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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
test speed of propagation
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
26
myelin
glial cells wrapped around segments of axons to produce layers of insuating fatty membranes
27
2 effects of myelin on cable properties of neurons
increase transmembrane resistance decrease effective membrane capacitance (thick) greatly increase length constant
28
nodes of Ranvier
short unmyelinated gaps exposed to extracellular fluid
29
myelin is laid down by two kinds of glial cells
schwann cells : PNS oligodendrocytes: CNS
30
saltatory conduction
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
31
is saltatory conduction fast?
yes, velocity of signal transmission enhanced
32
diseases of demyelination
multiple sclerosis: myelin sheath reduced in CNS compromises sensory perception and control of coordinated movement
33
electrical synapse
pre-syn neuron electrically connected to post-syn neuron by gap junctions rare
34
chemical synapse
APs in pre-syn neuron cause release of nt that diffuse across synaptic cleft
35
synaptic cleft
narrow gap separating membranes of pre and post syn neurons
36
neuromuscular junctions (NMJ)
synapses connecting motor neurons and the skeletal muscle fibers they control
37
some functions of nt
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
38
rectifying junctions
junctions where ionic current flows more readily in one direction than the other
39
fast/direct chemical synaptic transmission
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)
40
synaptic vesicles
membrane bound vesicles containing nt release nt by exocytosis
41
nt binding post-syn receptors has what effect
allows brief ionic current to flow through membrane of post-syn cell
42
slow/indirect chrmical synaptic transmission
affect post-syn cell by activating receptors that alter levels of signal molecules that modify ion channels multiple steps make it slower
43
fast chem synapses structure
small molecules release nt at active zones in pre-syn memb.
44
slow chem synapses structure
larger peptide molecules release nt at many sites in pre-syn terminal
45
what causes release of nt into cleft other than AP
AP stimulates release of Ca2+ from voltage gated Ca channels this initiates exocytosis
46
study of frog motor end plate (NMJ)
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
breakdown of ACh in cleft
performed by AChE acetylcholinesterase
48
endplate potentials (epps)
post-syn potentials in muscle fibers degrade with distance
49
study of synaptic transmission at frog NMJ
muscle fiber has a resting pot impale fiber with microelectrode at a point several mm from endplate to record resting pot and APs
50
curare
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
curare mechanism of action
interfere with synaptic transmission at NMJ blocks some post-syn receptors and reduces size of epps
52
how is curare useful
reduce size of epp below threshold so no AP, but can still record epps
53
postsynaptic current (psc)
change in rate of ion flow across post-syn mem
54
what drives psc
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
ions responsible for ps at NMJ
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
are psc shorter lived than postsynaptic potentials (psp)?
yes, ACh only opens channels momentarily
57
why does a psp last longer than psc
time depends on duration of psc and time constant of membrane
58
reversal potential (Erev)
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
excitatory postsynaptic potential (epsp)
any change in membrane potential of post-syn membrane that increases probability of an AP being generated in post-syn cell
60
inhibitory postsynaptic potential (ipsp)
any change in membrane potential of post-syn membrane that reduces probability of AP being generated in post-syn cell
61
if reversal potential of post-syn current is more pos than threshold the synapse is...
excitatory
62
if reversal potential is more negative than threshold the synape is...
inhibitory
63
inhibitory post-syn currents are typically carried through what channels
permeable to K and Cl-
64
ACh is excitatory in.... and inhibitory in....
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
presynaptic inhibition
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
postsynaptic inhibition
globally reduces excitability of post-syn cell
67
miniature endplate potentials
accidental release of nt from 1 vesicle resulting in a depol of .1mV
68
amount of transmitter released varies directly with...
amount of depol in presyn terminal more = more if low extracellular Ca, less postsyn response
69
function of Ca in nt release
concentration of Ca in NMJ must rise after an AP arrives in order to nt to be released
70
docking of vesicles at active zones
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
synaptotagmin
protein associated with memb of mature vesicles interacts with proteins of SNARE docking complex to permit fast Ca dependent membrane fusion
72
cholinergic
neurons that release ACh
73
agonist
molecules that mimic that action of a nt b/c they are analogs
74
antagonists
structural analogs that block nt binding sites
75
synaptic desensitization
if nt remains in cleft too long, receptors become inactivated
76
adrenergic neurons
neurons that use norepi or epi as transmitters can be excitatory or inhibitory
77
2 classes of ACh receptor
nicotinic (nAChR): NMJ; nicotine mimics action of ACh (fast direct mechanisms) muscarinic (mAChR): toxin from mushrooms; target cells of parasympathetic ns (indirect mechanisms)
78
electric ray and nAChR
high densities of these receptors in electroplax organ help them stun prey with high intensity electrical discharges
79
structure of AChR
5 subunits ligand must bind 2 alpha subunits to open channel
80
denervated muscle fiber
crushed axon causes AChR to spread out
81
other nt-gated channels in neurons that are fast direct acting
GABA, glutamate all have one subunit type that binds ligand
82
ionotrophic glutamate receptors (iGluR)
modifications in synaptic strength that underlie learning and memory 2 receptors named for sensitivity to specific agonists kainate AMPA NMDA
83
AMPA and NMDA
appear to worth together in post-syn memb. in CNS
84
NMDA opening
both gly and glu must bind to open AND depol must happen through AMPA channel --> NMDA (otherwise ion channel blocked by Mg)
85
AMPA selectivity
selective for Na ions
86
NMDA selectivity
allow Ca and Na to pass Ca intracellular messenger
87
G-proteins
membrane linked molecules that play a role in signal transduction and are linked to slow synaptic receptors
88
how does G protein complex work
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
metabotrophi gluatamate receptors lack...
an ion channel G-protein coupled that modify intracellular pathways
90
neuromodulation
pre-syn neuron can modify synaptic responses in post-syn neuron and other neurons in its vicinity last from secs to mins
91
synaptic plasticity
changes in synaptic efficacy that are longer lasting or permanent
92
fast epsp
ACh binds nAChR
93
slow epsp
ACh binds mAChR
94
late slow epsp
GnRH like peptide released from pre-syn neuron, but not directly onto post-syn neuron enhances fast responses
95
density of inhibitory synapses contacting many neurons is highest near the...
axon hillock
96
synaptic summation
addition of several post-syn potentials in post-syn neuron
97
spatial summation
summed inputs coming from 2 or more different neurons
98
temporal summation
summed inputs from a series of high-frequency APs arriving at a single synaptic terminal
99
neuronal plasticity
modification of neuronal function as a result of experience
100
homosynaptic modulation
activity in terminal itself causes a change in release of nt
101
heterosynaptic modulation
changes in pre-syn function induced by action of a modulator substance released from another close axon terminal
102
synaptic facilitation
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
tetanic stim (depression)
normal ca: reduced efficacy at NMJ b/c depleted vesicles low Ca: no depression b/c no depletion
104
tetanic stim (potentiation)
normal ca: occurs after depression, lasts a long time low ca: occurs immediately, short lived
105
heterosynaptic facilitation
amount of nt released increased by presense of modulator alters number of Ca ions that enter pre-syn terminals following AP
106
long term potentiation (LTP)
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
long term depression (LTD)
repeated low frequency stimulation of hippocampus

Animal Physiology (26 decks)

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