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Animal Physiology > Exam 2: Ch 6 Book > Flashcards

Exam 2: Ch 6 Book Flashcards

1
Q

2 ways signals move from point to point along the plasma memb.

A

graded potentials

action potentials

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2
Q

receptor potential

A

physical stimulus received and changes the membrane potential

graded potential in proportion with the stimulus

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3
Q

decremental transmission

A

sensory receptors lack voltage gated ion channels that produce APs so signal decays over distance

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4
Q

membrane at spike initiating zone of a sensory neuron contains

A

many voltage gated ion channels

if graded potential reaching this zone is still strong enough, AP generated

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5
Q

transfer of info between neurons is usually accomplished though

A

chemical signals carried by neurotransmitters

causes change in membrane potential of post-syn neuon

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6
Q

amount of nt released and thus the amplitude of the response from post-syn neuron depends on

A

number and frequency of AP arriving in terminals of pre-syn neuron

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7
Q

post-syn potential

A

change in membrane potential of post-syn neuon

graded signal (if large enough can initiate an AP in posy-syn neuron toward next neuron)

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8
Q

cable properties

A

electrical properties that affect conduction of a signal over distance

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9
Q

why would signal along longitude of an axon decay with distance

A

cytoplasm has resistance to flow of electrical signals

resistance of plasma membrane to electrical signals is high

charges leak out of the cell across plasma memb.

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10
Q

a perfectly insulated wire moves electrical signal without _______

A

decrement

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11
Q

membrane capacitance on signal decay

A

slows passive transmission of signal along axon

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12
Q

length constant

A

depends on resistance of membrane, cytoplasm, external solution

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13
Q

spread of electric current along interior of an axon in enhanced by

A

high membrane resistance

low cytoplasm resistance

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14
Q

in length constant equation what does each variable represent

A

Rm = resistance of a unit length of membrane

R1 = summed longitudinal internal and external resistance (Ri + Ro)

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15
Q

nonspiking neurons

A

very small neurons incapable of producing APs

graded signals conducted electrotonically to axon terminals without aid of APs

signals strong enough to release nt

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16
Q

where are nonspiking neurons found

A

retina

CNS

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17
Q

how does AP current move down an axon

A

Na current moves through activated patch of membrane, and depol adjacent patch

repolarized patch is refractory so AP travels in 1 direction

adjacent patch reaches threshold, current flows, and depol next patch

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18
Q

stim AP in middle of an axon

A

current moves in both directions but can’t get a backwards AP b/c membrane is in refractory state

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19
Q

propagation of an AP depends on 2 factors

A

passive cable properties that permit electrotonic spread of local current to adjacent patches of inactive memb.

electrical excitability of Na channels in axon memb.

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20
Q

why don’t neighboring axons excite each other when conducting current

A

high resistance of inactive membrane

small amount of current flowing is not enough to bring neighboring axon to threshold

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21
Q

speed of AP equation

A

v(p) = Δd / Δt

v(p) = velocity of propagation

Δ distance

Δ time

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22
Q

what does conduction velocity primarily depend on

A

how fast the membrane ahead of the active region is brought to threshold by local currents

higher length constant means farther the local currents can flow before they’re too weak to elicit threshold

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23
Q

how is length constant increased in squid, arthropods, annelids

A

increase in axonal diameter

reduces cytoplasmic resistance

why not in humans: takes up too much space

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24
Q

what do vertebrate do to increase length constant

A

myelinate axons

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25
Q

test speed of propagation

A

frog nerve muscle prep stimulated at 2 locations 3 cm apart

measure latency (time) to peak muscle twitch

muscle contraction moves a lever that scratches a piece of paper

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26
Q

myelin

A

glial cells wrapped around segments of axons to produce layers of insuating fatty membranes

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27
Q

2 effects of myelin on cable properties of neurons

A

increase transmembrane resistance

decrease effective membrane capacitance (thick)

greatly increase length constant

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28
Q

nodes of Ranvier

A

short unmyelinated gaps exposed to extracellular fluid

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29
Q

myelin is laid down by two kinds of glial cells

A

schwann cells : PNS

oligodendrocytes: CNS

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30
Q

saltatory conduction

A

occurs in myelinated axons

APs produced in small areas of membrane exposed at nodes of ranvier (Na moves in, tons of Na + K channels)

APs jump from node to node

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31
Q

is saltatory conduction fast?

