Neuro 3000 Exam #1 Set 2

Front 1

action potential

Back 1

used to conduct signal long distances without degradation

Front 2

-65mV

Back 2

resting potential

Front 3

action potential

Back 3

wave of positive charge, must depolarize the neuron to open up the ion channel

Front 4

reflex arc

Back 4

process by which sensory neuron come into the spinal cord via the dorsal root, internueron communicates and comes out the ventral root

Front 5

cytosol, plasma membrane, high resistance structure, membrane proteins

Back 5

structures needed to generate a resting potential

Front 6

phosphilipid membrane

Back 6

fluid, form new vesicles, phagocytize things,barrier to water and ions

Front 7

ion channels

Back 7

have both hydrophobic and hydrophilic regions, selective, proper structure of amino acids needed to go through

can be controlled to open and close

Front 8

ion pumps

Back 8

transport ions across the membrane against the concentration gradient using ATP as the energy source

Front 9

electric potential (voltage) and electrical conductance

Back 9

how much current flows depends in these two things

Front 10

conductance(g)

Back 10

relative ability for a charge to move from one place to another, depends on # particles available to carry the charge and how easily these can travel

Front 11

K+

Back 11

at rest this ion channel is always open, not gated or controlled

Front 12

equilibrium state

Back 12

occurs when diffusional and electrical forces are equal and opposite

Front 13

ionic equilibrium potential

Back 13

potential difference that balamces the ionic concentration gradient

Front 14

ionic concentrations

Back 14

large changes in membrane potential causes by tiny changes in this (.00001mM)

Front 15

K+

Back 15

high in the cell, low out

Front 16

Na+

Back 16

low in the cell, high out

Front 17

equilibrium potential

Back 17

ions move in the direction that moves the cell toward its...

Front 18

nernst equation

Back 18

can be used to calculate the exact eq potential of a cell

Front 19

charge and concentration difference

Back 19

used to determine whether inside of cell is positive or negative at eq for each ion

Front 20

-80 mV

Back 20

K+ eq potential

Front 21

62mV

Back 21

Na+ eq potential

Front 22

123 mV

Back 22

Ca+ eq potential

Front 23

-65 mV

Back 23

Cl- eq potential

Front 24

Na+/K+ ion pump

Back 24

pushes more K+ from outside the cell inside the cell and Na+ comes out, rquires ATP

Front 25

out of the cell

Back 25

transports Ca2+ pump transports it ____ of the cell, other proteins and channels help as well

Front 26

goldman equation

Back 26

eqn that shows thw relative permeability to multiple ions, the membrane voltage at any given time in the cell

useful in tracking action potential

Front 27

K+ channels

Back 27

mutations to these ion channels cause severe nuerological problems/death

Front 28

K+

Back 28

resting membrane potential close to this ion, due to the membrane being so permeable to this ion

Front 29

hodgkin and katz (1949)

Back 29

used manipulation of the external K+ concentration to show that resting potential of mostly set by K+ permeability of the neuron

Front 30

membrane potential

Back 30

external K+ concentration effects this

Front 31

spatial buffering

Back 31

helps keep brain from having too much K+ in one area

Front 32

astrocytes

Back 32

can take up K+ from environment or astrocyte and spread it out over wider area (regulate extracellular ion concentration)

Front 33

electrical synapses

Back 33

old evolutionarily, present at gap junctions

bidirectional, cells are electrotonically coupled, fast

formed by connexins, 6 of them make a connexon

common in mammalian CNS, glia,

Front 34

gap junction

Back 34

pore between two cells, channel allows ions to go through, not too selective, fairly large

when depolarized, signal will be transmitted to the other almost immediatelyc

Front 35

chemical synapses

Back 35

presynaptic and postsynaptic

cleft not empty but contains exracellular matrx proteins

highly orgamized

vesicles, secretory vesicles, active zones (presynaptic)

postsynaptic density: receptors and associated proteins

Front 36

CNS synapses

Back 36

-various sizes and configurations

-axodendritic, axosomatic, axoaxonic, dendrodendritic

grays type 1 and 2

Front 37

Gray's type 1 synapses

Back 37

synapse type with asymmetrical membrane thickness at synapse, usually excitatory (spheres)

Front 38

Gray's type 2 synapses

Back 38

synapse type that is symmetrical, usually inhibitory (oval shaped)

Front 39

neuromuscular junction

Back 39

synapses between motor neurons and muscle

learned much about synapses here

similar to CNS synapses

fast, large an reliable

Front 40

1. neurotransmitter synthesis

2. load neurotrans into synaptic vesicles

3. vesicles fuse to presynaptic terminal

4. binds to postsynaptic receptors

5. biochemical/electrical response in postsynaptic cell

6. removal of neurotrans from synaptic cleft

Back 40

6 principles of synaptic transmission

Front 41

dales principle

Back 41

neuron makes ONE neurotransmitter (found to be false)

Front 42

co-release and cotransmission

Back 42

dual transmitter neuron types (2)

