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HOM > Cellular Electrophysiology & Nerve > Flashcards

Cellular Electrophysiology & Nerve Flashcards

1
Q

what are the roles of the cell membrane?

A

compartmentalisation, control of fluxes, attachment of enzymes/cytoskeleton/secondary messenger models, sensory receptors, binding sites for hormones, secretion by exocytosis, uptake by pinocytosis, endocytosis and phagocytosis

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2
Q

what are the variables controlled by homeostasis?

A

concentration of ions, control of chemicals, physical characteristics of blood, concentration of blood gases, number of RBCs and WBCs, metabolic rate, body weight, bone density, muscle mass, temperature, heart rate

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3
Q

what is gain?

A

amount of output signal per unit error

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4
Q

what is a high gain?

A

large output from a small error

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5
Q

what is a low gain?

A

small output from a large error

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6
Q

what is feed-forward control?

A

predicted change in output necessary to maintain a constant level

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7
Q

what is the cephalic phase of insulin release?

A

feed-forward stage, when food smelt/enters mouth insulin released- minimises rise in blood glucose

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8
Q

what are the properties of hormones?

A

released into blood from endocrine glands, low concentrations so small changes have large effect, high specificity of binding, signal from 1 cell type to another

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9
Q

what are the types of hormone receptor?

A

GPCRs and RTKs

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10
Q

what type of receptor is the glucagon receptor?

A

a GPCR

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11
Q

what type of receptor is an insulin receptor?

A

a RTK

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12
Q

what is an ionotropic receptor?

A

coupled to ion channels, opens ion channel, used by fast neurotransmitters

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13
Q

what is an autocrine signalling molecule?

A

signalling molecule released by same cell type it acts on

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14
Q

what is a paracrine signalling molecule?

A

signalling molecule that acts locally via extracellular space on different cell type

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15
Q

what is the adenohypophysis?

A

anterior pituitary

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16
Q

what does the hypothalamus release in the cortisol release system?

A

CRH (corticotrophin releasing hormone)

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17
Q

what does the pituitary release in the cortisol release system?

A

ACTH (adrenocorticotropic hormone)

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18
Q

what does ACTH do?

A

inhibits CRH release, stimulates cortisol release and MSH release

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19
Q

what causes CTH release from the hypothalamus?

A

stress, starvation

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20
Q

what does CRH do?

A

stimulates ACTH release

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21
Q

what releases cortisol?

A

the adrenal cortex

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22
Q

what does the adrenal cortex do in cortisol release?

A

releases cortisol

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23
Q

what does cortisol do?

A

increases blood glucose, reduces inflammation, inhibits CRH and ACTH release

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24
Q

what happens in Addison’s disease?

A

adrenal gland can’t produce enough cortisol - leads to weakness, fatigue and hypotension, less inhibition so CRH and ACTH levels rise

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25
Q

what does MSH lead to?

A

more melanocytes so more pigmentation

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26
Q

what cause veterinary Cushing’s

A

excess ACTH from pituitary gland causes high cortisol levels

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27
Q

what are the properties of water? (6)

A

high boiling point, density decreases when freezes, high specific heat capacity and latent heat of vaporisation, electrical dipole, dissociates spontaneously and reversible, can act as solvent for ions

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28
Q

what is charge?

A

quantity of electricity (measure in coulombs) due to atoms/molecules that have gained or lost electrons

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29
Q

what is voltage?

A

difference in charge relative to another region (in volts)

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30
Q

what is capacitance?

A

amount of charge stored per volt

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31
Q

what is current?

A

number of charged particles flowing past a point per unit time

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32
Q

what is resistance?

A

restriction of flow of current

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33
Q

what is Ohm’s law?

A

voltage= current x resistance

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34
Q

what is resting potential?

A

potential across cell membrane at rest

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35
Q

what are excitable cells?

A

cells that can change their state from resting to excited and back again using bioelectricity

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36
Q

what is the cell membrane of nerve cells and muscle fibres composed of?

A

lipophilic phospholipid bilayer, transmembrane proteins that form ion channels and pumps and allow charged ions to move across the bilayer

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37
Q

what is a capacitor?

A

2 conductors separated by a non-conductor with different numbers of ions

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38
Q

what does membrane potential arise from?

A

different numbers of positive/negative charges across the membrane

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39
Q

what is a high resistance environment in terms of cell membranes?

A

no/closed ion channels

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40
Q

what are the 2 forces that determine movement of ions in solutions?

