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Neurobiology > Unit 2 Notes > Flashcards

Unit 2 Notes Flashcards

1
Q

movement at synapse

A
  1. ) voltage gated calcium channels open at synapse in response to depolarization caused by action potential
  2. ) calcium enters enters presynaptic neuron and binds to motor proteins which are on synaptic vesicles
  3. ) vesicles merge with presynaptic membrane
  4. ) insides released in synaptic cleft
  5. ) neurotransmitters bind to receptors on postsynaptic membrane
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2
Q

what makes AP start

A
  1. ) begin with receptor potential- graded (have to have high enough to open enough Na+ channels)
  2. ) greater graded potential, open more Na+ channels, depolarizes cell
  3. ) depolarize enough to hit threshold -> increase in Na+ conductance -> inward current of Na+
  4. ) conductance K+ also increases -> K+ outward to repolarize cell
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3
Q

voltage clamp experiments

A

-permits us to set membrane potential of cell almost instantaneously to any level and hold it there while recording current flow across membrane

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4
Q

capacitive current

A
  • initial brief surge of current
  • occurs b/c step from one potential to another alters charge in membrane capacitance
  • due to membrane properties
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5
Q

early inward current

A
  • due to Na+ inward current

- depolarize cell

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6
Q

leak current

A

-small K+ and Cl- outward current

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7
Q

why does current flip direction at +65 mV

A
  • beyond 62 (Na+ equilibrium)

- with greater depolarization, Na+ inward current becomes smaller and then reverses to outward current

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8
Q

Na+ channels

A
  • open quickly, so have inward current

- rises rapidly, but decreases to zero

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9
Q

K+ channels

A
  • open slowly relative to Na+ channels
  • outward current
  • once developed, remains high
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10
Q

absolute refractory period

A
  • no action potential is possible even with applied extracellular depolarization
  • due to Na+ channels having an inactivation gate on them
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11
Q

relative refractory period

A
  • can still get another AP, but would require a stronger stimulus
  • due to K+ channels still open (slow to close)
  • K+ conductance high (too high for Na+ to override)
  • threshold returns to normal, K+ channels close, Na+ inactivation removed
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12
Q

Hodgkin and Hukley findings

A

Depolariztion of membrane leads to…

  1. ) activation of sodium conductance mechanism
  2. ) subsequent inactivation of that mechanism
  3. ) delayed activation of K+ conductance mechanism
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13
Q

inactivation

A
  • decline to zero of Na+ current after it rises quickly
  • occurs b/c the potential is greater than the equilibrium potential of Na+ (65 mV)
  • occurs even if the cell is still depolarizing
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14
Q

potassium leaves cell

A
  1. ) depolarization decreased
  2. ) Na+ conductance decreases
  3. ) Na+ current decreases
  4. ) excess outward current causes repolarization
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15
Q

2 reasons nerve fiber can’t produce second AP immediately

A
  1. ) absolute refractory period- Na+ channel inactivation

2. ) relative refractory period- K+ channels slowly closing

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16
Q

CNS neuron

A
  • brief spikes w/ high frequency
  • activate and deactivate rapidly
  • rapid repolarization
  • rapid removal Na+ channel inactivation
  • more AP/given time
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17
Q

gating currents

A
  • generated by movement of charges in transmembrane helicies of ion channel
  • helicies move in response to change in membrane voltage, opening or closing gate
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18
Q

ball-and-chain model

A
  • responsible for inactivation of voltage activated Na+ channel
  • ball = clump of AA on cytoplasmic side (Mg2+)
  • chain = AA residues
  • depolarize -> ball binds to site inside channel and blocks pore b/c positive charge of pall pushed out of inside and up channel when repelled by positive charge accumulated from depolarization
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19
Q

channelopathies

A
  • channel being formed badly
  • startle disease
  • epilepsy, seizures- damage to K+ channels
  • cell fires when not supposed to
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20
Q

gate closed

A

positive charge in pore is attracted to cytosol

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21
Q

depolarize cell and gate

A

more positive inside results in the positive charges of pore moving up and gate opening

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22
Q

importance of calcium

A
  • keeps cell from being too excitable
  • acts like a charge buffer on outside of membrane between + and - charges
  • low Ca2+ environment- no charge buffer and membrane is more excitable (cells fire more readily)
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23
Q

lack of Ca2+

A

no buffer -> increase excitability of membrane (not good)