Front 43

corelease dual transmitter neurons

Back 43

type of neuron that has two different neurotransmitters in the same vesicle

Front 44

cotransmission dual transmitter neuron

Back 44

type of neuron that has more than one type of vesicle (more than one neurotrans made)

Front 45

nuerotransmitter synthesis

Back 45

process by which translation occurs in the rough ER and transport peptide granules to the end down microtubules (fast down axon) to the presynaptic terminal

Front 46

Ca+

Back 46

channels of this ion open when the cell is depolarized enough, influx of this ion into the cell

signals exocytosis

Front 47

exocytosis

Back 47

signalled by Ca+ influx, fusion of the synaptic vesicle with the membrane of the active zone, occurs rapidly

Front 48

peptides

Back 48

not released in the active zone, has a shorter time course, generally responds to higher internal calcium

only responds to G protein coupled receptors

Front 49

snares

Back 49

structures that help vesicles dock to the presynaptic terminal membrane

Front 50

v snares

Back 50

type of snare that is on the vesicle

Front 51

t snare

Back 51

type of snare that is attached to the terminal (presynaptic terminal membrane)

Front 52

neurotransmitter receptors

Back 52

100 different types

can be transmitter gated or ligand gated

g protein coupled

Front 53

transmitter gated channels

Back 53

pore (channel) usually closed until ligand binds

4-5 subunits, change conformation after ligand binds, channel opens within microseconds

not as selective as voltage gated ion channels

Front 54

AchR

Back 54

gates Na, K, Ca, excitatory, produce EPSPs

Front 55

Cl gated

Back 55

ion channel gated by this ion, produce IPSP, glycine, GABA

Front 56

EPSP

Back 56

moves cell to become more positive to the threshold, Na+ comes in

Front 57

IPSP

Back 57

drives cell to become more negative, Cl comes in

Front 58

reverse potentials, I-V plot

Back 58

tells which iosnw ill be flowing in and out at a given potential

linear line = no voltage dependence

tell you the nernst eq potential and reverse potential

Front 59

g protein coupled receptors

Back 59

neurotrans binds to receptor, conformational change, then opens the ion channel

slower acting

amino acids, amines, peptides

also called metabotropic receptors

(affects metabolism of the cell, changes Ca levels, second messengers)

Front 60

autoreceptors

Back 60

kind of receptors that are often g protein coupled

Front 61

signal termination

Back 61

neurotrans is destroyed/removed to compltete this

can be done by reuptake from specific transporters, or degradation by enzymes, or desensitization

Front 62

desensitization

Back 62

process by which receptor does not respond to neurotransmitter and no signal is sent

Front 63

antagonists

Back 63

block function of the nirmal neurotransmitter

Front 64

agonists

Back 64

increase activity of ntrans

Front 65

botulim toxin

Back 65

blocks ntrans release, damages snares, takes a while to regenerate, produces sort of paralysis while blocking ntrans activity

Front 66

black widow venom, causes increased ACh release

Back 66

this causes increased release of this ntrans, affectd Ca entry into the cell, sends signal for this to be released without an action potential, stimulate skeletal muscles, (spacticity, then desensitization, then paralysis)

Front 67

organophosphates

Back 67

inhibit the destruction of ntrans, causes overstim, desensitization, then paralysis

Front 68

synaptic integration

Back 68

process by which multipple inpute from the brain combine in one neuron and an output is determined

Front 69

integration of EPSPs

Back 69

thousands of channels

number that open depend on how much ntrans to be released

quantum number of ntrans in vesicle (several thousand)

mini postsyanptic potentials add up and is combo of how many vesicles were released

Front 70

spontaneuous release of ntrans

Back 70

the opening and closings called mini EPSPs thought to cause this

Front 71

quantal analysis

Back 71

used to determine amount of neurotrans that will make a release all at once into synaptic cleft, depends on numbers of vesicles that release ntrans

Front 72

EPSPs

Back 72

start to add up if stimulated a lot, can be temporal (diff times, same area) or spatial (diff areas same time)

Front 73

length constant

Back 73

lamda, where depolarization is 37%of original current

Front 74

length constant

Back 74

value that gives some idea how far away from the axon hillock the depolarization can still occur before the current dissipates too much

dendrites will have varying values of this

Front 75

internal resisitance and membrane resisitance

Back 75

two factors that determine the length constant

Front 76

internal resistance

Back 76

depends on diameter and electrical properties of the cytoplasm (constant in a mature neuron)

Front 77

membrane resistance

Back 77

depends on synaptic activity and how many ion channels are open

Front 78

low internal resistance, high external resistance

Back 78

ideal conditions for a large length contant

Front 79

dentrite

Back 79

not always electrically passive, some can have K+, Ca+, and Na+ channels

usually cant fire action potentials

opening of these channels can add current to propogate EPSPs

Front 80

shunting inhibition

Back 80

when Cl channels can open and drive cell toward -65mV (Cl eq pot), inhibitory synapes disspates the excitatory synapse on the dendrite

Front 81

modulation of synaptic transmission

Back 81

not super fast this way, adenylyl cyclase phosphorylates the protein kinase and channel opens