A

charge gradient and concentration gradient

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41
Q

when is ion flux at equilibrium?

A

when charge gradient and concentration gradient are balanced

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42
Q

what is the equilibrium potential of an ion?

A

the membrane potential at which the ion is at equilibrium

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43
Q

what is the Nernst equation used for?

A

to find the equilibrium potential of an ion

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44
Q

what is needed for the Nernst equation?

A

ideal gas constant (R), temperature (T in K), charge of the ion (Z), Faraday’s constant (F), [C] outside (ref) and inside (rest) (C is ion)

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45
Q

what are the assumptions of the Nernst equation?

A

only 1 ion at a time, membrane completely permeable to ion, ion at equilibrium

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46
Q

what is the Nernst equation at room temperature (20 degrees)?

A

E= 58 x log([ion]out/[ion]in)

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47
Q

what is the Nernst equation at body temperature?

A

61 x log([ion]out/[ion]in)

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48
Q

what are the typical ion concentration of mammalian neurons inside vs outside?

A

high [K+], low [Na+], [Cl-], [Ca2+] inside vs outside

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49
Q

in resting state what ion is primarily moving across neuron membranes?

A

K+

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50
Q

in active state what ion is primarily moving across neuron membranes?

A

Na+

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51
Q

what provides the driving force for ions to move across membrane?

A

difference between potential and equilibrium potential

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52
Q

what are microelectrodes?

A

recording devices attached to a voltmeter

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53
Q

what is resting membrane potential usually between?

A

-60 and -80mV

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54
Q

what dis Hodgkin and Keynes find when comparing resting membrane potential to the Nernst equation for K+?

A

fit very well at high [K+], deviated at low [K+]

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55
Q

what did Hodgkin and Keynes suggest as an equation for membrane potential?

A

Goldman equation, taking into account Na+

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56
Q

what does the Goldman-Hodgkin-Katz equation account for?

A

K+, Na+, Cl-, relative permeability of the membrane to the ions

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57
Q

which is the most permeant ion across the cell membrane at rest?

A

K+

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58
Q

why do K+ ions tend to move out of the cell?

A

high conc in cell at rest, driving force to reach equilibrium potential which is around -90mV

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59
Q

what is the equilibrium potential of K+?

A

around -90mV

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60
Q

what is the equilibrium potential of Na+?

A

around +50mV

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61
Q

what are the changes in membrane potential during an AP

A

starts at around -70mV, increase to -55mV, rapid increase to around +40mV, decrease to almost -90mV, return to around -70mV

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62
Q

what experiment can be used to record voltage signals during an AP?

A

current clamp

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63
Q

what does axonal malfunction arise from?

A

injury, degeneration, demyelination

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64
Q

what is the time constant of a membrane?

A

how long it will take for the membrane to get to 1/e of its original charge/time to charge capacitance to 63%

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65
Q

what does the time constant depend on?

A

membrane resistance and membrane capacitance

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66
Q

how is the time constant calculated?

A

membrane resistance x membrane capacitance

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67
Q

what does a larger time constant mean?

A

changes in membrane potential will be slower

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68
Q

what is length constant?

A

distance over which voltage decays to 37% of its initial value

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69
Q

what is length constant dependent on?

A

membrane resistance, extracellular resistance (assumed to be negligible), intracellular resistance

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70
Q

what does a smaller length constant mean?

A

voltage signal decays over shorter distance

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71
Q

how can length constant be improved?

A

myelination

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72
Q

how does myelination improve the length constant?

A

increases membrane resistance

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73
Q

what is myelination in the PNS?

A

Schwann cells which wrap membrane around axon to form 20-160 concentric layers of membrane

74
Q

what is myelination in the CNS?

A

oligodendrocytes wrap membrane around axon

75
Q

what is between the segments of myelination?

A

unmyelinated nodes of Ranvier

76
Q

how does myelination increase membrane resistance?

A

ions less likely to leak out of the membrane

77
Q

why are action potentials ‘all or none’ events?

A

if threshold potential is reached, an action potential will occur, if not then it won’t, size of action potential not changed by size of stimulus

78
Q

what is the absolute refractory period?

A

state when sodium channels cannot be opened as they are in inactive state, so new AP can’t be generated

79
Q

what does the absolute refractory period do?

A

prevents transmission of impulse in both directions

80
Q

what causes the relative refractory period?

A

K+ channels are delayed in closing so hyperpolarisation of membrane occurs- greater depolarisation required for new AP as further from threshold value

81
Q

what does increasing size of stimulus current do?

