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Electrophysiology Undergrad > Midterm 2 Material Questions > Flashcards

Midterm 2 Material Questions Flashcards

1
Q

List the flow of action potential generation during signal conduction.

A

Dendrites are the primary synaptic sites where info is sent to the cell soma, integrated and propagated along axons to other synaptic sites.
*Propagates along nodes of Ranvier

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2
Q

Where is the decision made regarding action potential generation?

A

The axon hillock

-Abundance of Na+ channels

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3
Q

What determines the firing pattern of action potentials in the cell?

A

-Type of ion channels expressed in the cell soma

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4
Q

True or False:

Axons act as active transporters of information from one cell soma to the next.

A

False.

-Passive transporters (majority)

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5
Q

At what site is an action potential turned into a chemical signal to act upon other cells?

A

The axon terminal

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6
Q

What are the predominant types of channels found at synaptic sites, including dendrites and the cell soma?

A
  • Ligand-gated channels

* Can also be found in axons

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7
Q

In what part of signal conduction are Na+ channels found in?

A

The axon

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8
Q

In what area do channels important in modulating firing pattern appear?

A

-The cell soma

The axon hillock is where this firing pattern may be transformed into an action potential

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9
Q

Ca2+ channels important in neurotransmitter release (example would be ACh release) appear at which part of signal conduction?

A

The axon terminal

chemical signal that can terminate on other cells

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10
Q

Burst firing of action potentials in the hypothalamus allows for what process in the human body?

A

-Allows for a bolus release of oxytocin and ejection of milk from the breasts

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11
Q

What law is responsible for the size and shape of passive responses in a cell?

A

Ohm’s Law
V= I x R
*current, resistance and capacitance

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12
Q

True or False:

Passive responses decay with time, whereas Active responses do not decay over time.

A

True

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13
Q

What is characteristic of an EPSP?

A

A depolarization
(cell becoming more positive)
–>If strong enough, can trigger an action potential.

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14
Q

What is characteristic of an IPSP?

A

A hyperpolarization

cell becoming more negative

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15
Q

What causes a passive response to decay with time??

A
  • Current leak through the membrane

- Cytoplasmic resistance

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16
Q

True of False:
Post-synaptic potentials attenuate.
(signal’s decline in amplitude before reaching the soma)

A

True.

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17
Q

True or False:
-Length constant increases when membrane resistance increases (membrane becomes less leaky).

-Length constant increases when internal resistance decreases (larger axon).

A

True.

-Signals propagate further if the membrane doesn’t leak, as well as if the axon is larger.

–> Larger length constant= less resistance of current propagation= signal changes Vm faster and further.

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18
Q

Do signals travel faster or slower in large axons compared to small axons?

A

Signals travel faster in thicker (larger) axons.
–>Leads to a larger length constant, meaning a faster and larger passive signal.

-Signal is larger when membrane resistance increases (membrane is less leaky) and when internal resistance decreases.

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19
Q

Approximate size comparison of length constants of squid axons versus mammalian axons.

A

Squid axon length constant: 13 nm

Mammalian axon length constant: 0.2 nm

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20
Q

Intermittent myelination leads to what kind of action potential propagation?

A

Saltatory conduction

-Spreading of action potentials along nodes of Ranvier

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21
Q

Na+ channels are densest in which regions of cell transduction?

A

-The axon hillock and the nodes of Ranvier

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22
Q

How does myelination increase speed of signal transduction (increase length constant) ?

A
  • Myelination increases membrane resistance (insulation- makes the membrane less leaky) and decreases membrane capacitance.
  • This leads to a decrease in time constant and an increase in length constant.
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23
Q

Which two factors lead to an increase in speed conduction of signals?

A
  • Increase in length constant

- Decrease in time constant

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24
Q

True or False:
Oligodendrocytes in the CNS and Schwann Cells in the PNS speed up transmission by increasing membrane resistance and decreasing membrane capacitance.

A

-True.

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25
Q

True or False:

Neurons can proliferate, whereas Glial Cells can not.

A

False.

Glial Cells can proliferate but neurons can’t.

