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NSC 201 > Unit 2: Neurophysiology > Flashcards

Unit 2: Neurophysiology Flashcards

1
Q

Electrical potential

A

Voltage, all living cells have it across their membranes (Vm)

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2
Q

How do water molecules bind to ions?

A

Electrostatically

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3
Q

Hydrated diameter

A

The water/ion molecule complex has a larger diameter than the ion itself, important limiting factor for ions moving through pores (channels) in membrane

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4
Q

Ohm’s Law

A

Voltage (V)= I (current) R (resistance)
OR
Current= Voltage*Conductance (G=1/R)

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5
Q

How do non-polar, fat soluble (lipophilic/hydrophobic) molecules cross membrane?

A

They dissolve in the lip bilayer

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6
Q

How do polar, water soluble (lipophobic/hydrophilic) molecules cross membrane?

A

They only cross through ion channels or carrier molecule “poles” in membrane

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7
Q

Ion channels/ what they are composed of

A

They are complex proteins composed of 4-6 polypeptide subunits (has hydrophobic surface that associates with phospholipid bilayer), form an aqueous pore (opening) where ions can pass

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8
Q

Ion channels show 4 levels of protein structure

A
  1. Primary: chain of AAs linked by peptide bonds
  2. Secondary: membrane spanning segments, lipophilic AAs, coil into alpha helices
  3. Tertiary: folded alpha helices create a subunit
  4. Quaternary: multiple subunits assemble together
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9
Q

Fundamental properties of channels (3)

A
  1. Channels are gated (open –> closed)
  2. Channels are selective (selectivity based on chemical properties of AA and diameter of pore)
  3. Ion flow is passive
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10
Q

Channel types (5)

A
  1. Random
  2. Voltage
  3. Chemical
  4. Chemical AND voltage-gated
  5. Mechanical-gated
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11
Q

Random channels

A

Open or close randomly, leakage channels

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12
Q

Voltage channels

A

Open or close depending on membrane voltage

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13
Q

Chemical channels

A

Open or close by binding with a “ligand” often referred to as a “messenger” (extracellular messenger: “neurotransmitter“; intracellular messenger: “second messenger”)

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14
Q

Chemical and voltage-gated channels

A

Opened by binding transmitter only when membrane voltage is favorable

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15
Q

Mechanical-gated channels (“stretch” channels)

A

Opened by membrane deformation

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16
Q

Diffusion

A

Movement of substances down a concentration gradient

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17
Q

Random (Brownian) Motion

A

Motion of molecules in solution eventually distributes substances uniformly within a compartment

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18
Q

What causes the formation of a chemical gradient?

A

Lipid bilayer lacking channels resists movement across it

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19
Q

Concentration Gradient

A

Difference in (ion) concentration within compartment or across a barrier

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20
Q

What does the magnitude of the concentration gradient (Wc) depend on?

A

Log ration of extracellular to intracellular concentration

Wc=RT (ln[out] -ln[in])= 2.3RTlog10([out]/[in])

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21
Q

Equilibrium

A

Ion exchange is equal in magnitude, and opposite in direction

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22
Q

What does separation of charge cause?

A

Voltage difference across membrane

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23
Q

What does a voltage difference cause?

A

Electrical gradient that drives ion currents through open channels

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24
Q

Can current flow if there is an electrical gradient but there is no concentration gradient?

A

Yes

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25
Q

Direction of current flow

A

Left to right (by convention, current flows in the direction of positive charge)

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26
Q

What ion does current go with?

A

Na+ (Cl- goes opposite way)

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27
Q

What is magnitude (strength) of electrical gradient (We) determined by?

A

Product of 3 variables (z=valence/charge of ion, F=Faraday’s constant, E=voltage across membrane)

We=-zFE

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28
Q

Initial conditions for equilibrium potential (2)

A
  1. K concentration gradient exists across membrane, but no open K ion channels
  2. Intracellular and extracellular compartments are electrically “balanced” (neutral)
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29
Q

What happens when K channels open?