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24
Q

afterhyperpolarizaing potentials

A
  • right after AP
  • occurs b/c delayed rectifier channels continue to open for period that outlasts AP
  • results in increasing K+ conductance, which drives membrane toward K+ equilibrium potential
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25
Q

Calcium-activated potassium channels

A
  • Ca enters with Na
  • leads to K channels opening
  • brings the excitability of the cell down- diminishes response
  • habituation
  • cell essentially calms down
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26
Q

why doesn’t AP degrade

A
  • signal refreshed along conduction

- axon is excitable along length

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27
Q

myelinated cell

A
  • facilitate current flow
  • Nodes of Ranvier in between myelin
  • lots of Na+ channels accumulated at nodes
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28
Q

spike initiation zone

A
  • sensory nerve endings
  • axon hillock
  • spike initiation more likely at sites where there is a high density of voltage-gated sodium channels
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29
Q

distribution of sodium channels

A

-piled up densely at nodes of Ranvier and sensory nerve endings

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30
Q

orthodromic

A
  • AP travels in one direction

- typically from soma to terminal

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31
Q

antidromic

A
  • backward propagation

- usually experimentally driven

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32
Q

typical conduction velocity

A

10 m/s

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33
Q

length of AP

A

2 milliseconds

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34
Q

what determines spread of AP along membrane

A

axon structure

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35
Q

axon excitability

A
  • depends on diameter (bigger -> faster)

- depends on # voltage-gated channels

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36
Q

habituation

A

adaptation so don’t respond vigorously every time

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37
Q

electrotonic potentials

A

as you increase distance from current passing electrode in nerve fiber, the potential become smaller and slower
*decay of response with distance is exponential

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38
Q

membrane resistance low relative to cytoplasm

A

current leaks outward through membrane before it can spread far

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39
Q

high resistance membrane

A
  • allow significant portion of current to spread laterally before escaping to the external solution
  • depends on surface area of fiber
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40
Q

length constant properties

A
  • increases with membrane resistance

- decreases with internal longitudinal resistance

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41
Q

length constant

A

distance that a electric potential will travel along neuron via passive conduction

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42
Q

fiber diameter increase

A
  • internal resistance decreases more rapidly than membrane resistance
  • results in more membrane resistance than internal
  • further conduction
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43
Q

why is potential rise slower at points more distant to electrode

A

internal longitudinal resistance reduces current flowing

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44
Q

what influences rate of AP propagation

A
  1. ) space constant- want large

2. ) time constant- want small

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45
Q

small time constant

A

membrane will depolarize to threshold quickly and conduction velocity will be high

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46
Q

saltatory conduction

A
  • ions cannot flow easily in or out of high-resistance myelin, so AP “jumps” from one node of Ranvier to the next
  • increases conduction velocity
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47
Q

electrically coupled

A

-special intercellular structures allow processes of one neuron to be in electrical continuity with the next (allow current flow between them)
cardiac, smooth muscle, epithelial, gland cells, and neurons

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48
Q

gap junction

A
  • electrical synapse
  • low resistance connection that allows transfer of electrical signals from one cell to the next
  • collection of connexons
  • fast link between pre and post synaptic cell
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49
Q

connexon

A

proteins that form aqueous channels between cytoplasms of adjacent cells

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50
Q

oligodendroglia

A

-myelinate in CNS

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51
Q

extrastriate area

A
  • region of occipital cortex that is sensitive to motion and perception
  • integration
  • more complex receptive fields
  • neural connections diverge
  • motion, color, and form
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52
Q

myelogenesis

A

glial cell development

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53
Q

when are axons fully myelinated

A
  • about age 25

- athletes peak in mid 20s

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54
Q

plasticity

A

-neural connections and networks change

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55
Q

higher peak

A
  • action potential big

- fiber myelinated

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56
Q

synaptic transmission

A
  • how cells communicate with one another
    1. ) direct
    2. ) indirect
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57
Q

direct communication

A
  1. ) chemical synapse (ionotropic)