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26
Q

When intracellular calcium levels are low, how is the structure of the gap junction affected?

A
  • The pore remains open.
  • Connexin subunits stay tilted 7-8 degrees from the axis perpendicular to the plane of the membrane.

–>Parallel shift causes closing of the pore.

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27
Q

Describe the relationship of current as it passes through one cell to another through a gap junction.

A

-Current entering the second cell will be a mirror image of the graph of current exiting the first cell.

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28
Q

True or False: Humans and rats have very similar connexion sequences.

A

True.

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29
Q

Chemical Transmission of ACh on nicotinic receptors:

A

An action potential enters the presynaptic terminal, causing voltage gated calcium channels to open and Ca2+ enters the presynaptic terminal. An increase in (Ca2+)i causes synaptic vesicles to fuse with the presynaptic membrane. This allows the transmitter molecules to diffuse through the synaptic cleft to bind to their receptors of the post-synaptic cell.

  • Bound receptors activate post synaptic cell.
  • The transmitter is broken down by enzyme or taken back up into the pre synaptic terminal.

(Neurotransmitter release is dependent on depolarization of the presynaptic membrane.)

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30
Q

What can prevent neurotransmitter release?

A

-Blocking Ca2+ channels blocks calcium influx.

Ex. of a calcium blocker is Cadmium.

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31
Q

What is BAPTA?

A
  • Ca2+ chelator which buffers Ca2+ ions

- ->Prevents neurotransmitter release

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32
Q

What is synaptic delay and what are it’s causes?

A
  • Large delay between Ca2+ influx and the post-synaptic response.
  • IS MUCH LONGER THAN SIMPLE DIFFUSION OVER A MEMBRANE (approx. 50 nm)

-Highly temperature dependent- suggests the delay is mainly due to the neurotransmitter release mechanism

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33
Q

True or False:

The higher the temperature, the shorter the synaptic delay.

A

True.

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34
Q

What is the effect of using curare on the neuromuscular junction?

A

-Competitive neuromuscular blocker

Blocks ACh binding

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35
Q

What is the effect of using neostigmine on the neuromuscular junction?

A
  • AChE Inhibitor

- Allows ACh to stay in the synapse longer.

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36
Q

Describe quantized release of ACh?

A

-The quantal event corresponds to ACh release from one synaptic vesicle.

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37
Q

What are individual Miniature End Plate Potentials? (MEPP’s)

A

-Small depolarization’s that occur in discrete multiples of a unitary amplitude (same size).

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38
Q

What occurs after the ACh binds the nicotinic receptor?

A
  • ->EPSP
  • Leads to an excitatory post synaptic potential which decays from its site of action.
  • Size is decreased with presence of curare.
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39
Q

What is an End Plate Potential?

A

Action potential in the post synaptic cell.

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40
Q

True or False:

EPP’s increase with intracellular calcium and decrease with intracellular Mg2+.

A

-True.

Mg2+ blocks Ca2+ channels

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41
Q

What is one quantum?

A

-One quantum generates a MEPP which is the smallest amount of stimulation one neuron can send to another neuron.

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42
Q

What is the summation of MEPP’s?

A

EPP

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43
Q

What pump is responsible for sending ACh into the synaptic cleft of the neuromuscular junction?

A
  • ACh-H+ exchanger.

* Active secondary pump dependent on the H+ gradient of the proton pump.

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44
Q

How do vertebrae’s neuromuscular junction use ACh?

A

-The vertebrae synapse is designed to release a large amount of ACh from synaptic vesicles to cause maximal activation of the post synaptic muscle cells in response to action potential in the motor neuron.

(Pumps ACh into the synaptic cleft)

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45
Q

How do carbon fibre microelectrodes detect neurotransmitters?

A

Neurotransmitters oxidize with H+

Seretonin as an example

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46
Q

What is Full Fusion?

A

Vesicles bind membrane and dispenses contents fully into the synaptic cleft.

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47
Q

What is “Kiss and Run” Fusion?

A

-Vesicle binds membrane and PARTIALLY dispenses contents- then moves back to the interior to have its store of neurotransmitters replenished.