A

Allows for outflow (“efflux”) of K+ down its concentration gradient, creating a (net) outward K current

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30
Q

What does K efflux result in?

A

Separation of charge across membrane that creates a voltage differences and acts as an electrical gradient opposing outward K+ current, electrical gradient flows stronger as K efflux continues

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31
Q

What does net negative charge inside membrane attract?

A

K+ because there are fewer K+ inside to balance A-

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32
Q

When are ion currents equal?

A

When efflux of K down its concentration gradient equals influx of K down its electrical gradient (Wc=We, zero net current)

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33
Q

Equilibrium Potential (Eion)

A

No net current in membrane potential (Vm=Eion)

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34
Q

Ions inside vs Outside

A

Inside: K+
Outside: Na+ and Ca2+

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35
Q

Nernst Equation

A

Describes equilibrium potential when electrical potential stops chemical potential from going down gradient

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36
Q

Distribution of ions across membrane

A

K+: 1:20 (outside/inside)
Na+: 10:1
Cl-: 12:1
Ca2+: 10,000:1

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37
Q

Ions in cytoplasm (inside)

A

High K, low Na and Cl

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38
Q

Ions in extracellular fluid (outside)

A

High Na and Cl, low K

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39
Q

***Equilibrium/Reversal Potentials

A

ENa+: +62 mv
ECa++: +123 mv
ECl-: -65 mv
EK+: -80mv

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40
Q

Ionic driving force

A

Difference between Vm and Eion, which causes either net inward or net outward current

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41
Q

Large changes in membrane potential are caused by…

A

Tiny changes in ion concentration

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42
Q

Where does separation of electrical charge exist?

A

Only across the membrane

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43
Q

Capacitance

A

Membrane stores electrical charge

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44
Q

Are intra- and extracellular fluids charged or neutral?

A

Electrically neutral: equal number of + and - charges in each compartment

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45
Q

What is membrane potential (Vm) determined by?

A

Weighted sum of all ion channel currents

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46
Q

Ion current contribution to Vm is proportional to…

A

Relative density of its channels (i.e. total conductance) in a patch of membrane

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47
Q

Godman-Hodgkin-Katz equation

A

Extension of the Nernst equation, expresses the contribution of each ion to Vm as the weighted sum of each ion’s concentration gradient

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48
Q

Density of K+ channels at rest

A

Much higher than Na+ or Cl- channels

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49
Q

Permeability of K to Na

A

pK: pNa= 1 : 0.05 (Vm is strongly dependent on EK+***)

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50
Q

Increasing [K+]out….

A

Depolarizes the membrane (makes it less negative than at rest)

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51
Q

Depolarization

A

Membrane potential becomes less negative (positive ions in)

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52
Q

What 2 things play a role in regulation of [K+]out?

A

Blood-brain barrier and astrocytes

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53
Q

“Leakage” currents

A

At rest, Vm=-65 mv so Cl- is close to equilibrium. Ions not in equilibrium give rise to leakage currents and could cause concentration gradients to decline if unchecked

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54
Q

Ion pumps

A

Transport proteins, they establish and maintain concentration gradients, critical for long-term maintenance of resting potential

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55
Q

What do ion pumps do?

A

Pumps expend energy from breakdown of ATP to exchange ions against concentration gradients (“active transport”)

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56
Q

What is the neuronal membrane highly permeable to at rest?

A

Potassium because of open membrane potassium channels

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57
Q

Movement of potassium ions across membrane, down concentration gradient, leaves inside of neuron…

A

Negatively charged

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58
Q

Polarized

A

Negative membrane potential

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59
Q

Other names for action potentials (3)

A

Spikes, discharges, impulses

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60
Q

Action Potential

A

Brief reversal of the resting membrane potential (inside briefly becomes positive relative to outside)

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61
Q

Excitable Membranes

A

Membranes that generate APs are called “excitable” (mostly found in neurons and muscle fibers)

62
Q

What underlies AP activity?

