels at the nodes of ranvier only! (less doors to open)

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32
Q

what does myelin do?

A

it decreases the amount of decay when you go across the axon so you need less regeneration points!!

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33
Q

why is myelination faster?

A

less channels to open/regenerate at

myelin is faster travel

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34
Q

which disorder is damaged myelin related to?

A

Multiple Sclerosis (MS)

  • damages myelin and transmission
  • 55-75k in canada (highest rate in the world)
  • damage is in the form of lesions or plaques
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35
Q

what are the charictaristics of the two types of potentials? PSPs and APs?

A

psps: graded, amplitude modulated, fast (speed of light*), decremental
aps: not graded, frequency modulated, less fast (regeration required), not decremental

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36
Q

what effect does the action potential have on a presynaptic membrane?

A

it causes vesciles to fuse!

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37
Q

how does a vesicle fuse with the membrane?

A

kiss and run! quickly opens and closes
they’re made of the same phospholipid bilayer
-under some conditions, the vesicle is depleted and there isn’t enough time to push things back into the vesicles

38
Q

what are receptors?

A

closed channels that open when they bind with NTs!

  • specific channels (pores/holes)
  • gated by binding (ligant gated)
39
Q

why do we get EPSPs? how are they generated?

A

epsp’s are generated from binding to the receptor which causes a sodium channel to open up
***some channels allow sodium IN AND potassium OUT

40
Q

what was the classic model of neurotransmission based on?

A

the neuromuscular junction!

  • in a squid :)
  • between muscle fibers and the nerve cell
  • when receptors bind, sodium flows!
41
Q

what are the 5 claims of the classic model?

theyre wrong

A
  1. each cell has a single input
  2. NT are deactivated by enzymes
  3. NTs product either EPSPs or IPSPs
  4. each NT has a single receptor
  5. Each cell releases a single NT
42
Q

WITW: why is this wrong?

“each cell has a single input”

A

in the NMJ: each muscle fiber recieves input from only one motor neuron (others died off in development)

in the rest of the body: there are so many synapses per neuron, 10,000 in purkinje cells (look at shape of dendrites)
NMJ is an exception!

43
Q

WITW:

“neurotransmitters are deactivated by enzmes”

A

at NMJ: enzyme deactivates ACh
-when you want your mucles to move/when you don’t want them to move

this is actually rare at non-cholinergenic synapses

rest of body: enzyems clear up synapses so your leg doesn’t keep on moving, but the primary mechanism is reuptake.

44
Q

what is reuptake?

A

energetically favourable process, take the same NT and stuff it back into a vesicle and keep using it !
-uses PUMPS as reuptake proteins
(things can be reuptake inhibitors like drugs and such)

45
Q

what are the 3 ways of NT cleanup?
**
confusing look for readings or ask Jay

A
  1. diffusion: floating away into extracellular space
  2. enzyme degradation: broken down into metabolites
  3. reuptake (pre-synaptic or astrocytes): the things that end in T (NET, PMAT, DAT) move things back into the cell for repackaging
46
Q

what happens to metabolites in the body?

A

they filter out through the rest of the body or are turned back into NTs through an enzymatic process

47
Q

what role do astroglia play in neurotransmitter cleanup?

A

maintain synaptic environment, break down NTs if there are too many and then transport them back into presynaptic vesicles

48
Q

WITW:

“neurotransmitters produce one of either ESPSs or IPSPs”

A

at NMJ: yes, ACh produces EPSP at the junction

everywhere else: can produce epsp either ipsp (not just one OR the other)
depending on the RECEPTOR not the NT.
- some glutamate receptors will have an inhibitory effect

49
Q

WITW:

“Each neurotransmitter has a single receptor”

A

at NMJ: ACT receptors can be artificially stimulated and when you do, you see that some of them resond to nicotine and others don’t some respond to muscarine and others dont? why is this?
IONOTROPOIC AND METABOTROPIC RECEPTORS!
nicotinic and muscarinic are iono and metabo respectively!

50
Q

what is an ionotropic receptor?

A 
ligant gated ion channels
exitiatory or inhibitory
FAST on/off effect!
like an ion channel
EPSPs and IPSPs are relaly good for transient signals
51
Q

how do you hyperpolarize an ionotropic receptor?

A

you open up chloride ions! they will flow on in

52
Q

what is a metabotropic receptor?