A

yes, velocity of signal transmission enhanced

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32
Q

diseases of demyelination

A

multiple sclerosis: myelin sheath reduced in CNS

compromises sensory perception and control of coordinated movement

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33
Q

electrical synapse

A

pre-syn neuron electrically connected to post-syn neuron by gap junctions

rare

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34
Q

chemical synapse

A

APs in pre-syn neuron cause release of nt that diffuse across synaptic cleft

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35
Q

synaptic cleft

A

narrow gap separating membranes of pre and post syn neurons

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36
Q

neuromuscular junctions (NMJ)

A

synapses connecting motor neurons and the skeletal muscle fibers they control

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37
Q

some functions of nt

A

inc/dec # of ion channels inserted into membrane of post-syn cell

alter excitability of post-sun neuron by changing rate at which ion channels open or close

modify sensitivity of channels to activating signals

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38
Q

rectifying junctions

A

junctions where ionic current flows more readily in one direction than the other

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39
Q

fast/direct chemical synaptic transmission

A

found at the NMJ and CNS

AP reaches axon terminals and vesicles release nt that diffuses across cleft and binds receptors in post-syn membrane (opens ligand gated ion channels)

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40
Q

synaptic vesicles

A

membrane bound vesicles containing nt

release nt by exocytosis

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41
Q

nt binding post-syn receptors has what effect

A

allows brief ionic current to flow through membrane of post-syn cell

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42
Q

slow/indirect chrmical synaptic transmission

A

affect post-syn cell by activating receptors that alter levels of signal molecules that modify ion channels

multiple steps make it slower

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43
Q

fast chem synapses structure

A

small molecules

release nt at active zones in pre-syn memb.

44
Q

slow chem synapses structure

A

larger peptide molecules

release nt at many sites in pre-syn terminal

45
Q

what causes release of nt into cleft other than AP

A

AP stimulates release of Ca2+ from voltage gated Ca channels

this initiates exocytosis

46
Q

study of frog motor end plate (NMJ)

A

muscle membrane has junctional folds under depression (where pre-syn axon branches are to inc surface area)

active zones above folds release nt ACh and vesicles recycled

ACh causes post-syn Na and K ion channels to open

47
Q

breakdown of ACh in cleft

A

performed by AChE

acetylcholinesterase

48
Q

endplate potentials (epps)

A

post-syn potentials in muscle fibers

degrade with distance

49
Q

study of synaptic transmission at frog NMJ

A

muscle fiber has a resting pot

impale fiber with microelectrode at a point several mm from endplate to record resting pot and APs

50
Q

curare

A

blow dart poison

applied to frog nerve-muscle preparations

at some concentration APs fail and muscle does not contract

APs in motor neuron unaffected though and muscle can generate AP if current directly injected

51
Q

curare mechanism of action

A

interfere with synaptic transmission at NMJ

blocks some post-syn receptors and reduces size of epps

52
Q

how is curare useful

A

reduce size of epp below threshold so no AP, but can still record epps

53
Q

postsynaptic current (psc)

A

change in rate of ion flow across post-syn mem

54
Q

what drives psc

A

nt binding receptors to change amount of ionic current crossing membrane

direction and intensity of psc controlled by size of conductance and electrochemical driving force

55
Q

ions responsible for ps at NMJ

A

influx of Na partly canceled normally by smaller efflux of K

both move through post-syn ACh channels (less selective than voltage gated ion channels)

56
Q

are psc shorter lived than postsynaptic potentials (psp)?

A

yes, ACh only opens channels momentarily

57
Q

why does a psp last longer than psc

A

time depends on duration of psc and time constant of membrane

58
Q

reversal potential (Erev)

A

resting potential at which there is no change in voltage in post-syn cell

no net driving force on ions so no net charge movement

for 1 ion its the nernst potential

59
Q

excitatory postsynaptic potential (epsp)

A

any change in membrane potential of post-syn membrane that increases probability of an AP being generated in post-syn cell

60
Q

inhibitory postsynaptic potential (ipsp)

A

any change in membrane potential of post-syn membrane that reduces probability of AP being generated in post-syn cell

61
Q

if reversal potential of post-syn current is more pos than threshold the synapse is…

A

excitatory

62
Q

if reversal potential is more negative than threshold the synape is…

A

inhibitory

63
Q

inhibitory post-syn currents are typically carried through what channels

A

permeable to K and Cl-

64
Q

ACh is excitatory in…. and inhibitory in….

A

excitatory: NMJ opening Na/K channels
inhibitory: parasympathetic neurons innervating the heart (K channels open longer reducing frequency of spontaneous depolarizations that drive heart beat)

65
Q

presynaptic inhibition

A

inhibitory transmitter released from a terminal that ends on the pre-syn terminal of an excitatory axon

reduce amplitude of AP invading excitatory axon

66
Q

postsynaptic inhibition

A

globally reduces excitability of post-syn cell

67
Q

miniature endplate potentials

A

accidental release of nt from 1 vesicle resulting in a depol of .1mV

68
Q

amount of transmitter released varies directly with…

A

amount of depol in presyn terminal

more = more

if low extracellular Ca, less postsyn response

69
Q

function of Ca in nt release

A

concentration of Ca in NMJ must rise after an AP arrives in order to nt to be released