Front 82

intracellular and extracellular electrodes

Back 82

can be used to record action potentials

Front 83

Na + enters the cell

Back 83

extra cellular area gets more negative (microvolts) an intracellular gets more positive (mV)

Front 84

K+ channels open

Back 84

these ion channels open in the rising phase

Front 85

Na+

Back 85

these channels close in the falling phase

Front 86

undershoot

Back 86

when extra K+ ion channels open in response to the influx of Ca+ ions in the action potential

Front 87

action potentail

Back 87

caused by entry of pos charge into the cell

Front 88

absolute refractory period

Back 88

channels cannot open until cell gets back to -65mV takes a least one ms

Na channels inactivated, cant be deinactivated until membrane pot is more negative

Front 89

relative refractory period

Back 89

longer because there is an undershoot, more current is required to fire action potential, some K+ channels remain open and make it hard to get back to resting potential

cell is hyperpolarized until K channels open up

Front 90

firing frequency

Back 90

amount of depolarization controls this, increases after the depolarizing current increases

Front 91

hodgkin and huxley

Back 91

researchers who used the voltage clamp, figured out a lot about action potential, propose channels allow Na to come in and K to leave

predicted existence of voltage gated ion channels

Front 92

squid giant axon

Back 92

used with voltage clamp to study axons

Front 93

voltage clamp

Back 93

method used to figure out the eq potential of the cell, inject current as channels open and close to compensate for current an see which and how much current is needed to open a channel

Front 94

nernst eq

Back 94

used to determine the eq pot of the cell used by hoghkin and huxley

Front 95

Na+

Back 95

higher outside the cell

Front 96

k+

Back 96

higher inside the cell

Front 97

Na+

Back 97

early inward current is carried by this ion

Front 98

K+

Back 98

late outward current carried by this ion

Front 99

-40

Back 99

Na+ channels open at this potential and close quickly

Front 100

time and voltage

Back 100

membrane volatge changes depend on these two things

Front 101

depolarization

Back 101

caused by an influx of sodium ions

Front 102

repolarization

Back 102

caused by efflux of K+ ions (flowing out of the cell)

Front 103

rising phase

Back 103

due to inward Na+ current

Front 104

falling phase

Back 104

due to outward potassium current

Front 105

sodiu channel

Back 105

made up by 1800 AAs

each domain looks like subunit of it

each domain has s4 voltage sensor which can manipulate voltage where it opens by changing AAs

has conformational changes

Front 106

pore loop

Back 106

this part of the sodium channel determines selectivity to K+ or both K+ and Na+

Front 107

-40mV

Back 107

potential where sodium channel is opened, huge driving force for Na+ to come into the cell since the eq pt of Na+ is ~60

Front 108

water molecules

Back 108

important for Na+ channel selectivity (too small for K+ and this molecule to get through)

Front 109

patch clamp

Back 109

can measure how long the channel is open

used to isolate single channel activities, forms gigaseal between pipette and membrane

whole cell technique form continuous environment with the cell membrane

can set system to current

more sophistocated

Front 110

absolute refractory period

Back 110

ball and chain model used to describe this process, ball out of the Na+ channel, Na+ flows through, then ball inside channel, then ball back out with channel closed to end this and action potential can be generated again

Front 111

tetodotoxin

Back 111

blocks sodium channel from the outside

Front 112

lidocaine

Back 112

binds reversibly to the sodium channels and makes a good pain medication, can localize the effects

Front 113

K+ channels

Back 113

do not open right after depolarization, but are delayed

Front 114

delayed rectifier channels

Back 114

one of the types of K+ channels, don't open immediately but take a few ms to open

open the membrane is depolarized, slow inactivation, repolarizes membrane after an action potential

Front 115

overshoot

Back 115

when the membrane pot approaches the eq pot of Na and it is greater than 0mV

Front 116

membrane pot threshold

Back 116

point at which Na channels open and cell is more permeable to Na

Front 117

rising phase

Back 117

Na ions enter cell due to large driving force, past resting potential for a bit

Front 118

falling phase

Back 118

Na channels inactivate, K channels open, large driving force for K to leave cell

Front 119

undershoot

Back 119

membrane pot moves toward K eq pot, hyperpolarizes the cell and makes it not very permeable to Na (therefore no action pot)

Front 120

orthodromic

Back 120

action potentials that start from the cell body

Front 121

antidromic

Back 121

action potentials that start backward

Front 122

Na

Back 122

during action potential conduction, this ion diffuses down axon and depolarizes, extra locations where this ion comes in, passive is not enough

Front 123

casper

Back 123

helps localize Na channels to the nodes of rancier so Na can get in where there is no myelin

Front 124

saltatory conduction

Back 124

increases the membrane resistance, so length constant is much larger

completed by nodes of ranvier Na channels

Front 125

spike initiation zone

Back 125

where the action pot usually starts, the axon hillock

Front 126

neurons

Back 126

fire at diverse rates (eg stellate faster and mre frequent than pyramidal)