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Physiology > B1W2: Physio > Flashcards

B1W2: Physio Flashcards

1
Q

Assumptions of Action potential

A
  1. AP does not decrease in amplitude as it propagates
  2. AP occurs duet o decrease in transmembrane resistance i.e. increase in conductance/ion permeabilities
  3. Cooling axon slows AP and widens it
  4. Reducing [Na]o decreases amplitude, magnitude of pos. overshoot and velocity (sodium hypothesis bc makes GHK more neg.)
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2
Q

What amount of Na+ is needed to make an AP?

A

VERY SMALL AMOUNT

Exception: large diameter axons

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3
Q

Signifigant increase in [Na+] and decrease in [K+]

A

Will screw up ATP Na+/K+ pump if it isn’t already blocked by ischemia/hypoxia

Constant stimulation

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4
Q

Voltage clamp on action potential

A

Measures specific currents at Vm

  • no ionic current at hyperpolarization (-140 mV)
  • at depolarized (-20 mv), positive current inward followed by outward
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5
Q

Tetrodoxin

A

TTX, blocks Na+ channels

Leads o respiratory paralysis and death

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6
Q

Dihydropyridines

A

Block Ca2+ channels

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7
Q

TEA

A

tetraethylammonium

Blocks K+ channels

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8
Q

What happens if you clamp Vm at the E of an ion?

A

Current=0

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9
Q

What happens if you clamp Vm at more pos. than -30mv?

A

Inward current starts to lessen

After the ENa, Na+ will go in opposite direction!

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10
Q

Equation for current of ion w/ voltage clamp

A

i of ion=g(ion) x (Eion-Eclamp)

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11
Q

Channel activations

A
  1. action potential initiated
  2. causes Vm to more positive level by opening voltage-gated channels
  3. gNa and gK up, but gNa faster so its peak occurs sooner
  4. Reaches threshold, Vm at which iNa=iK
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12
Q

Electrical excitability

A

Ease of firing AP

Proportional to 1/(Vth - Vm)

Want to increase excitability by making Vth more neg. or Vm more pos.

Need to decrease (Vth-Vm)

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13
Q

Incease in [Ca2+] o and excitability

A

Moves Vm towards +

Decreases excitability because Ca2+ binding to membrane proteins, more pos. charge need to be removed to depolarize

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14
Q

Decrease in [Ca2+]o and excitability

A

Increases excitability by decreasing current of Ca2+

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15
Q

[K]+ o increase affect on excitability

A

moves Vm towards Vth, up excitability

Current of K+ out of cell is down so Vm stays more +

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16
Q

Properties of ion channels

A

Selective (due to specific amino acids)

Inactivation/activation controlled

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17
Q

S4 voltage-gated protein domain

A

Lysine and arginine positive residues

Senses voltages

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18
Q

S5-S6 voltage-gated channels

A

Pore region

Has amino acids that recognize substrate

19
Q

Activation of ion channels in Na+

A

S4 helices attrached to inside membrane usually

Depolarization causes helix to be attracted to extracellular side, opening pore

20
Q

Inactivation/closing of ion channels

A

In Na+: hinged lid

In K+: ball and chain, amino acids near NH3+ work

Channels can only be reactivated by going back to resting state

21
Q

Depolarization blockade

A

Can’t initiate AP because Na+ channels remain in inactive state due to depolarization

Na+ channels remain inactivated because S4 still has AP charges on it

22
Q

Ways to initiate depolarization blockade

A

Increase in neurotransmitters (i.e. succinylcholine, not broken down as quickly as Ach)

Increase anesthetics–bind to Na+ channel while inactivated

Increase H+: blocks Na+ from binding, leading to coma, respiratory acidosis, decrease in renal function

23
Q

General properties of electrical synapses

A
  • Fast
  • pre/post synapses sealed by low-resistance gap junctions
  • Connexons (of 6 connexins)= gap junctions
  • use little energy, biodirectional
  • stimulate multiple cells simultaneously
24
Q