A

increases frequency of action potentials

81
Q

where are voltage gated ion channels concentrated in myelinated axons?

A

at Nodes of Ranvier

82
Q

what is saltatory conduction?

A

rapid jumping of current from node to node

83
Q

how are axons classified?

A

speed of conduction, myelination, diameter of axon, function

84
Q

what is the general rule for characteristics of large diameter neurons?

A

heavily myelinated, low thresholds for electrical stimulation, rapid conduction

85
Q

what did Cole and Curtis observe in 1939?

A

AP clearly over-shot 0mV and change in membrane resistance during AP

86
Q

what did Hodgkin and Huxley find about the AP using squid giant axon?

A

AP overshot to around +40mV, sodium movement responsible for AP

87
Q

what are examples of conditions involving damage to axons?

A

prolapsed intervertebral disc, poliomyelitis, motor neurone disease, hypo-myelinating neuropathy

88
Q

what is the C fibre afferent?

A

type of sensory afferent fibre that is important for alerting brain to harmful stimuli

89
Q

what are local anaesthetics?

A

class of drugs that can cross membrane and block VGNaCs from inside- shut down APs in pain fibres

90
Q

why do voltage gated ion channels have selective permeability?

A

due to amino acids

90
Q

what are the reversal potentials for closing VG ion channels?

A

the Nernst equilibrium potential for the permeant ion

91
Q

what is capacitive current? (voltage clamp experiment)

A

current needed to be injected

92
Q

what is the command voltage? (voltage clamp experiment)

A

the membrane potential decided by the experimenter

92
Q

how is the command voltage reached in the membrane? (voltage clamp experiment)

A

microelectrodes record actual membrane potential, compare it with command voltage, then inject current into axon to change it to command voltage

93
Q

what is the recording taken in the voltage clamp experiment?

A

how much current had to be injected to reach command voltage- and if positive or negative- shows current passing through the open membrane channels at the command voltage

94
Q

what is the current injected equivalent to when command voltage is made more positive in voltage clamp experiment?

A

the current moving across the membrane during the depolarisation phase of an AP

95
Q

what is seen in the voltage clamp experiment?

A

rapid capacitative current (current injection), rapid transient inward current, delayed outward current

96
Q

what is seen in the control experiment for voltage clamp experiment (membrane potential changed in opposite direction by same amount)?

A

only capacitative current and no ionic current

97
Q

what does voltage clamp experiment prove?

A

currents ‘gated’ by specific voltage change

98
Q

what suggested that the rapid transient inward current in the voltage clamp experiment may be due to Na+ ion flux?

A

initially got larger with more depolarisation, as membrane potential approached +50mV (equilibrium potential of Na+) started to get smaller

99
Q

what suggested the delayed outward current was due to K+ in the voltage clamp experiment?

A

increased with more depolarisation suggesting equilibrium potential of ion moving was more negative

100
Q

how was the importance of Na+ for the transient inward current proved?

A

by removing the Na+ in the seawater bathing the axon or by blocking the VGNaC conductance using tetrodotoxin

101
Q

how was the importance of K+ for the delayed outward current proved?

A

by using TEA to block VGKCs- can’t change intracellular K+ concentration

102
Q

what are channelopathies?

A

clinical conditions associated with non-functional mutated ion channels

103
Q

what is the structure of the VGNaC?

A

single α-subunit polypeptide with associated β-subunits

104
Q

what key functional features are present in the α-subunit of VGNaCs?

A

sensitivity to voltage, selectivity to Na+ ions

105
Q

how many repeating domains do VGNaCs have?

A

4

106
Q

how many membrane spanning regions do the domains of VGNaCs contain?

A

6 (S1-S6)

107
Q

how are the 4 domains of VGNaCs arranged?

A

around a central ion channel pore

108
Q

where is the voltage sensor located in VGNaCs?

A

around S4

109
Q

what is the ion channel pore formed from in VGNaCs?

A

the linker sequence between S5 to S6

110
Q

how long after opening will the VGNaC inactivate?

A

1ms

111
Q

what region of the VGNaC determines selectivity?

A

loop between S5 and S6

112
Q

how is the intracellular pore of VGNaCs opened?

A

when S4 detects voltage S5 moves, opening the pore

113
Q

what happens in the inactivated state of the VGNaC?

A

intracellular loop blocks channel

114
Q

what causes a positive feedback cycle of VGNaCs opening?