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48
Q

What is Botulism toxin? What is it’s mechanism of action?

A

-Endopeptidases that cleave synaptobrevin, SNAP-25 or syntaxin.

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49
Q

What is Tetanus toxin’s mechanism of action?

A

-Cleave synaptobrevin

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50
Q

What are ionotropic receptors?

A

-Ligand Gated Ion channels

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51
Q

What are metabotropic receptors?

A

-G-protein linked receptors

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52
Q

ACh binds a nicotinic receptor through which kind of receptor activity?

A

Ionotropic: Ligand gated ion channel

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53
Q

ACh binds a muscarinic receptor through which kind of receptor activity?

A

Metabotropic: G protein coupled receptor

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54
Q

What is characteristic of G protein coupled receptors?

A

-Typically have 7 transmembrane regions, a neurotransmitter binding site on the extracellular side, and a G protein interaction on the cytosolic side of the membrane.

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55
Q

Common examples of metabotropic receptors:

A

-Muscarinic, glutamate receptors, GABA receptors, ect.

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56
Q

Describe the cAMP pathway.

A

-Activation of a G protein which leads to the activation of adenylyl cyclase which converts ATP into cAMP, which leads to the activation of Protein Kinase A. This leads to the activation or inhibition of several different secondary pathways due to phosphorylation.

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57
Q

How do G proteins modulate pathways?

A
  • Can modulate pathways through a diffusible second messenger
  • Can also involve direct channel modulation by the beta-gamma subunit.
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58
Q

Signal Amplification through the G protein coupled cascade?

A

Usually depends on the activation of adenylyl cyclase, PKA and the phosphorylation of different pathways.

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59
Q

Muscarinic activation of G proteins in the heart muscle leads to what activity?

A

-Leads to opening of K+ channels through a direct effect of the beta-gamma subunit.

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60
Q

How do G proteins regulate as secondary messengers?

A

-Regulate adenylyl cyclase and can be inhibitory of stimulatory, to increase or decrease production of cAMP.

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61
Q

Describe the IP3 pathway.

A
  • PLC splits PIP2 into IP3 and DAG, both which acts as secondary messengers and activate different pathways.
  • ->IP3 causes an increase in (Ca2+)i
  • ->DAG activates Protein Kinase C
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62
Q

What is the different between diverging and converging transmitter actions?

A

Diverging transmitters activate several different pathways, whereas converging transmitters come together to all activate the same pathway (ie. They all activate the same G protein)

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63
Q

What are the 3 subunits of G proteins?

A

Alpha, beta and gamma

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64
Q

What is the difference between spactically focused and widely divergent synaptic connection?

A

-Spatically focused is when one neuron has effects on several other neurons under one neuron branch, and widely divergent means one neuron has several effects on different neuronal branches.

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65
Q

NE example of modulation of AHP current.

A

NE decreases AHP by blocking Ca2+ dependent K+ channels and therefore decreases spike frequency adaptation.

66
Q

Beta adrenergic stimulation modulation example.

A

Beta adrenergic receptor stimulation enhances Ca2+ current through a cAMP dependent mechanism.

67
Q

Muscarinic inhibition of M type current example.

A

-Muscarinic inhibition of the M current results in a depolarization/ increases excitability
(M currents block depolarization’s)

68
Q

Examples of diffuse systems affecting excitability in the brain.

A
  • NE and serotonin systems are involved in the RAS system (reticular activating system- sleep and wake)
  • Hallucinogenic drugs and anti-depressants effect levels of serotonin.
  • Dopamine system originating in the substantia nigria is involved in the initiation of voluntary movement and its degeneration is responsible for the motor symptoms of Parkinsons disease.
  • Dopamine systems in the ventral tegmental area is involved in rewards systems in the brain- also involved in addictions.
69
Q

Where is ACh stored and taken to from synaptic vesicles?

A

ACh is stored in the cytoplasm, taken up by secretory vesicles and released through Ca2+ dependent exocytosis.
(Taken back up by endocytosis or destroyed by AChE)

70
Q

What is the reverse potential, as well as the type of channel that binds ACh?

