Ape2

Front 1

What non-ionic source contributes to the charge within cells? What is this charge?

Back 1

Proteins, negative

Front 2

How is an ion gradient maintained within a cell?

Back 2

Na-K pump

Front 3

What is the Na-K distribution like in a cell?

Back 3

More Na on outside, more K on inside

Front 4

Typical resting potential of a cell?

Back 4

-70mV

Front 5

What two forces pull on ions in cells?
Where does Potassium want to go based on these forces? Why?
How about Sodium?

Back 5

Concentration gradient, charge differences

K:
Conc: Wants to leave
Charge: wants to stay

Na:
Conc: wants to come in
Chrge: wants to come in

Front 6

What happens when sodium ions are allowed to pass through ion channels? Which direction do they proceed in?

Back 6

Decreased membrane potential, enters the cell until reaches an equilibrium.

Front 7

What are the 5 types of channels within a neuronal cell membrane? Describe their mechanism of opening/closing.

Back 7

Passive (leak): always open
Active (gated): open/close in response to stimuli
Chemical (ligand)
Voltage
Mechanically

Front 8

Label diag 7.

Back 8

1. Central canal
2. Epyndymal cells
3. Grey matter
4. Neurons
5. Myelinated axons
6. Microglia
7. Astroglia
8. Oligodendrocyte
9. White matter

Front 9

Describe the steps of a graded potential.

Back 9

Membrane is exposed to a chemical that opens sodium ion channels, sodium ions enter cell membrane and produce a local current that depolarizes adjacent portions of he cell membrane.

Front 10

Would sodium ion leakage result in depolarization or hyperpolarization?
How about K+ ions?

Back 10

Na: Depolarization
K: Hyperpolarization

Front 11

What are the general steps of an AP?

Back 11

Mebrane depolarizes to threshold, sodium channels open, close, potassium channels open, return to normal permeability.

Front 12

What must a graded potential do in order to generate an AP?

Back 12

Reach threshold.

Front 13

How does the amplitude of an AP vary?

Back 13

It doesn't.

Front 14

What is a refractory period? What are the two types? When do they occur?

Back 14

New action potential cannot occur until recovery.
Absolute: NO AP NO MATTER HOW MUCH OF A DEPOL (under peak)

Relative: Possible is stimuli large enough (undershoot)

Front 15

Place in order of increasing speed:
Type A fibers
Type B fibers
Type C fibers

Why do they differ in speed?

Back 15

A, B, C

Diameter, myelination

Front 16

Describe how nonmyelinated axons propagate APs.
Same for myelinated axons.
What are these methods used known as?

Back 16

nonmy:
Ap develops in initial segment, local current depol adjacent portion of membrane to threshold, AP develops, initial segment enters refractory, repeat.

AP at initial segment, depol at node 1, repol at initial segment, repeat.

Continous Conduction
Saltatory Conduction

Front 17

Relationship between graded potentials and distance traveled? Action potentials?

Back 17

Decrease with distance.
No effect.

Front 18

Effect of Excitatory NTs on AP?
Inh?
Will an NT always be excitatory?

Back 18

Cause dpol, promote AP
Hyperpol, suppress AP

Nope, can promote or inhibit based on receptor

Front 19

NT in cholinergic synpases?
Why is there a synaptic delay?
What happens to ACh once it's broken down?
When doe synaptic fatigue occur?

Back 19

ACh
Ca++ influx and NT release take time
Reabsorbed and recycled by Presyn Neuron
When you run out of ACh

Front 20

Synapses ACh involved in?

Back 20

All neruomusc junctions
Neuron-neuron in PNS
Parasymp post-ganglion

Front 21

Steps of a cholinergic synapse?

Back 21

AP arrives, depolarizes synaptic knob, extracellular Ca++ enters and triggers release of ACh (exocytosis), ACh binds receptors and depol post syn mem, AChE removes ACh

Front 22

Why does ACh have a direct effect on receptors?

Back 22

WHen it binds, it causes a conformational change in the receptor, making it open.

Front 23

List effects and whether INH/EXC:
Norepi
DA
5HT
GABA

Back 23

Exc: brain, AutoNS
Exc/Inh, movement, muscle tone
------attention, emotoin, sleep/wake
Inh, reduce anx

Front 24

Role of neuromodulators? Direct or indirect effect?
Major class? Suffix?

Back 24

Influence post syn resp to NTs
Both
Opiates, phins, ins

Front 25

How do neurotransmitters exert effect in indirect fashion? Give examples of such NTs.

Back 25

G protein system (second messengers)

Epi, NE, DA, GABA, Hist

Front 26

Give examples of direct NTs.

Back 26

ACh, glut, asp.

Front 27

What kind of effect do NO and CO have? Direct or indirect? Describe the pw.

Back 27

Indirect-->lipid soluble, activate second messengers that effect receptor opening.

Front 28

What are some ways neuronal signaling can be altered?

Back 28

Promote depolarization, channel blockers, depress membrane sensitivity, remove myelin, block/promote release, block NT binding, stimiulate receptors, block inactivation of NTs

Front 29

Classify as hyperpol or depol:
EPSP
IPSP

Back 29

Depol
Hyperpol

Front 30

Describe temporal and spatial summation.

Back 30

Graded potentials timed (release one after the other at the same pre syn term)

Spatial: simultaneous graded potential from two different pre syn neurons.