A

if nearby VGNaCs are close enough for the resulting depolarisation from 1 opening to be at threshold value they will also be opened

115
Q

what is the difference between the structure of VGNaCs and VGKCs?

A

the α-subunit in VGKCs is equivalent to a single domain of the VGNaC so 4 α-subunits are needed to form VGKCs

116
Q

what were the 2 theories of transmission between neurons and targets?

A

electrical and chemical

117
Q

what did Dale and colleagues show in 1913?

A

IV injection of ACh inhibits heartbeat of cat, as does parasympathetic nerve stimulation, suggesting parasympathetic nerve stimulation could be chemical

118
Q

what did Otto Loewi find in 1921?

A

put 2 beating hearts in 2 containers filled with Ringer’s solution. stimulated vagus nerve in one, heart rate slowed. took solution from this container, put in other container- heart rate of other heart slowed- seemed a substance released by vagus nerve slowed heart rate- chemical

119
Q

who used microelectrodes to directly record chemical synaptic transmission at the NMJ?

A

Katz

120
Q

where are neurotransmitters stored?

A

in vesicles in the presynaptic axon terminals

121
Q

what is an advantage of chemical over electrical transmission?

A

diversity of neurotransmitters and their receptors in the post-synaptic membrane produces different types of response

122
Q

what does an AP cause when it reaches the axon terminal?

A

activation of VGCaCs so rapid influx of Ca2+

123
Q

what is the structure of VGCaCs similar to?

A

VGNaCs

124
Q

what is intracellular concentration of Ca2+ like and why?

A

kept very low by buffers/transporters/pumps

125
Q

what are examples of proteins that keep intracellular Ca2+ concentration low?

A

the Na+/Ca2+ exchanger, the calcium pump (pumps 1 Ca, 2 H ion out, uses 1 ATP)

126
Q

what does influx of Ca2+ cause?

A

the neurotransmitter containing vesicles to fuse with the presynaptic membrane and release the neurotransmitter by exocytosis

127
Q

how is the vesicle membrane recovered after neurotransmitter release?

A

endocytosis

128
Q

what are electrical synapses called?

A

gap junctions

129
Q

how are gap junctions formed?

A

a connexon on the pre and post-synaptic membrane form a gap junction channel, conducts ions if there is depolarisation in 1 of the neurons to the 2nd neuron

130
Q

what forms a connexon?

A

6 connexins

131
Q

what enzyme is used to synthesis ACh?

A

choline acetyltransferase (ChAT)

132
Q

what are end plate potentials?

A

depolarisations when ACh binds to receptors at the post-synaptic region of the muscle cell in the NMJ

133
Q

what do EPPs cause?

A

depolarise the muscle membrane enough to open VGNaCs in the muscle cell membrane causing a muscle AP

134
Q

why will an AP in the motor neuron reliably produce an AP in the muscle cell?

A

AP in the motor neuron causes the release of sufficient ACh to open VGNaCs in the muscle cell

135
Q

what enzyme inactivates ACh in the synaptic cleft?

A

acetylcholinesterase (AChE)

136
Q

what are MEPPS?

A

miniature EPPs- represent the smallest unit of chemical synaptic transmission- spontaneous small depolarisations at endplate when motor neuron not being stimulated

137
Q

what is the quantal theory of synaptic transmission based on?

A

neurotransmitter is released in parcels (quanta), giving rise to MEPPs; EPP amplitudes correspond to the sum of MEPPs

138
Q

what is 1 quantum (MEPP) equivalent to?

A

1 vesicle of neurotransmitter

139
Q

what is the model for number of MEPPs?

A

number of quanta x probability of release

140
Q

what happens if the NMJ is bathed in low Ca2+ solution?

A

EPPs are much smaller in amplitude- fewer quanta released

141
Q

what is the post-synaptic receptor for ACh on the NMJ?

A

nicotinic ACh receptor

142
Q

what is curare?

A

antagonist of the nAChR- reduces amplitude of EPPs

143
Q

where are nAChRs found in the post-synaptic membrane?

A

junctional folds

144
Q

what is the function of junctional folds?

A

increase the SA available for synaptic transmission at the NMJ

145
Q

what sort of protein is the nAChR?

A

ligand-gated ion channel

146
Q

what does ACh binding to the nAChR cause?

A

opening of an integral ion channel pore in the receptor protein

147
Q

what is the pore of the nAChR permeable to?

A

Na+ ions and K+ ions

148
Q

what is the sodium pump coupling ratio?