A

-Usually around 0mV because nicotinic receptors do not differentiate between Na+ and K+ well as they are NON-SELECTIVE CATION CHANNELS.
(This means the same amount of Na+ and K+ inside the cell as outside the cell)

71
Q

Describe the structure of the nicotinic ACh receptor.

A
  • 5 transmembrane subunits make up the channel
  • Each subunit has 4 transmembrane regions.
  • ->Large extracellular region is involved in binding.
  • 2 ACh must bind the receptor in order to open the pore.
  • ->Subunit composition: 2Alpha, Beta, Gamma & delta
  • ->Alpha subunits contains M1, M2 M3 and M4 transmembrane regions.
72
Q

What segment of the ACh receptor forms the pore?

A

M2 segment for the pore of Nicotinic ACh receptor channels.

73
Q

What is the role of M1-M2 Linkers of the Nicotinic ACh receptor?

A

-Important for sites of modulation

74
Q

What is the role of M3- M4 Linkers of the Nicotinic ACh receptor?

A

Phosphorylation, oxidation, Ca2+ binding site, ect.

More modulation.

75
Q

What is the thought on ancestry of ligand gated channels with pentametric structures?

A

-Very similar, so it is thought that they diverge from a common ancestor over time.

Anion/ Cation selective –> GABAr, GLY, nAChR, ect.

76
Q

Which channel is the most ancient ligand-gated channel?

A
  • Glutamate channels

* Come from a different evolutionary line than the other channels.

77
Q

Which is the main excitatory neurotransmitter in the CNS?

A

Glutamate

78
Q

What are the 2 main types of Ionotropic glutamate receptors?

A

AMPA receptors- mediate vast majority of fast excitatory neurotransmission

NMDA receptors- slower, sensitive to Na+/ K+ but highly permeant to Ca2+
*Important in neuronal plasticity

79
Q

Examples of Ionotropic glutamate receptors:

A

GluR# for AMPA and NMDAR# for NMDA

80
Q

What ions cause a voltage block of Ca2+ current?

A

Mg2+ ions block Ca2+ current

81
Q

Describe AMPA and NMDA current flow.

A

At low potentials (very negative) NMDA channels do not open because Mg2+ blocks the current, and only fast current can pass through AMPA channels. At higher potentials, NMDA current and AMPA current can be activated (Mg2+ is pushed out at positive potentials)

82
Q

Why is NMDA current important?

A

-Allows for the passage of Ca2+ and slower kinetics.

83
Q

What type of channels mediate inhibitory post synaptic potentials (IPSP’s) ?

A

-Anion Channels (-) !

84
Q

What are 2 main types of anion channels?

A

GABAa and Glycine channels act by opening Cl- channels.

-Glycine receptors are blocked by Strychnine.

85
Q

Defects in the glycine receptor leads to what disease?

A

-Startle disease (HYPEREKPLEXIA)

86
Q

What is the main CNS inhibitory neurotransmitter?

A
  • GABAa receptors
  • Glycine mediates the rest (smaller amount)
  • Synaptic inhibition is tightly regulated
  • -> Too little= unconsciousness and coma
  • -> Too much= seizures
87
Q

What inhibitory receptors are important in the brain, particularly for mediating the effects of barbiturates and benzodiazepines?

A

GABAa receptors

–>Increase inhibitory potentials!

88
Q

What are the 2 types of vesicles which store neurotransmitters?

A
  • Small clear vesicles (low frequency stimulation)

- Large dense core (high frequency stimulation)

89
Q

True or False:

Bursts of high frequency stimulation is required for the release of both types of vesicles.

A

-True.

90
Q

What are synapses?

A

Synapses are the physical sites of memory storage for the brain!

91
Q

What is the relationship underlying synaptic strength?

A
  • The relationship between presynaptic activation and the amplitude of the post synaptic response.
  • ->Sensitivity of a synapse can lead to a long term change in it’s future effectiveness- builds memories as a circuit.
92
Q

What is “Working Memory”?

A
  • Short term memory
  • Seconds- Minutes
  • Continual series of fleeting memories
93
Q

What is “Long Term Memory”?