A

G-protein-coupled receptor that MODULATES the cel and has longer slower signals
cause SIGNAL CASCADES
a big bundle of amino acids
NT binds on the outside and G proteins on the inside break off and do a bunch of work inside the cell (receptor has changed shape to let this happen)

53
Q

what do the cascading signals in metabotropic receptors do?

A

modify existing channels
tell receptors to be brought to the sruface
can go to DNA and cause transcription changes
Modulatory roles
NOT an on/off signal
last longer

54
Q

WITW:

“each cell releases a single NT”

A

there has been lots of “coexistence” within cells in NS
usually a peptide/OR gas AND a small molecule NT
-located in different vesicles and released into another place (extra-synaptic)

55
Q

what is a Gas Nt and whats it’s issue?

A

can pass through any membrane, can’t be stored in a vesicle so must be made ON DEMAND

56
Q

what are some more examples of neurotransmitters?

A

gas NT
membrane permeable NTs
Retrograde transmission

57
Q

what is the benefit of membrane permeable NTs?

A

receptors can be anywhere, even on the inside of the cell or in the nucleus!

58
Q

what are the two types of presynaptic receptors?

A

autoreceptors
-binds the same NT that the axon is releasing
-on the edges of the synapse
-during periods of high activity, they slip out of the cleft and tell the cell that theres too much acvitivy going on.
Mostly metabotropic
NOT used in reuptake

heteroreceptors: recepton on acon that binds a different NT - extrasynaptic (around edges) usually another synapse nearby that is used to MODIFY a signal (turning up or down the volume on existing signals)

59
Q

what is an example of a heteroreceptor action?

A

“spider on your arm”

- you notice more now that its been said. the signal has been AMPLIFIED

60
Q

What is an agonist/antagonist?

A

agonist: increase function of that sytem (bind to receptors or bock reuptake)

Antagonist: decrease function of that system

61
Q

describe gluatmate

A

primary excitatory NT
used throughout the brain
mostly IOnotropic (AMPARs, NMDA, Kainate)
Metabotropic with an inhibitory role (autoreceptors) i.e. mGluR

62
Q

what are some gluatmate drugs?

A

all antagonists!

  1. Barbiturates, kill u in high doses
  2. Nitrous Oxide: laughing gas
  3. Ketamine: tranquilizer
  4. Ethanol: booze!

slows down and dampends everything

63
Q

what happens if you have a glutamate agonist?

A

anxiety and seisure territory!! unprovoked activity in many many cells

64
Q

describe Gaba

A

primary inhibitory NT
used throughout brain
ionotropic (GABA A) and metabotropic (GABA B)
not the best target for drugs

65
Q

what are some Gaba drugs?

A

all agonists!

  1. Benzodiazepines: anti anxiety (xanax)
  2. Ethanol: alcohol
  3. Chloroform: knocks ya out
  4. Ether: anasthetic but can be dangerous

all anti anxiety, increasing inhibition, sedating effect

66
Q

what are the amines?

A 
dopamine
Epinephrine (adrenaline)
Norepinephrine
Histamine
Serotonin

Like “watering the lawn”. theyre either not targetting or targeting many different neurons. attempting to modulate a whole brain region

All metabotropic and play modulatory roles

67
Q

what is the study about motivation and brain stimulation all about?

A

olds and milner thought dopamine was the pleasure molecule, so they stimulated the VTA to Nucleus accumbens

They initially tried to hit the brainstem but failed and hit these axons.

Needle hooked up to battery and level, when its pressed the rats keep doing it above all else!

BUT MAYBE its cause they felt compelled and not because they felt ‘pleasure’

68
Q

what do all addictive drugs have in common?

A

dopamine release indirectly (heroine/nicotine) or directly

69
Q

what is a thought of secondary treatment for neurodegernerative disorder?

A

stimulating axons from the VTA to the nucleus accumbens

70
Q

which is the area responsible for dopamine in parkinsons disease

A

the SNc (substantia nigra)

71
Q

what is a treatment for Parkinson’s disease?

A

l-dopa! because dopamine can’t cross the blood brain barrier and there are enzymes in your brain which can convert it for you

72
Q

how many neurons have died by the time someone shows sympotoms of parkinsons?

A

90%

73
Q

what are the symptoms of parkinsons?

A

very hard to initiate/stop movement, (voluntary movement)

NOT a lack of pleasure directly

74
Q

what is the issue in patients with schizophrenia?

how do drugs help?

