General Things To Remember - Block 1 M1

Front 1

Synapsin

Back 1

Anchors synaptic vesicles to the cystoskeleton for storage - has to be phosphorylated to release them for synaptic transmission.

Front 2

Rab3A

Back 2

Guides released vesicles to dock at the active zone in a synapse.

Front 3

Synaptotagmin

Back 3

A molecule on vesicle membranes that when bound to Ca2+ allows them to dock to the plasma membrane's active site.

Front 4

Glycine

Back 4

Inhibitory CNS neurotransmitter; opens Cl- channels and prevents opening of voltage-gated channels.

Front 5

GABA

Back 5

Major inhibitory neurotransmitter at multiple synapses in both brain and SC

Front 6

Ecl for mammalians

Back 6

-70

Front 7

VGluT

Back 7

specific transporter for Glutamate uptake into synaptic vesicles

Front 8

mGluR2

Back 8

Glutamate autoreceptor for feedback inhibition of synthesis and release at Glutamatergic neurons

Front 9

System activated by NE

Back 9

reticular activating system

Front 10

How many types of glutamate uptake receptors for inactivation

Back 10

5 - all work by sodium cotransport

Front 11

Things in the CELL

Back 11

K
Acid
Protein
Phosphates

Front 12

Things in the ECF

Back 12

NaCl
Ca
Glucose

Front 13

What gives ion channels selectivity?

Back 13

P loops - 5 amino acids facing inner pore

Front 14

Mechanical event that opens ion channels:

Back 14

Movement of Pos Arg residues on S4 Gate to outside
-makes inside of memb pos
-makes outside of memb neg

Front 15

How to close a Na channel:

Back 15

Hinged Gate - loop blocks the hole

Front 16

How to close a K channel:

Back 16

Ball and Chain - amino terminus swings up to plug the hole with its positive charge.

Front 17

Contributions to the Em:

Back 17

95% = K diffusion
5% = Na/K Atpase

Front 18

How Na/K Pump works:

Back 18

3 Na out
2 K in
Net neg charge on inside

Front 19

Ultrafiltration

Back 19

Reverse osmosis - the movement of water up its concentration gradient due to hydrostatic force.

Front 20

Edema

Back 20

-RH or LH failure
-Loss of plasma proteins
-Renal failure
-Brain damage

Front 21

Dehydration

Back 21

-Hypovolemia
-Hypotension
-Cholera
-Diabetes insipidus
-Hyperglycemia

Front 22

Oubain

Back 22

noncompetetive inhibitor of Na/K ATPase - prevents K binding

Front 23

Mechanism of Oubain:

Back 23

1. Inhibit Na/K Pump
2. Sodium accumulates in cell
3. Sodium/Ca exchanger stops working b/c no gradient for Na
4. Ca accumulates in SR and increased contraction force

Front 24

Botox

Back 24

prevents neuromuscular junction release of NT by inhibiting SNAREs

Front 25

Nerve gas

Back 25

inhibits acetylcholinesterase - no stop of neuromusc transmsn.

Front 26

DHPR

Back 26

Dihydropyridine receptor - the Voltage gated Ca channel on muscle cells within the T-tubule

Front 27

RyR

Back 27

Ryanidine receptors - Calcium gated calcium channels in the SR - activated by the calcium that came in via DHPR rec on cell surface

Front 28

Curare

Back 28

blocks AcH receptors so no EPP is generated at the NMJ

Front 29

Neostigmine
-action
-treatment for

Back 29

Anti-AChesterase - keeps it around longer
-treats myasthenia gravis

Front 30

Malignant hyperthermia

Back 30

SR channels fail to close - Ca leaks out; constant contraction; generates lots of heat and increased metabolism.

Front 31

Cause of malignant hyperthermia:

Back 31

Genetic - induced by Anesthesia

Front 32

4 Ways to change contractile force in a skeletal muscle:

Back 32

1. Length-tension relationship
2. Summation
3. Tetany
4. Fatigue

Front 33

2 Types of summation:

Back 33

1. Frequency (temporal)
2. # motor units (quantel)

Front 34

What does the Length-tension curve tell?

Back 34

Longer length = more passive F
Active F goes to zero if too long.

Front 35

What does the Force-velocity curve tell?

Back 35

The larger the load (force) the slower velocity
The lighter the load the faster velocity.

Front 36

Can you change the Force/Velocity curve?

Back 36

For skeletal: no
For cardiac: yes - via vagal versus sympathetic stim

Front 37

Fast muscle fibers

Back 37

-White
-Glycolytic
-Extensive SR

Front 38

Slow muscle fibers

Back 38

-Oxidative
-Myoglobin
-Red
-Extensive blood supply

Front 39

What type of muscle is tonic?

Back 39

Aorta

Front 40

What type of muscle is phasic?

Back 40

Jejunum

Front 41

What stimulates aorta?

Back 41

NE

Front 42

What stimulates jejunum?

Back 42

AcH

Front 43

What inhibits aorta?

Back 43

AcH

Front 44

What inhibits jejunum?

Back 44

NE

Front 45

What is an EMG

Back 45

Electromyography - changes in electrical signal allow you to see recruitment of muscle fibers

Front 46

What happens to a skeletal muscle when you increase voltage with fixed resistance?

Back 46

Current changes because you recruit more motor units

Front 47

What is motor unit recruitment?

Back 47

Quantel summation

Front 48

What's the other type of summation?

Back 48

Frequency summation

Front 49

What is frequency summation?

Back 49

Decreasing the time between two impulses so that they add together to make one big impulse.

Front 50

What is Delay Time?

Back 50

Time between release of Ca from SR and the actual release of Troponin from Actin - about 8-10 ms

Front 51

What was the cause of muscle fatigue if you see fast recovery?

Back 51

-Glycogen depletion
-K+ buildup in ECF (depolarizing)

Front 52

What causes small motor unit fatigue?

Back 52

Loss of calcium

Front 53

What fibers fatigue first?

Back 53

Fast twitch - run out of glycogen first and can't do oxidative metabolism

Front 54

3 Types of Calcium channels:

Back 54

N type - neurons
L type - Atria/ventricles
T type - SA and AV nodes