A
  • Many last for hours to decades
  • Strongly resists disruption and replacement.
  • Allows for the accumulation of knowledge over time.
94
Q

What is Facilitation involved in high frequency stimulation?

A

Allows for the release of neurotransmitters for 10-100 ms (rapid & ends quickly)

95
Q

What is Potentiation involved in high frequency stimulation?

A

Allows for the release of neurotransmitters from seconds to minutes (attenuates)

96
Q

What is Depression involved in high frequency stimulation?

A

This is a short term decrease in neurotransmitter release which can occur during high frequency stimulation.

97
Q

What is Habituation involved in low frequency stimulation?

A

-A slowly progressing decrease that occurs during relatively low frequency activation.

98
Q

What is likely the cause of Facilitation in high frequency stimulation??

A

-An accumulation of Ca2+ in the presynaptic terminal causing an enhancement in the probability of release of individual quanta of neurotransmitter

(larger release)

–>Low (Ca2+)i = smaller release

99
Q

What may cause depression in high frequency stimulation?

A

May be caused by a depletion of vesicles from the synaptic terminal.

100
Q

What are the advantages of studying synaptic plasticity on Aplysia Californica ?

A
  • Simple nervous system

- Simple behavioral repertoire

101
Q

The gill and siphon of the Aplysia Californica undergo what type of frequency stimulation?

A

Low frequency stimulation

  • ->Habituation
  • Occurs due to receptive stimulation of the sensory neuron, leading to a progressive decrease in the size of the post synaptic neuron response.
  • Show classical conditioning
102
Q

What is the Classical Conditioning?

A

-A learning process that occurs when 2 stimuli are repeatedly paired.

–>Paired stimuli gives the largest response.
Changes in synaptic strength can be long lasting.

103
Q

What is Long Term Potentiation (LTP)?

A

–>Trains of high frequency stimulation of a specific synapse which can lead to long lasting increases in synaptic strength.

-Hippocampal neurons can undergo this long term increase in synaptic efficacy.

104
Q

In what region of the brain has LTP been most intensely studied?

A

The Hippocampus

105
Q

Is an increased number in quanta a pre or post synaptic response?

A

LTP does not change the size of response but it changes the number of quanta detected in the post synaptic cell.

*Due to the insertion of AMPA receptors

106
Q

Describe insertion of AMPA receptors on LTP.

A

-One type of LTP is due to the insertion of AMPA receptors into the post synaptic spine, which converts a “silent” synapse into an active synapse.

107
Q

What is Associative LTP?

A

-LTP activation requires activation of the presynaptic terminals that occurs at the same time as depolarization of the post synaptic neuron.

  • Achieved by rapid repetitive stimulation of one input, or by coincident activation of two or more inputs.
  • Cooperative Activation= Summation
108
Q

What happens when the post synaptic cell is depolarized?

A

-LTP is evoked.
–>REQUIRES NMDA RECEPTORS
(Causes the release of glutamate which leads to the depolarization)

109
Q

What is Long Term Depression (LTD) ?

A
  • Long term decrease in synaptic efficacy

- Type of low frequency stimulation over a long period of time (causes a decreased response)

110
Q

True or False:

Both LTP and LTD depend on an increase in Ca2+ concentration in the post synaptic neuron.

A

True

111
Q

What is the proposed mechanism for LTP and LTD?

A

Glutamate is released from the presynaptic terminal and activates NMDA receptors, which allows for Ca2+ to enter the post synaptic cell and depolarize the cell.

-Glutamate is also able to activate AMPA receptors.

112
Q

What happens when there are high levels of Ca2+ inside the cell due to high frequency stimulation?

A

-Leads to net activation of protein kinases and phosphorylation of one or more synaptic proteins that regulate synaptic strength.

113
Q

How could LTP be initiated?

A

One hypothetical pathway has the phosphorylated/ dephosphorylated synaptic proteins modulating the AMPA receptor channels.
–>Increase in (Ca2+)i leads to the phosphorylation of synaptic proteins and LTP activation.

114
Q

What is a pathway that may lead to LTD?