A

3Na pumped out for 2K pumped in

149
Q

what is the resting MP of the endplate of a muscle cell?

A

around -100mV

150
Q

what is the threshold for an AP in skeletal muscle?

A

around -65mV

151
Q

where are VGNaCs located in the endplate?

A

at the bottom of junctional folds

152
Q

what is myasthenia?

A

muscle weakness

153
Q

what is an autoimmune cause of myasthenia gravis?

A

immune system attacking the nAChR

154
Q

what is the main treatment for autoimmune myasthenia gravis?

A

prolonging duration of ACh activity in the synapse

155
Q

what is a large difference between electrical and chemical synapses?

A

in electrical membrane of the 2 neurons very close together, in chemical larger synaptic cleft

156
Q

what is a motor unit?

A

1 motor neuron plus all the muscle fibres it stimulates

157
Q

what is a neuromuscular junction?

A

synapse between motor neuron and skeletal muscle end plate

158
Q

what is the electron microscopy evidence for the quantal theory of synaptic transmission?

A

vesicles shown near membrane at rest and fusing with membrane after stimulation

159
Q

what does postsynaptic response amplitude depend on?

A

amount of NT released and number of NT receptors

160
Q

in a reflex response where is the ‘decision’ to contract a muscle made?

A

at the sensory afferent synapses onto the motor neuron

161
Q

in voluntary movements where in the ‘decision’ to contract a muscle made?

A

at the level of cortical brain neurons

162
Q

difference between synapses in the CNS vs NMJ?

A

many different NTs in CNS, just ACh in NMJ; synapses can be excitatory or inhibitory in CNS, just excitatory in NMJ; axons can contact different parts of neurons in CNS; neurons contact other neurons in CNS; an EPSP in excitatory neurons in the CNS doesn’t always cause an AP- an AP depends on input of all the different neurons; voltage changes produced at most synapses in CNS smaller than EPPs at NMJ

163
Q

why are voltage changes produced at most synapses in the CNS smaller than EPPs at the NMJ?

A

NMJ is a larger synapse with more vesicles of ACh in the presynaptic terminal of the motor neuron, more nAChRs in junctional folds, than CNS synapses

164
Q

what is an EPSP?

A

an excitatory postsynaptic potential

165
Q

why is it beneficial for strong signals to be required to evoke a response in CNS post-synaptic neurons?

A

ensure energy isn’t wasted generating non-essential signals in brain and spinal cord, keeps good levels of response specificity

166
Q

what neurotransmitter are EPSPs due to at most CNS synapses?

A

glutamate

167
Q

what are the receptors for glutamate on post-synaptic receptors?

A

AMPA receptors, NMDA receptors, Kainate receptors

168
Q

what are IPSPs in CNS synapses in the brain mediated by?

A

GABA

169
Q

what are IPSPs in CNS synapses in the spinal cord mediated by?

A

glycine

170
Q

how can glutamate cause excitation and inhibition?

A

causes excitation via AMPA receptor, and inhibition via GPCR

171
Q

how does the knee jerk reflex work?

A

sensory afferent fibres from the muscle synapse with efferent extensor motor neuron, projects back to quadriceps muscle. glutamate released from pre-synaptic terminal of sensory neuron, binds to AMPA receptors in dendrites of the motor neuron. AMPA receptor activation leads to a depolarisation of the motor neuron dendrites. glutamate also binds to AMPA receptors present on inhibitory interneurons in spinal cord, excite the interneuron, which releases glycine to bind to glycine receptors on the motor neuron to the antagonist (flexor) muscle causing this muscle to be inhibited so both muscles don’t contract simultaneously against each other

172
Q

what is synaptic integration?

A

combining of all the synaptic inputs in the dendrites of a CNS neuron

173
Q

what is temporal summation?

A

when a single presynaptic neuron is activated several times to cause multiple rounds of neurotransmitter released- if response to the rounds of release occurs before 1st response fully decayed they add together to generate a larger EPSP

174
Q

what is spatial summation?

A

when more than 1 presynaptic neuron is activated near-simultaneously causing neurotransmitter release at multiple sites, each EPSP adds together to generate a larger EPSP

175
Q

what is shunting inhibition?

A

when an IPSP happens in the path of an EPSP- inward Cl- movement effectively pulls positive current out of the dendrite reducing the EPSP

176
Q

what is primary active transport?

A

energy provided directly by ATP

177
Q

what is secondary active transport?

A

energy provided from the Na+ or H+ gradients set up by ATP pumps

HOM (9 decks)

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