Properties of chemical synapses–ionotrophic

A

i.e. nicotinic

  • Receptor=ion channel
  • NTs activate (i.e. Ach)
  • works at medium speed
25
Q

Metabolism of Ach in synapse

A
  • Made from choine and acetyl coA in presynaptic terminal, uses Ach-H transporter to package
  • Degraded by acetylcholine esterase in synapse if too much
26
Q

Properties of chemical synapses–metabotrophic

A

(i.e. muscarnic)

  • G protein coupled receptor
  • Can be very slow
  • Example: in cardiac muscle, Ach binds and releases B subunit; this in turn causes K+ channels to open and hyperpolarization (chronotrophic inhibition)
27
Q

Skeletal muscle synapse structure

A

Down myeliated axon –> bouton per muscle fiber

This is the motor unit/end plate

28
Q

Steps of skeletal muscle synapse

A
  1. depolarization
  2. Ca2+ floods cell to release vesicles, fuse vesicles with membrane and have vesicles open above active zone
  3. Ach binds to ligand channels, causes EPP due to the Na+ current that causes AP
29
Q

EPP

A

Due to Ach opening ion channels, local depolarization generated with amplitude that decreases with distance (unlike AP)

30
Q

Curare

A

Competitive inhibitor AcH at ionotrophic receptor

i.e. poison darts

Reduced EPP amplitude so no AP

Paralysis

31
Q

Myeesthenia gravis

A

Muscular weakness and fatigue

Antibodies compete for Ach receptors (autoimmune disease)

32
Q

alpha-bungarotoxin

A

snake venom that causes muscle paralysis

Ach competitive inhibitor

can be used to degrade effects of myesthenia gravis

33
Q

Botulinus toxin

A

Blocks the proteins that regulate movements of vesicles to excitatory presynaptic neurons, preventing release of glutamate

Leads to muscle weakness, paralysis, ANS issues

34
Q

Tetanus toxin

A

Blocks vesicle movement to inhibitor presynaptic membranes; muscle rigidity, lock jaw

GABA or glycine, inhibitors, are being blocked from release

35
Q

Organophosphates

A

inhibit Ach esterase in synapse, leading to parasympathetic activation because too much Ach

SLUDGE: salivation, lacrimation, urination, defecation, GI, emesis

Examples: chemical warfare agents, agricultural insecticides

Use atropine, a competitive inhibitor for muscarinic receptors, to save people

36
Q

Different types of synaptic connections in nerve cells

A

Axo dendritic: synapse with dendrite

Axosomatic: synapse with soma

Axoaxonic: synapse with axon

Axospinous: synapse with spine

37
Q

Long term potentiation

A

When increased activity of nerve makes moe spines grow, causing increase in postsynaptic intracellular [Ca2+] and EPSP amplitude

38
Q

Two types neural netwoks

A

Discrete/spatiall focused: specific, fast, focused, aroused

Widely divergent/diffuse: modulates memory, motor control, mood, etc.

–central core in brainstem

39
Q

Excitatory synapses (EPSP)

A

Glutaminergic

  • brain visual cortex pyrimidal cell
  • local, non-propagated
  • glutamate/aspartate
  • opens Na/K –> Vm toward threshold –> depolarization
  • unlike EPP, low amplitude at single synapse
40
Q

Inhibitory synapses (IPSP)

A
  • brain visual cortex pyramidal cell
  • GABA or glycine
  • opens Cl- –> Cl- in cell –> hyperpolarization
  • Cl- follows conc. gradient; in CNS neurons, Ecl is near or more negative than the resting potential
41
Q

Voltage clamping experiments with EPSP

A
  • at -65 mV, an EPSP causes local depolarization
  • at Vm=0, EPSP=0; this is because iNa=iK
  • Any higher, hyperpolarization and reverse potential
42
Q

Voltage clamping experiments with IPSP

A
  • at Em=-65, gCl increases and iCl increases, hyperpolarization
  • at Em=-71 mV, Ecl=-71, Icl=0, IPSP=0
43
Q

Spatial summation

A

several axons send signal to cell

44
Q

Temporal summation

A

same axon sends many signals over time

Physiology (9 decks)

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