A

A moderate increase in (Ca2+)i produced by low frequency stimulation preferentially activates protein phosphatases which dephosphorylate synaptic proteins in LTP activation- leads to LTD.

115
Q

What type of channel is responds to capsaicin, the hot sensation produced by chili peppers?

A 
TRP Channels 
(Transient receptor potential channels)
116
Q

What kind of receptor is a TRPC Receptor?

A

Classical

First discovered

117
Q

What kind of receptor is a TRPV Receptor?

A

Vanilloid

  • Capsaicin Receptors
  • Also responds to warm sensations
118
Q

What kind of receptor is a TRPM Receptor?

A

-Melastatin

Tumour sensor in mice

119
Q

What kind of receptor is a TRPA Receptor?

A

Ankyrin

120
Q

True or False:

-All neurons are sensitive to temperature, but some have evolved into thermoreceptors.

A

True.

-There are specialized sensory neurons, however, whose activity changes dramatically with temperature.

121
Q

Where are the main peripheral/ core temperature sensors in the body?

A

Skin and the hypothalamus

122
Q

What is a Tonic response?

A

-Steady response to changes in temperature
(as long as the stimulus is present)
–>Always present- the eyes are always in-taking light so you can see.

123
Q

What is a Phasic response?

A

Response only to change
(stimulus is off the peak of the usual response)
–>Response to change only.
–>Clothing example- you forget you’re wearing clothing

124
Q

What are receptive fields?

A

1mm area on the skin receptive to changes in temperature.

-Correspond to individual sensory fibres (most likely individual nerve endings)

125
Q

What is likely the main contributor to Thermosensation?

A

Ion passage through ion channels

126
Q

What temperature does TRPV1-4 respond to?

A

Transduce Warm Temperature Sensations

127
Q

TRPV1 Channel corresponds to?

A

Vanniloid receptor activated by vanniloid compounds

  • Capsaicin
  • ->High temperature threshold approx. 43 degrees
  • Other TRPV channels are activated at more moderate temperatures.
128
Q

What does TRPV8 correspond to?

A

Mediates sensation of moderate cold (menthol receptor)

129
Q

The sensation of hearing depends on the detection of what?

A

-Vibration of the hair cells which is dependent on mechanosensitive TRP channels.

130
Q

What type of cells are Hair Cells?

A
  • Modified epithelial cells (NOT NEURONS).

- Constantly exposed to 2 different extracellular solutions.

131
Q

How do hair cells mediate the opening of TRP channels?

A
  • Vibration of the stereovilli in one direction causes the opening of TRP channels (likely TRPA1), while deformation in the other direction causes them to close.
  • Opening of these TRP channels leads to an influx in K+ ions because the endolymph draws in K+.
  • Leads to a resultant depolarization, Ca2+ influx and transmitter release.
132
Q

What structures links Stereovilli?

A

Tip Links

  • Keeps them mechanically connected.
  • Tall stereovilli don’t have tip links, indicating that channels are seen to be located at the BOTTOM of tip links of smaller stereovilli.
133
Q

True or False:

-We can smell over 400,000 odorants.

A

True.

*80% smell bad for human protection.

134
Q

What is Rhodopsin? What pathway binds to Rhodopsin and moves in conjunction with bound light allowing people to see?

A
  • A receptor that responds to light.
  • Constructed from retinal and protein opsin
  • Rhodopsin is bound to retinal, and when light hits the ligand, a conformational change occurs and the channel is flipped.
  • Leads to activation of a G protein, leading the conversion of cGMP which turns off dark current and hyperpolarizes the cell.
  • The signal is sent through the optic nerve and to the brain.
135
Q

True or False:

A blockade of K+ Channels can POTENTIATE ACh release (dendrotoxins).

A

True

136
Q

Blockade of Ca2+ channels by which toxins causes the blocked release of ACh?

A

w-conotoxin and q-agatoxin

137
Q

What is Botulism and Tetanus mechanism of action?

A

Block exocytotic release of ACh by degrading synaptic proteins.

138
Q

What is the effect/ mechanism of action of black widow spider poisoning?