A

they have high (hyperactive) dopamine levels (but they aren’t happier persay)

All drugs to help schizophrenia treat positive symptoms of schiz by blocking the function of dompamine by blocking their receptors

75
Q

what is a study that demonstrates how dopamine is not the pleasure molecule.

A

Salamone 1990s
experiment where there are 2 choices for a rat (work for 4 pellets or get 2 for no work)
3 conditions
1. baseline (rats trained to do the tast both ways
2. given dopamine antagonist
3. give dopamine antagonist plus remove the barrier

when given the antagonist they are LAZIER and don’t want to work for the pellets, but when the arm is removed they still WANT the extra pellets.

when they’re on the drug they aren’t willing to work for the treat

76
Q

what’s norepinephrines story?

A

originates in locus coreluous (activating system)
enhances memory by stress and emotion
MODIFY OR ENHANCE existing signals
- tells other neurons whats going on/whats important

when you have norepineprine release, you have stronger activity at the synapse are are more likely to retain a memory

77
Q

what is PTSD’s implication with norepinephrine?

A

when using beta blockers (blocking norepinephrine) and asking pateints to recount their experiences, they recall the memory but reconsolidate it to be less stressful. they don’t FORGET it persay, but they have less of a stress response when they recall it later.

78
Q

why do beta blockers work for PSTD?

A

when you reconsolidate a memory, you reactivate synapses and the memory becomes vulnerable to change (which is why stories change after you tell them sometimes)

79
Q

what is serotonin?

A

associated with happiness etc.
found in raphe nucleus (brain stem)
precursor is tryptophan

80
Q

what is tryptophan? how does it work?

A

serotonin precursor, carbs must be present for it to cross BBB
in high amino acid foods

81
Q

what happens in serotonin depletion studies?

A

someone stays in lab and they eat a tryptophan depleted diet: serotonin levels DROP

  • increased impulsivity
  • increased aggression
  • worse on stroop tests
  • if you have a family history of depression, it will effect their mood!
82
Q

whats a stroop test?

A

saying the colours or written colours and not the word itself

83
Q

what are SSRIS?

do they work?

A

taken for depression, they block reuptake of serotoin, so it has more time to be active
Prozac/Fluoxetine

depression is an imbalance of monoamines

ssris take effect quick on the brain but take weeks-month to notice improvements

lots of side effects (weight gain, sexual dysfunction)

84
Q

what did a meta analysis find for the efficacy of SSRIS?

A

Pharmaceuticals didn’t release data that didn’t agreee with them when letting SSRIs hit the shelves

  • no better than placebo for mild depression
    May help with major depression
    VERY SMALL EFFECT SIZE, cycling happens

maybe depression isn’t caused by lack of serotonin but a lack of something in yoour life - Jay

85
Q

what is the story of acetylcholine?

A

used at the NMJ!
also in the Basal Forebrain!

wakefulness
attention

Nicotine acts this way as well, and nicotine can be a mild psychostimulant for the 1st dose

86
Q

what are endocannabinods?

A

travel RETROGRADE

  • weaken connection between cells at a synpase!
  • bind to the same receptors that cannabis does!

this breaks a lot of rules

87
Q

why does the brain have a system for weakening systems (endocannabinoids)

A

you don’t want to remember EVERYTHING, things that aren’t important and whatnot
can also work as a negative feedback loop

88
Q

what is adenosine? what’s its story?

A

the A from ATP.
A is a byproduct of the usage of ATP

Adenosine has an inhibitory effect on brain function - DAYTIME SLEEPINESS

however there ARE adensoine receptors and caffeine works on the same ones!
- caffeine is an adenosine antaonist

89
Q

how does adenosine respond to caffiene in the brain?

A

it makes MORE receptors, building your tolerance to caffeine over time, so that if you dont have it, you have a bunch of receptors that are making you tired!

90
Q

what are endogenous opiod? what drugs act on this system?

A

endorphins!

  • giant peptide NTs
  • exogenous opioids (heroin) mimic this system
  • pain relief and anesthetic AND pleasure
  • dangerous drugs like fentanyl are strong agonists of these receptors

Receptors are are GPCRs***

Receptors found in spinal chord, periacueductal grey, nucleus accumbens and more

91
Q

what happens at high levels of fentyal use?

A

since inhibition is so high, it can cause too much inhibition and inhibit lifesustaining processes like the BRAINSTEM

92
Q

what is naloxone?

A

its an opiod receptor ANTAGONIST

- blocks the effect on the brainstem

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