B1W2: Physio

Question 1

Assumptions of Action potential

Answer 1

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.)

Question 2

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

Answer 2

VERY SMALL AMOUNT

Exception: large diameter axons

Question 3

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

Answer 3

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

Constant stimulation

Question 4

Voltage clamp on action potential

Answer 4

Measures specific currents at Vm

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

Question 5

Tetrodoxin

Answer 5

TTX, blocks Na+ channels

Leads o respiratory paralysis and death

Question 6

Dihydropyridines

Answer 6

Block Ca2+ channels

Question 7

TEA

Answer 7

tetraethylammonium

Blocks K+ channels

Question 8

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

Answer 8

Current=0

Question 9

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

Answer 9

Inward current starts to lessen

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

Question 10

Equation for current of ion w/ voltage clamp

Answer 10

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

Question 11

Channel activations

Answer 11

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

Question 12

Electrical excitability

Answer 12

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)

Question 13

Incease in [Ca2+] o and excitability

Answer 13

Moves Vm towards +

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

Question 14

Decrease in [Ca2+]o and excitability

Answer 14

Increases excitability by decreasing current of Ca2+

Question 15

[K]+ o increase affect on excitability

Answer 15

moves Vm towards Vth, up excitability

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

Question 16

Properties of ion channels

Answer 16

Selective (due to specific amino acids)

Inactivation/activation controlled

Question 17

S4 voltage-gated protein domain

Answer 17

Lysine and arginine positive residues

Senses voltages

Question 18

S5-S6 voltage-gated channels

Answer 18

Pore region

Has amino acids that recognize substrate

Question 19

Activation of ion channels in Na+

Answer 19

S4 helices attrached to inside membrane usually

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

Question 20

Inactivation/closing of ion channels

Answer 20

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

Question 21

Depolarization blockade

Answer 21

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

Question 22

Ways to initiate depolarization blockade

Answer 22

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

Question 23

General properties of electrical synapses

Answer 23

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

Question 24

Properties of chemical synapses–ionotrophic

Answer 24

i.e. nicotinic

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

Question 25

Metabolism of Ach in synapse

Answer 25

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

Question 26

Properties of chemical synapses--metabotrophic

Answer 26

(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)

Question 27

Skeletal muscle synapse structure

Answer 27

Down myeliated axon --\> bouton per muscle fiber This is the motor unit/end plate

Question 28

Steps of skeletal muscle synapse

Answer 28

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

Question 29

EPP

Answer 29

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

Question 30

Curare

Answer 30

Competitive inhibitor AcH at ionotrophic receptor i.e. poison darts Reduced EPP amplitude so no AP Paralysis

Question 31

Myeesthenia gravis

Answer 31

Muscular weakness and fatigue Antibodies compete for Ach receptors (autoimmune disease)

Question 32

alpha-bungarotoxin

Answer 32

snake venom that causes muscle paralysis Ach competitive inhibitor can be used to degrade effects of myesthenia gravis

Question 33

Botulinus toxin

Answer 33

Blocks the proteins that regulate movements of vesicles to excitatory presynaptic neurons, preventing release of glutamate Leads to muscle weakness, paralysis, ANS issues

Question 34

Tetanus toxin

Answer 34

Blocks vesicle movement to inhibitor presynaptic membranes; muscle rigidity, lock jaw GABA or glycine, inhibitors, are being blocked from release

Question 35

Organophosphates

Answer 35

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

Question 36

Different types of synaptic connections in nerve cells

Answer 36

Axo dendritic: synapse with dendrite Axosomatic: synapse with soma Axoaxonic: synapse with axon Axospinous: synapse with spine

Question 37

Long term potentiation

Answer 37

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

Question 38

Two types neural netwoks

Answer 38

Discrete/spatiall focused: specific, fast, focused, aroused Widely divergent/diffuse: modulates memory, motor control, mood, etc. --central core in brainstem

Question 39

Excitatory synapses (EPSP)

Answer 39

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

Question 40

Inhibitory synapses (IPSP)

Answer 40

* 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

Question 41

Voltage clamping experiments with EPSP

Answer 41

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

Question 42

Voltage clamping experiments with IPSP

Answer 42

* at Em=-65, gCl increases and iCl increases, hyperpolarization * at Em=-71 mV, Ecl=-71, Icl=0, IPSP=0

Question 43

Spatial summation

Answer 43

several axons send signal to cell

Question 44

Temporal summation

Answer 44

same axon sends many signals over time