A

-Causes an explosive release of ACh in the synapse

139
Q

What is ALS (amyotropic lateral sclerosis) or Lou Gehrig’s disease?

A
  • Results from the degeneration of motor neurons and is characterized by the gradual loss in motor function leading to paralysis.
  • Death usually occurs within 5 years.
140
Q

What is Myasenthia gravis?

A

-A disease characterized by muscle weakness brought on by an autoimmune response to the ACh receptors at the NMJ.

141
Q

What can be used to treat Myasenthia gravis?

A

-AChE inhibitor (increasing the time ACh stays in the synapse)
Ex. Neostigmine

142
Q

What is Lambert- Eaton Syndrome?

A

An autoimmune disease caused by antibody block against presynaptic Ca2+ channels- meaning Ca2+ can’t cause muscle contraction.
-Characterized by weakness and fatigue.

143
Q

Where do Parasympathetic nerves originate?

A

-Originate in the medulla and sacral spinal cord.

144
Q

Where do Sympathetic nerves originate?

A

-Originate in the thoracic and lumbar spinal cord.

145
Q

True or False:

The adrenal medulla is activated as part of the parasympathetic response.

A
  • False

- ->Sympathetic response.

146
Q

Chromaffin cells secrete what catecholamine into the blood?

A

Epinephrine

147
Q

What is the name of the drug which is an alpha1 agonists used to treat nasal congestion.

A

Phenylepherine

148
Q

What is the name of the drug which is a beta1 antagonist used to treat hypertension?

A

Propanolol

149
Q

What is the name of the drug which is a beta2 adrenergic agonist used to treat asthma?

A

Isoproterenol

150
Q

What kind of drug is Atropine and how is it used clinically at the eye doctor?

A
  • Muscarinic antagonist

- Pupil dilator for eye exams (causing mydraisis)

151
Q

What are autonomic varicosities?

A

Axons of postganglionic neurons make multiple points of contact with their targets.

152
Q

What is the resultant PSP from nicotinic receptor activation?

A

Quick EPSP

153
Q

What is the resultant PSP from muscarinic receptor activation?

A

Slow EPSP

154
Q

What is the result of the activation of M type current?

A

Inhibits firing over a relatively long time scale, which can lead to neuronal hyperexcitability.
–>Causes only 1 action potential instead of constant firing.

155
Q

What occurs after the addition of Muscarine to muscarinic receptors?

A

-Results in a steady state depolarization, and blocks M-type current.

156
Q

True or False:
Cotransmission can modulate responses in the ANS, as the rate and pattern of action potential firing influences the release of transmitters at the presynaptic terminal.

A

True!

157
Q

What pathway affects ATP binding to cause contraction of smooth muscle?

A

ATP binds to a purinoceptor (a ligand-gated cation channel) on the smooth muscle cell, leading to depolarization, activation of voltage-gated Ca2+ channels, increased [Ca2+]i, and the rapid phase of contraction.

158
Q

What pathway affects NE binding to cause contraction of smooth muscle?

A

NE binds to an alpha 1-adrenergic receptor, which-through a Gq/PLC/IP3 cascade, leads to Ca2+ release from internal stores and the second phase of contraction.

159
Q

What pathway affects Neuropeptide Y binding to cause contraction of smooth muscle?

A

Neuropeptide Y binds Y1 receptor and causes an increase in intracellular calcium, leading to contraction
*Slowest phase of contraction

160
Q

What are the 2 ways Nitric Oxide diffuses through Smooth Muscles?

A
  • Nitric Oxide can be released due to interactions with endothelial-1 to produce NO which can diffuse through smooth muscle, or ACh binds M3 receptors leading to NO production.
  • ->NO is not stored as it is a gas, and diffuses through smooth muscle causing relaxation.
161
Q

What pathway describes how NO cause relaxation in smooth muscle?

A
  • Both sources of NO activate guanylyl cyclase and raise cGMP intracellularly, which leads to phase 1 relaxation.
  • Neuropeptide VIP binds to receptors and causes an increase in (cAMPi) and a decrease in (Ca2+i) in the cell, leading to DELAYED relaxation.

Electrophysiology Undergrad (1 decks)

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