2. ) electrical synapse

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58
Q

indirect communication

A
  • via chemical receptor changes cell behavior, but not in regards to resting membrane potential
  • g-protein coupled receptor (metabotropic)
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59
Q

electrical synapse (gap junction)

A
  • incredibly fast transmission
  • no lag
  • presynaptic has full AP
  • post synaptic has a much smaller AP- indicates that not a ton of ions actually go thru
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60
Q

chemical synaptic transmission

A

-secretion of specific chemical by a nerve terminal and its interaction with specific postsynaptic receptors

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61
Q

bouton

A
  • nerve terminal swelling
  • pre-synaptic membrane has electron dense regions with clusters of synaptic vesicles
  • lots of mitochondria for ATP
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62
Q

excitatory post synaptic potential (EPSP)

A

synaptic potential that excites a post synaptic cell

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63
Q

inhibitory post synaptic potential (IPSP)

A

synaptic potential that inhibits a post synaptic cell

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64
Q

curare

A

block postsynaptic receptors, reducing end plate potential amplitude below threshold

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65
Q

ionophoresis

A

method of ejecting charged molecules, such as ACh, from pipettes

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66
Q

ACh and permeability

A
  • ACh produces a nonspecific increase in permeability of the postsynaptic membrane to small ions (Na+, Ca2+, and K+)
  • does not increase Cl- permeability
  • general increase in cation permeability
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67
Q

reversal potential

A
  • membrane potential at which a neurotransmitter causes no net current flow of ions through that neurotransmitters receptor channel
  • aka- equilibrium potential
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68
Q

differences between CNS synapses and neuromuscular junction

A
  1. ) principal excitatory transmitter is L-glutamate (not ACh)
  2. ) there are 2 glutamate ionotropic receptors (AMPA and NMDA)- neither structurally homologous to nicotine receptor
69
Q

AMPA

A
  • glutamate receptor in CNS
  • similar permeability and function as nicotine receptor in neuromuscular junction
  • mediates fast excitatory transmission throughout CNS
70
Q

NMDA

A
  • glutamate receptor of CNS
  • blocked by Mg2+ at normal RMP
  • not involved in fast signaling b/c of Mg2+
  • gate slowly
  • higher permeability to Ca2+
71
Q

Mg2+ binding to NMDA channel

A
  • binds extracellularly
  • even if activated, current can’t flow until cell depolarized towards zero
  • bound tightly b/c attracted to negative RMP
  • binding loosens as cell depolarizes
72
Q

NMJ inhibition

A

-increasing anion permeability

73
Q

NMJ excitation

A

-increasing cation permeability

74
Q

reciprocal inhibition

A
  • due to way circuits are built
  • when extensor firing, flexor is not
  • inhibitory interneurons go to excitatory interneuron of one that should not be firing
75
Q

interneuron

A
  • neuron that forms connection between other neurons

- Ex: neuron from toe to spine -> interneuron in spine -> neuron to brain

76
Q

presynaptic inhibition

A
  • preventing EPSP from happening in first place
  • or modulating transmitter release
  • much more specific than post-synaptic inhibition
  • often targets one input
  • before synapse excitatory input shut down
  • timing is everything
77
Q

post synaptic inhibition

A
  • basically shutting cell down

- preventing from fire

78
Q

why delay in excitation

A

-neurotransmitter has to drift across synapse

79
Q

post synaptic receptors and inhibition

A

-receptors on postsynaptic respond to GABA binding by opening Cl- binding

80
Q

glycine without chloride extracellularly

A
  • Cl- efflux
  • no change in membrane potential or input resistance upon glycine binding to inhibitory channel
  • no ions besides Cl- pass through inhibitory channels
81
Q

inhibitory response key

A

-involves increase in Cl- permeability, so reversal potential for inhibitory current is equal to chloride equilibrium (-62 mV)

82
Q

what binds and activates chloride channel

A
  • GABA

- glycine

83
Q

maximum presynaptic inhibitory effect

A
  • impulse must arrive in inhibitory presynaptic terminal before action potential arrives in excitatory terminal
  • timing is everything
84
Q

autoinhibition

A
  • glutamate and GABA spill over from synaptic cleft, back onto presynaptic terminals
  • activates metabotropic (g protein) receptors
85
Q

metabotropic receptors presynaptic terminal

A
  • suppress calcium entry into the terminals
  • reduce neurotransmitter release b/c no Ca2+ to bind to motor proteins carrying vesicles
  • slower than presynaptic inhibition through ionotropic receptors, but lasts longer
86
Q

delayed timing of presynaptic metabotropic receptors

A

-due to time takes for receptor to activate a g protein and inhibit Ca2+ channels