A

Voltage-gated ion channels

63
Q

Characteristics of APs (3)

A
  1. All-or-nothing event
  2. Duration is very brief (0.5-2.0ms)
  3. Does not require energy (PE–>KE)
64
Q

Phases of a “spike”

A

Resting potential –> Threshold –> Rising phase –> Overshoot –> Falling phase –> Undershoot

65
Q

Nav channels

A

Voltage-gated Na+ channels

66
Q

Threshold

A

Membrane at rest, only resting K+ channels and Na+ channels open, Nav and voltage gated K+ channels closed

67
Q

Rising Phase

A

Threshold to open Nav channels is more positive than Vrest, caused by inward Nav channel current

68
Q

When depolarized to Nav threshold, wha happens to inward vs outward current?

A

Inward current through Nav channels just exceeds outward “leakage” current via open resting K channels

69
Q

Positive feedback process

A

Inward current depolarizes membrane further and opens more Nav channels–> explosive amplification of inward depolarizing current

70
Q

Falling Phase/AP is terminated by (2)

A
  1. Nav “inactivation”

2. Falling phase: gK»gNa, so Vm rapidly repolarizes toward Vrest

71
Q

Delayed Rectifier

A

Group of slow opening and closing voltage-gated K+ channels compared to Nav

72
Q

What accelerates repolarization of membrane?

A

Outward (+) current moving through Kv channels (persists because it is delayed=”undershoot”)

73
Q

Refractory Period

A

Brief period (1-2ms) during and after generation of the AP when membrane is unable, or less able (inhibited, not impossible), to generate another AP

74
Q

Importance of refractory period (3)

A
  1. Affects duration of AP
  2. Sets upper limit of firing rate
  3. Prevents AP from re-invading membrane that has just discharged so that AP propagates away from site of intiation
75
Q

Absolute Refractory Period

A

Time during AP overshoot when all available Nav channels are either open or inactivated, threshold for generating another Ap is effectively infinite

76
Q

When does the relative refractory period take place?

A

Follows the ARP, associated with AP falling phase and undershoot

77
Q

Cause of relative refractory period

A

Prolonged outward K currents through Kv channels (high threshold, slow inactivating)

78
Q

Threshold during RRP

A

Elevated but not infinite, initiation requires stronger supra threshold depolarization that can open more Nav channels to overcome outward K currents causing afterpotential

79
Q

Sub-threshold inward currents

A

“Graded” i.e. proportional to the strength of the stimulus (different amplitudes?)

80
Q

Supra-threshold inward currents

A

(via resting ion channels) may result in repetitive generation of APs

81
Q

Supra-threshold depolarization

A

Elicits AP due to activation of enough voltage-gated channels to exceed outward currents through resting channels

82
Q

When can APs repeat?

A

If depolarization is sustained above threshold because channels repeatedly cycle between open and closed states

83
Q

Stimulus strength causes…

A

Stronger stimulus –> greater depolarizing current –> faster membrane reaches threshold to initiate another AP

84
Q

What is firing rate proportional to?

A

Stimulus strength

85
Q

What is firing rate limited by?

A

Duration of the absolute refractory period

86
Q

Patch Clamp technique

A

Sakmann & Neher, electrode that can form a tight electrical seal with membrane, resolves minute currents carried by single ion channels

87
Q

Structure of voltage-gated channels

A

Proteins with subunits, has a selectivity filter and voltage sensor

88
Q

Selectivity filter in voltage-gated channel

A

Loop segments located in the pore restrict channel to specific ion(s)

89
Q

Voltage sensor in voltage-gated channel

A

Membrane-spanning segments of each domain are charged, making them voltage-sensitive

90
Q

What causes voltage-gated channels to open?

A

When membrane is depolarized to threshold, electrostatic migration of charge in voltage sensor causes conformational change

91
Q

“Ball and chain” model

A

Pore becomes plugged by + charged internal loop of channel protein complex, has to close/plug channel or it will die after it fires once

92
Q

How to unplug pore (aka “deinactivate”)

A

Vm must become more negative than threshold, has to “rearm” it to open again if depolarized to threshold

93
Q

Voltage-gated Potassium channels (subunits and pore)

A

Subunits: KCNA gene, determine channel subtypes
Pore: selectivity for K ions by stripping water off K but not sodium

94
Q

Where does current flow during AP?