70
Q

docking of vesicles at active zones

A

SNARE proteins located in vesicular membrane (v-SNARE) and in plasma memb of active site (t-SNARE)

v and t SNARES form a complex to dock vesicles

71
Q

synaptotagmin

A

protein associated with memb of mature vesicles

interacts with proteins of SNARE docking complex to permit fast Ca dependent membrane fusion

72
Q

cholinergic

A

neurons that release ACh

73
Q

agonist

A

molecules that mimic that action of a nt b/c they are analogs

74
Q

antagonists

A

structural analogs that block nt binding sites

75
Q

synaptic desensitization

A

if nt remains in cleft too long, receptors become inactivated

76
Q

adrenergic neurons

A

neurons that use norepi or epi as transmitters

can be excitatory or inhibitory

77
Q

2 classes of ACh receptor

A

nicotinic (nAChR): NMJ; nicotine mimics action of ACh (fast direct mechanisms)

muscarinic (mAChR): toxin from mushrooms; target cells of parasympathetic ns (indirect mechanisms)

78
Q

electric ray and nAChR

A

high densities of these receptors in electroplax organ help them stun prey with high intensity electrical discharges

79
Q

structure of AChR

A

5 subunits

ligand must bind 2 alpha subunits to open channel

80
Q

denervated muscle fiber

A

crushed axon

causes AChR to spread out

81
Q

other nt-gated channels in neurons that are fast direct acting

A

GABA, glutamate

all have one subunit type that binds ligand

82
Q

ionotrophic glutamate receptors (iGluR)

A

modifications in synaptic strength that underlie learning and memory

2 receptors named for sensitivity to specific agonists

kainate

AMPA

NMDA

83
Q

AMPA and NMDA

A

appear to worth together in post-syn memb. in CNS

84
Q

NMDA opening

A

both gly and glu must bind to open

AND depol must happen through AMPA channel –> NMDA (otherwise ion channel blocked by Mg)

85
Q

AMPA selectivity

A

selective for Na ions

86
Q

NMDA selectivity

A

allow Ca and Na to pass

Ca intracellular messenger

87
Q

G-proteins

A

membrane linked molecules that play a role in signal transduction and are linked to slow synaptic receptors

88
Q

how does G protein complex work

A

nt receptor protein (spans membrane) gets nt bound extracellularly and activates G protein on cytoplasmic face

G protein regulates activity of effector proteins which could be ion channels, enzymes (control [ ] 2nd messengers) or both

89
Q

metabotrophi gluatamate receptors lack…

A

an ion channel

G-protein coupled that modify intracellular pathways

90
Q

neuromodulation

A

pre-syn neuron can modify synaptic responses in post-syn neuron and other neurons in its vicinity

last from secs to mins

91
Q

synaptic plasticity

A

changes in synaptic efficacy that are longer lasting or permanent

92
Q

fast epsp

A

ACh binds nAChR

93
Q

slow epsp

A

ACh binds mAChR

94
Q

late slow epsp

A

GnRH like peptide

released from pre-syn neuron, but not directly onto post-syn neuron

enhances fast responses

95
Q

density of inhibitory synapses contacting many neurons is highest near the…

A

axon hillock

96
Q

synaptic summation

A

addition of several post-syn potentials in post-syn neuron

97
Q

spatial summation

A

summed inputs coming from 2 or more different neurons

98
Q

temporal summation

A

summed inputs from a series of high-frequency APs arriving at a single synaptic terminal

99
Q

neuronal plasticity

A

modification of neuronal function as a result of experience

100
Q

homosynaptic modulation

A

activity in terminal itself causes a change in release of nt

101
Q

heterosynaptic modulation

A

changes in pre-syn function induced by action of a modulator substance released from another close axon terminal

102
Q

synaptic facilitation

A

when the amplitude of a second stim (summation) is greater than adding the two stims together

due to lingering Ca in pre-syn terminal (more nt release)

103
Q

tetanic stim (depression)

A

normal ca: reduced efficacy at NMJ b/c depleted vesicles

low Ca: no depression b/c no depletion

104
Q

tetanic stim (potentiation)

A

normal ca: occurs after depression, lasts a long time

low ca: occurs immediately, short lived

105
Q

heterosynaptic facilitation

A

amount of nt released increased by presense of modulator

alters number of Ca ions that enter pre-syn terminals following AP

106
Q

long term potentiation (LTP)

A

neurons innervating hippocampus stimulated at high frequency

increase in amplitude of post-syn potentials long after stim ends

excitatory nt glutamate

AMPA/NMDA receptors contribute

107
Q

long term depression (LTD)

A

repeated low frequency stimulation of hippocampus

Animal Physiology (26 decks)

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