87
Q

dystrophin glycoprotein complex

A
  • links together the myofiber cytoskeleton, membrane, and ECM
  • provides structural support for muscle cell
  • plays a key role in AChR localization
88
Q

rapsyn

A
  • AChR-associated proteins

- key role in linking MuSK and AChRs to cytoskeleton

89
Q

localizing ACh receptors

A
  • plasticity- developing motor circuits
  • how motor neurons make synapses with muscle tissue
  • motor neuron releases agrin
  • agrin affiliates with MuSK receptor post-synaptically
  • MuSK interacts with other proteins in postsynaptic cell
  • proteins aggregate cholernergic receptors
90
Q

remembering

A
  • changing circuits

- plasticity

91
Q

long-term potentiation (LTP)

A

-change to synapse that makes cell more likely to fire (plasticity)
-associated with insertion of AMPA receptors at synapses
-change due to having more receptors in place
synapse strengthened

92
Q

long-term depression (LTD)

A
  • leads to forgetting

- connections are plastic

93
Q

forgetting at cellular level

A
  • LTD
  • AMPA receptors retract
  • synapse loses strength
94
Q

what makes neuromuscular junctions

A
  • agrin

- cholernergic receptors

95
Q

where are electrical synapses

A
  1. ) reflex pathways where fast response is necessary

2. ) where electrical transmission assists in coordinating or amplifying activity of other neurons

96
Q

crayfish escape reflex

A
  • electrical synapse between pre and post synaptic neurons

* rectified- not bidirectional

97
Q

rectify

A
  • electrical coupling across electrical synapse goes in one direction only
  • pre -> post synaptic cell
  • not common of most electrical synapses, but present in crayfish
98
Q

coupling ratio

A
  • degree of electrical coupling between cells

- Ex: 1:4 means 1/4 presynaptic voltage appears on post synaptic cell

99
Q

strong coupling

A
  • resistance of junction between cells must be low

- must have reasonable match between sizes of pre and post elements

100
Q

chemical and electrical synapses together

A
  • chemical presynaptic potential is preceded by electrical presynaptic potential
  • occurs widely in vertebrates
101
Q

electrical synaptic transmission advantage

A
  1. ) absence of synaptic delay
  2. ) more reliable
  3. ) less likely to fail due to synaptic depression or toxins blocking
  4. ) intracellular transfer of Ca2+, ATP, and cAMP
102
Q

blend of neurotransmitter

A
  • each neuron has own specific blend
  • cotransmitters
  • typically dominated by a certain nt
103
Q

how to identify neurotransmitter

A
  1. ) synthesized and stored by cell
  2. ) released
  3. ) produces effect in target cell
  4. ) removed from cleft
104
Q

identify serotonergic structure

A
  • identify serotonin synthesizing enzymes
  • identify synaptic vesicle transporters
  • identify reuptake transporters
  • don’t find degradative NZs
  • look at slide for rest
105
Q

methods of localizing neurotransmitter systems

A
  1. ) immunocytochemistry
  2. ) in situ hybridization
  3. ) microionophoresis
106
Q

immunocytochemistry

A

-using fluorescently labeled secondary antibodies to identify neurotransmitter and structures

107
Q

in situ hybridization

A
  • uses labeled complementary DNA strand to localize specific sequences
  • bright areas show mRNA for particular neurotransmitter
108
Q

microionophresis

A
  • using micropipette to push out positively charged current
  • looking at synaptic function
  • is synapse using chemical you think it is
109
Q

ACh release

A
  • little released at rest (continuously synthesized)
  • bunch released at stimulation
  • can act on both ionotropic and metabotropic receptors
110
Q

blocked cholenergic reuptake

A
  • blocks choline from re-entering cell
  • release of ACh drops significantly
  • supports that choline is necessary for ACh to by synthesized
111
Q