A

Flows in through voltage-gated sodium channels

95
Q

Electrotonic flow

A

Passive flow, depolarization spreads from site of AP initiation to adjacent membrane in both directions

96
Q

Where does AP begin?

A

“Spike initiation zone” in axon initial segment (AIS)

97
Q

Why do APs begin in AIS? (2)

A
  1. Nav channels are clustered at high density in AIS

2. AIS has lowest threshold for generating an AP

98
Q

Membrane Cable Properties (3)

A
  1. Cytoplasmic Conductance: gi( =1/Ri)
  2. Membrane Conductance: gm(=1/Rm)
  3. Membrane Capacitance
99
Q

Cytoplasmic Conductance

A

Proportional to fiber diameter/volume, limits current flow along the membrane

100
Q

Membrane Conductance

A

Proportional to resting ion channel density and ion channel conductance, limits current flow across membrane

101
Q

Membrane Capacitance

A

Created by the phospholipid bilayer, which separates and stores charge, affects how fast membrane potential changes when ion channels open

102
Q

Length Constant (λ)

A

Distance over which a change in membrane potential falls to 37% (1/ε) of its original magnitude

λ = (Gi/Gm)^½

103
Q

Longer length constant=

A

Further potential will travel (faster conductance)

104
Q

Time Constant (τ)

A

Rate of membrane potential change, expresses time it takes membrane to reach 63% of a new steady-state potential in response to an instantaneous change in membrane potential

105
Q

What is time constant directly & indirectly proportional to?

A

Membrane capacitance (Cm) and indirectly proportional to conductance (Gm)

106
Q

The shorter/faster/lower the time constant, the…

A

Shorter the latency to generate APs

107
Q

Nerve conduction velocity

A

Speed at which APs propagate down their axon

108
Q

What optimizes propagation of APs? (2)

A
  1. Increased fiber diameter (has a higher internal conductance)
  2. Myelination (ex: security line at airport, speed up so you can’t look back at loved ones)
109
Q

Myelin

A

Increases λ by decreasing Gm (conductance), decreases τ by lowering Cm (capacitance-inversely proportional to membrane thickkness)

110
Q

Where are Nav channels restricted to?

A

Node of Ranvier

111
Q

Kv1.1 Shaker channels

A

Low-threshold/rapid activation, segregated from Nav channels, reducing effect on rate of AP initiation

112
Q

Kv3.1 Shaw channels

A

High threshold/rapid activation, co-localized with Nav channels in the node, enhancing speed of AP reolarization

113
Q

Types of communication in the NS (4)

A
  1. Ephatic
  2. “Gas-transmission” (nitric oxide)
  3. Electrical
  4. Chemical
114
Q

Ephatic communnication

A

Intercellular current spread due to membrane apposition (positioning), known to occur in the cerebellum

115
Q

“Gas-transmission” comunication

A

NO is a free-radical gaseous signaling molecule, short half-life (few sec), powerful neuromodulator, vasodilator

116
Q

Electrical communication

A

Direct communication between neurons

117
Q

Chemical communication

A

Communication via chemical messengers

118
Q

Electrical synapses

A

Low-resistance junctions that conduct electrical potentials directly from one cell to another, neuron-to-neuron, neuron-to-glial cell

119
Q

Bi-directional current flow

A

Non-rectifying

120
Q

Uni-directional current flow

A

Rectifying, can only go in one direction

121
Q

Gap junction structure

A

Narrow cleft with membrane-bridging channels (connexons)

122
Q

What do connexons do?

