Neurobiology 1: Bioelectricity & Synapses Flashcards

1
Q

What are the 3 main types of neurons?

A

sensory(bring info into CNS), motor (send info out from CNS),and interneurons (connects those two, most brain neurons)

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2
Q

function of glial cells in CNS?

A
  • supporting cells that are not excitable (no rapid change in mem pot), but do have a resting potential (ALL CELLS HAVE A RESTING POT. ALL)
  • provide nutrient support (glucose, lactose)
  • In CNs: (blood brain barrier): astrocytes (type of glial cell) that filter toxic compounds flowing through blood…lay in between blood and neurons
  • glia are all around neurons
  • NT reuptake
  • K+ homeostasis
  • in PNS: oligodendrocytes (another kind of glial cell) wrap myelin around axon
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3
Q

function of glial cells in PNS?

A
  • provides insulation by wrapping myelin sheaths around axons
    • myelin is composed of FA
  • comprises grey matter–> where most of neuronal cell bodies are outside brain
  • white matter in the middle is composed of axons that connect the cell bodies in grey matter
    • reverse in spinal cord: white matter outside, grey matter in middle
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4
Q

why is there a resting potential (Vm)?

A

1) conc diff of ions across mem

2) diff permeability to ions of K+, Na+2, Cl-, Ca+2

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5
Q

what molecules have a negative charge in the cell

A

proteins and nucleic acids

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6
Q

Which ions are abundant in cytoplasm vs extracellular?

A

High anions in cytosol
High K+ in cytosol
Low Na+ in cytosol
Low Cl- in cytosol

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7
Q

why is there a membrane pot in a cell

A

high permeability to K+ and low permeability to Na+ and Cl-

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8
Q

If the mem was 100% permeable to K+, what would the Ek be?

A

-92 mV

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9
Q

If the membrane was 100% permeable to Na+ what would the ENa be?

A

+62 mV

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10
Q

What is the driving force?

A

Difference between E and resting mem pot

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11
Q

What is the driving force for K+?

A

Since Ek = -92 but resting mv is -60, wants to make cell more neg so pushes K+ out but is WEAK

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12
Q

What is the driving force for Na+?

A

Both conc gradient and E wants to pull Na+ in so STRONG…opposite direction with K+

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13
Q

What is the driving force for Cl-?

A

high conc of Cl- outside, so wants to go in but the - charge clashes with an alr neg cytosol so WEAK

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14
Q

What is the driving force for Ca+2?

A

LOTS of Ca+2 outside so conc gradient drives, in and +2 outside attracted to neg cytosol so STRONG

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15
Q

What happens if inc permeability to Na+?

A

Na+ comes in–> depolarize

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16
Q

what happens if inc permeability to K+

A

K+ leaves–> hyperpolarize

17
Q

what happens if inc permeability to Cl-

A

Ca+2 comes in–> STRONG depolarization

18
Q

How does the Na+/K+ pump work?

A
  • uses ATP
  • keeps Na+ low and K+ high inside to maintain Vm
    • Na+ enters from inside
    • ATP, conformational change to open
    • releases Na+ and K+ enters from outside
19
Q

detail an axon potential

A

at rest, K+ ion channels alr open, Na+ voltage act gate is closed, inact is open
When threshold is reached, activ gate opens, transient influx of Na+ inside, inact closes
As inside of cell gets more (+), K+ voltage gate opens so mem is 100% permeable to K+
K+ leaves, so mem is less (+) which brings depolarization down

20
Q

what is the mem threshold

A

mV that opens Na+ activ gate

21
Q

detail the propagation of an action potential

A

spreads to one direction down axoplasm… first area that got depolarized before it is repolarized to resting b/c of Na+ inact gate closing and K+ opening so the once super (+) inside is now less (+)

22
Q

how is the duration the action potential determined?

A

kinetics of opening of Na+, and K+ channels and inactiv of Na+ channel

23
Q

how is the direction of the action potential determined?

A

can’t go backwards b/c inact gate closes…can only go forward to Na+ channels available for depolarization

24
Q

What is the significance of the diameter of axons in invertebrates?

A

small diameter= slow AP, high resistance to current flow, frequent voltage gates along axon
large diameter = fast AP, less resistance, travel farther, fewer voltage gates required

25
Q

what 3 factors determine speed of conduction of an AP?

A

speed of current flow in axoplasm
leakage of ions across PM
kinetics of channels opening/closing

26
Q

what regenerates action potentials?

A

voltage ion gates (K+ and Na=)

27
Q

In vertebrate axons, where are the ion channels located?

A

nodes of Ranvier

28
Q

what is the function of myelin sheaths

A

dec leakage of ions thru mem

29
Q

What are the 2 types of synapses?

A
  1. electrical- not as commons, good for firing in synchrony, mediated by gap junctions, can’t be easily modulated, can only be excitatory, can’t be summated temporally
  2. chemical- NT released from presynaptic cell and diffuses across a cleft
30
Q

List 9 types of NT and whether they are excitatory or inhibitory

A
  1. ACh- excitatory…btwn motor neurons and muscle cells
  2. Serotonin- generally inhibitory
  3. dopamine- generally excitatory
  4. glutamate- excitatory
  5. norepinephrine- either
  6. glycine- inhibitory..opens Cl- channels
  7. GABA- inhibitory… opens Cl- channels
  8. neuropeptides (substance P)
  9. NO
31
Q

What happens at the neuromuscular junction?

A

depolarization at axon terminus opens Ca+2 channels so large influx
this stimulates fusion of synaptic vesicles to release NT into cleft
Na+ channels open in post synaptic –> depolarization

32
Q

what breaks down ACh?

A

acetylcholinesterase

33
Q

IPSP and EPSP

A
IPSP = inhibitory in post synaptic = hyperpolarize
EPSP = excitatory in post synaptic = depolarize
34
Q

function of the axon hillock

A

beginning of axon, not myelinated, many voltage-gate channels
where the decision to fire an AP occurs
cell body has no voltage gated ion channels
EPSP and IPSP flow passively to axon hillock

35
Q

what are the 2 types of chemical receptors

A
  1. ionotropic receptors
    • the receptor is the channel
    • ex ACh
  2. metabolic receptor
    • GPCR but instead of adenyl cyclase, it’s an ion channel
    • ex. cardiac adrenergic opens Ca+2 channels via activation of PKA
36
Q

what are the 3 ways NT are removed from cleft

A
  1. degraded by enzymes (ACh by acetylcholinesterase)
  2. diffuses out
  3. taken up by glial cells or transporters and recycled