ACh synthesis

A
  • made from acetyl CoA and choline
  • acetyl CoA and choline brought together by choline acetyltransferase
  • ACh transporter puts into vesicle with ATP
  • vesicle releases ACh in cleft
  • AChE breaks excess ACh into acetate and choline
  • choline brought back into cell (acetic acid diffuses away)
112
Q

classical low molecular weight neurotransmitters

A

-produced within axon terminal from cellular metabolites and are incorporated into small synaptic vesicles for storage and release
Ex: ACh and NE

113
Q

neuropeptide transmitters

A
  • synthesized in cell body
  • packaged in large dense-core vesicles, and shipped down axon
  • slow process
114
Q

reducing ACh cytoplasmic concentration

A
  • sequester ACh into vesicles

* balance between synthesis and vesicular uptake is critical

115
Q

feedback inhibition

A
  • rate-limiting step in a biosynthetic pathway is inhibited by the final product
  • Ex: norepinephrine
116
Q

catecholamines

A
  • dopamine
  • norepinephrine
  • epinephrine
  • no fast NZ to degrade in cleft- typically take back up
117
Q

cocaine and NE

A
  • blocks mechanism that brings NE back into cell

- NE in cleft longer -> drives pleasure response

118
Q

NE, dopamine, and epinephrine accumulation

A
  • all 3 inhibit tyrosine hydroxylase

- inhibition doesn’t occur until steady state is reached- rate of synthesis is equal to rate of degradation and release

119
Q

tetrahydrobiopterin

A
  • necessary cofactor for tryptophan hydroxylase in serotonin synthesis
  • necessary cofactor for tyrosine hydroxylase in NE synthesis
120
Q

tryptophan

A
  • found in meats, grain, and dairy

- neurons can’t synthesize, so must be transported from blood into CSF

121
Q

Factors influencing serotonin abundance

A
  1. ) amount of tryptophan in blood

2. ) amount of available tetrahydrobiopterin

122
Q

pyridoxal phosphate

A

-cofactor necessary for GABA synthesis

123
Q

glutamate synthesis

A
  • major excitatory neruotransmitter in brain
  • synthesized from glutamine in releasing neurons
  • after release some taken up in presynaptic cell, most taken up by glial cells
  • glial cells convert to glutamine and release at nerve terminals
  • nerve cell converts glutamine to glutamate
124
Q

amino acidergic neurotransmitters

A
  • GABA
  • glutamate
  • glycine
125
Q

solute carrier transporters (SLC)

A
  • mediate accumulation of transmitters in synaptic vesicles
  • some transport more than one nt (b/c not enough different kinds for all nts)
  • poor substrate specificity
126
Q

axonal transport

A

-movement of mitochondria, synaptic vesicles, lipids, and proteins along axon from neuron cell body to axon terminal

127
Q

anterograde

A

-soma to terminal

128
Q

retrograde

A
  • terminal to soma
  • used for recycling or degradation of membrane-enclosed organelles in cell body
  • crucial for movement of nerve growth factor from axon to cell body
129
Q

tracers

A
  • used to map synaptic connections by visualizing axons and cell bodies
  • fluorescently labeled structures are observed during axonal transport
130
Q

kinesin

A
  • accessory factor

- powers anterograde transport along microtubule tract (toward terminal)

131
Q

dynein

A
  • accessory factor

- powers retrograde transport along microtubule tract (toward soma)

132
Q

how is direction of organelle movement regulated

A

-specific receptors for either kinesin or dynein on surface of organelles

133
Q

mechanisms for transmitter removal from synaptic cleft

A
  1. ) diffusion
  2. ) degradation
  3. ) uptake into glial cells or nerve terminals
    * prompt removal is crucial for normal synaptic function
134
Q

direct excitatory neurotransmitter in CNS

A

glutamate

135
Q

direct inhibitory nts in CNS

A

GABA and glycine

136
Q

indirect transmitters

A
  • ACh
  • neuropeptides
  • monoamines
  • ATP
  • all act on G protein-coupled receptors (ACh and ATP also act on ionotrophic)
137
Q

glutamate

A
  • excitatory transmitter of CNS

- activates both AMPA and NMDA receptors

138
Q

GABA and glycine receptors

A

-homologous to ACh receptors, but permeable to Cl- instead of cations

139
Q

site of ACh release cholinergic receptors CNS

A
  • major difference between CNS and PNS cholinergic systems
  • release at varicosities (swellings) along axon that don’t make contact with post synaptic neuron
  • still fast
140
Q

volume transmission

A

-neurotransmitter is released distal to receptors (variscosities) and must diffuse to receptor
-behave more like hormones
Ex: ACh in cortex