A

Permit ions and other small polar molecules to pass from one cell to another

123
Q

Advantages of Electrical Transmission (4)

A
  1. Reliable
  2. Fast (no delay)
  3. Efficient
  4. Tough
124
Q

Chemical synapse structure (3 parts)

A
  1. Presynaptic endings (terminals): synaptic vesicles, secretory granules, active zones
  2. Synaptic cleft
  3. Postsynaptic membrane: receptors, enzymes, signaling molecules, structural proteins
125
Q

Synaptic Transmission

A

Chemical messenger (NT) is released by terminal in response to depolarization and binds to selective receptors

126
Q

Synaptic efficiency (chemical** vs electrical)

A

Chemical: activity in terminals can have graded (excitatory and inhibitory effects) on postsynaptic neuron activity
Electrical: response in postsynaptic neurons in less than or equal to that in pre-synaptic neuron

127
Q

Plasticity (chemical vs electrical)

A

Chemical: effectiveness can be modified by “experience”, trophic factors, hormones, etc.
Electrical: little to none

128
Q

Is chemical or electrical transmission favored more? Why?

A

Chemical because it is more flexible and plastic

129
Q

Small neurotransmitters (3)

A
  1. Acetylcholine
  2. Amino Acids: Glutamate, GABA, Glycine
  3. Biogenic amines: Dopamine, Epinephrine, Norepinephrine, Serotonin, Histamine
130
Q

Large NTs

A

Neuropeptides

131
Q

Neuropeptide characteristics

A

Over 30 identified, co-released with classical transmitter, cleaved from larger peptides, referred to as neuromodulators (mediate long-term changes in excitability)

132
Q

Coexistence

A

Many neurons contain 2 NTs: one small in small vesicles and one large packaged in larger vesicles

133
Q

Transmitter Release

A

See slides/textbook

134
Q

Activation of Receptors

A

“Lock and Key”

1. Transmitter is released and diffuses across cleft 2. Binds to receptors which are specific for given NT

135
Q

Ionotropic Receptors

A

Associated with ligand-activated ion channels, direct, fast and shot-acting, result is post-synaptic potential
EPSP: Na+ or Na+/K+
IPSP: K+, Cl-

136
Q

Metabotropic Receptors

A

Associated with signal proteins and G proteins, indirect, slow and longer-lasting, result: varied, modulatory

137
Q

Where are metabotropic receptors located?

A

Pre-synaptic membrane, autoreceptor function is to maintain appropriate level of (subsequent) NT release

138
Q

Termination of Transmittion (4)

A
  1. Re-uptake
  2. Enzymatic degradation
  3. Diffusion
  4. Scavenging
139
Q

Re-uptake

A

Free NT directly taken up by terminal, re-packaging into vesicles of enzymatically destroyed

140
Q

Enzymatic degradation

A

Breakdown of NT by enzymes, followed by breakdown products, re-synthesis of NT in nerve terminal (Ach)

141
Q

Diffusion

A

NT concentration in cleft declines

142
Q

Scavenging

A

Free NT taken up by astrocytes via specialized membrane transporters

143
Q

Steps in synaptic transmission (7)

A

See slides

144
Q

Postsynaptic Potentials (PSPs)

A

Membrane potential changes caused by synaptic activity

145
Q

Functional Classes of PSPs (3)

A
  1. Excitatory (EPSP)
  2. Inhibitory (IPSP)
  3. Shunting
146
Q

EPSP

A

Net inward cation (e.g. Na+) current (depolarizing), increases probability of reaching AP threshold

147
Q

IPSP

A

Net outward current (hyperpolarizing), decreases likelihood of reaching AP threshold

148
Q

Shunting

A

Open channels prevent/reduce depolarization by “clamping” Vm near Eion

149
Q

Location of ionotropic receptor

A

Dendrite

150
Q

Nicotinic acetylcholine (nAchR) receptors

A

Permeable to cations (both Na and K), reversal potential Er~0mv

151
Q

Negative Vm=

A

Net inward current (depolarizing, INa>Ik)

152
Q

Positive Vm=

A

Net outward current (hyperpolarizing, Ik>INa

NSC 201 (5 decks)

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