141
Q

Alzheimer’s disease

A

-degeneration of the basal forebrain cholinergic neurons and of their cortical and hippocampal terminals

142
Q

biogenic amines

A
  • NE, histamine, dopamine, serotonin
  • influence attention, sleep, arousal, and mood
  • volume transmission out of unmyelinated axons
  • activate G-protein coupled receptors
143
Q

locus coeruleus

A
  • part of pons where noradreneric neurons are concentrated

- Ex: norepinephrine big player

144
Q

raphe nuclei

A
  • concentration of serotonergic neurons in brain stem

- regulate sleep wake cycle and food intake

145
Q

dopamine

A
  • intermediate in NE pathway unless neuron lacks dopamine hydrozylase
  • role in pleasure and reward
146
Q

dopaminergic neurons

A
  • concentrated in brain stem- substantia niagra
  • concentrated in ventral tegmental area- goes to frontal lobe (pleasure)
  • control prolactin secretion
147
Q

cocaine

A
  • inhibits dopamine transporter and increases dopamine levels (feels good)
  • nicotine also increases levels, but by different mechanism
148
Q

histamine

A
  • anti-inflammatory and causes drowsiness

- histamine-containing neurons abundant in hypothalamus

149
Q

Substance P

A

-neuropeptide involved in pain

150
Q

Opioid peptides

A
  • involved in control of pain

- activate inward rectifying K+ channels, inhibiting neurons

151
Q

orexins

A
  • neuropeptides that regulate sleep and appetite
  • glucose and leptin inhibit orexin release
  • ghrelin stimulates release
152
Q

oxytocin and vasopressin

A

-affect social behavior
-oxy- milk (cuddley)
vaso- thirst

153
Q

enkephalins

A

-neuropeptide related to opiate that inhibits neurotransmitters in the pathway for pain and emotion

154
Q

treatment for depression

A
  • SSRIs

- serotonin remains in cleft longer

155
Q

why does AP only go one way

A

-once it starts region behind is refractory

156
Q

large dendrite

A
  • synaptic potential larger b/c more channels

- synaptic potential will spread farther toward cell body

157
Q

Golgi vs Ramon and Cajal

A
  • Golgi: thought neurons were continuous with one another
  • Ramon and Cajal: thought neurons were within contact with one another
  • both were correct
158
Q

Gap junction key points

A
  1. ) speed

2. ) crayfish escape reflex

159
Q

ACh channel closing

A

-ACh is rapidly hydrolyzed in cleft by AChE, so concentration falls quickly, preventing further channel opening

160
Q

Postsynaptic and presynaptic inhibition differences

A
  1. ) post- reduces excitability of entire cell

2. ) pre- specific, aims at particular input, so post can respond to other inputs

161
Q

ionotropic presynaptic inhibition receptors

A

-channels respond to rapidly upon transmitter binding

162
Q

microtubules

A
  • organelles (vesicles and mitochondria) attach to microtubules, which use ATP to transport along track in axons
  • have polarity with positive end pointing toward terminal
  • responsible for fast axonal transport
163
Q

ACh left in synapse for too long

A
  • receptor becomes desensitized
  • muscle becomes refractory
  • paralysis
  • AChE crucial when this happens
164
Q

feel good

A

-dopamine and serotonin

165
Q

Parkinson’s

A
  • loss of dopaminergic cells in substantia niagra

- substantia niagra big role in output of movement

166
Q

rate limiting step catecholinameinergic neurons

A
  • hydroxylation of tyrosine

- coversion of tyrosine to dopa via tyrosine hydroxylase

167
Q

MAO

A
  • monoamine oxidase
  • bound to outer membrane of mitochodria
  • helps degrade excess dopamine (not rapid like AChE)
168
Q

ambien

A

dumps massive amounts of serotonin

Neurobiology (4 decks)

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