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Physio Neurons > Neurons > Flashcards

Neurons Flashcards

0
Q

What is Playtoxin?

A

A toxin found in marine animals, which binds and locks the Na/k toxin in a way that causes it to allow passive diffusion of ions. Kills the gradient. Extremely toxic

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1
Q

What do Digoxin and Ouabain do?

A

Bind and inhibit Na/k ATPase in the heart and increase contracibility

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2
Q

What creates the membrane potential across neurons?

A

Leaky K + channels, also sometimes known as background channels, because they are always open

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3
Q

What maintains the membrane potential of a cell?

A

The na/k ATPase pump

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4
Q

What are isoflurane and halothane

A

They are general anesthetic gases that activate leaky potassium channels, making neurons less excitable

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5
Q

What is the name of the potassium leak channels that set the resting potential in Cardiac Myocytes?

A

Inward Rectifier Potassium Channels

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6
Q

Example of ligand gated voltage channel?

A

Neurotransmitter binding at synapse

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7
Q

Example of Phosphorylation mediated ion channel?

A

Leaky potassium channels

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8
Q

Example of voltage gated ion channel?

A

Voltage gated Na+ channel
VG K+ channel
VG Ca 2+ channel

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9
Q

What are the 3 factors that cause K+ channels to open slightly slower than Na+ channels?

A
  1. Na+ channels activate more quickly
  2. Na+ channels activate a positive feedback loop, while K+ channels activate a negative feedback loop
  3. The K+ channel’s V1/2 occurs at a more depolarized potential than Na+ channel.
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10
Q

What is the speed of activation and deactivation in vNa+?

A

Fast activation and Fast deactivation

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11
Q

What is the speed of activation and deactivation in vK+?

A

Activates slowly, and stays open for longer

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12
Q

What are the three states of a vNa+ channel?

A

Closed, Inactive, Open

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13
Q

What’s the difference between the closed and inactive state of vNa+?

A

The inactive state is not competent to open even due to depolarization. The closed state can be induced to open due to depolarization.

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14
Q

What is the absolute refractory period?

A

The absolute refractory period is period where regardless of the stimulus, an action potential cannot be fired. This is due to the vNa+ being in the inactivate form.

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15
Q

What is the relative refractory period?

A

This is a period where an action potential can be fired, however, the stimulus must be larger than normal, because at this point the membrane potential is more negative than the resting potential (hyperpolarization) due to the vK+ channels being opened for a long time.

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16
Q

What is orthodromic?

A

Means that the action potential moves from the axon hillock to the terminal synapse. In normal neurons.

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17
Q

What is antidromic?

A

An experimental condition where the action potential moves from the terminal synapse to the axon hillock.

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18
Q

What is Accomodation?

A

it occurs when there is a prolonged depolarization. It makes it so that the threshold for depolarization is higher. This is due to inactivated vNa+ channels

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19
Q

What are Lidocaine and Procaine, and what is their mechanism of action?

A

They are local anesthetics which function by blocking vNa+ channels

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20
Q

What are Phenytoin and Carbamazepine, and what is their mechanism of action?

A

They are antiepilepletical/anticonvulsatory drugs which inhibit vNa+ channels

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21
Q

What is Dofetilide, and what is its mechanism of action?

A

It is an antiarythmic agent, which functions by blocking delayed rectifer vK+ channels

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22
Q

What are Tetrodotoxin and Saxitoxin, and what is their mechanism of action?

A

They are natural toxins which are paralytic. They inhibit sodium channels. Saxitoxin is found in certain shellfish, and sometimes administered in proper dosages by sushi chefs to give a tingle

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23
Q

What is propofol?

A

It is a general anesthetic which functions by blocking vNa+ channels as well as GABA

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24
Q

What are the two ways to get channelopathies?

A

Genetic or acquired

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25
Q

What are periodic paralysis?

A

Periodic paralysis is a group of rare genetic diseases that lead to weakness or paralysis. The underlying mechanism of these diseases are malfunctions in the ion channels in skeletal muscle cell membranes that allow electrically charged ions to leak in or out of the muscle cell, causing the cell to depolarize and become unable to move, because action potentials can’t be generated. Could lead to myotonia, which is uncontrolled contraction of muscle

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26
Q

What is Myotonia?

A

It is the inability to relax your muscle. Myotonia often diminishes with the repeated contractions. It doesn’t affect strength.

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27
Q

What is the characteristic EMG abnormality of myotonia?

A

The EMG has a characteristic abnormality known as the myotonic run, which consists of repetitive discharges that persist for several seconds after a voluntary contraction

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28
Q

What does myotonia sound like on a speaker?

A

like a chainsaw revving up.

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29
Q

What is the defected channel in hyperkelemic periodic paralysis and paramyotonia congenita? What type of inheritance is it?

A

Defect in the Nav 1.4 channel. Dominant inheritance.

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30
Q

Where is vNa1.4 expressed?

A

In skeletal muscle

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31
Q

which synapse is bidirectional? Which is one-directional?

A

Electrical synapse is bidirectional, chemical synapse is one directional

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32
Q

Which occurs faster: electrical or chemical synapse?

A

Electrical. it has no delay

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33
Q

An electrical synapse is connected by gap junctions. What is a gap junction made up of?

A

It is made up of two hemmicahnnels that connect

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34
Q

What is a hemmichannel made up of?

A

A hemmichannel is made up of 6 connexins

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35
Q

What are two disease associated with defective gap junctions?

A
  1. Charcot Marie Tooth Syndrome

2. Metestatic Cancer. Gap junctions function in holding the cells together.

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36
Q

How would you describe electrical synapse transmission?

A

It is graded, so even when the threshold isn’t reached, the signal is transmitted to the post synaptic cell.

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37
Q

What organ has a large distribution of gap junctions, that are integral to its function?

A

The heart. Gap junctions are necessary to transmit signals causing the cells to contract in tandem.

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38
Q

Do muscles contain excitatory or inhibitory neurotransmitters or both?

A

Just excitatory

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39
Q

Is Acetylcholine excitatory, inhibitory, or both?

A

It is both. It is seen as excitatory in the nicotinic receptor, which is in muscles. And it is excitatory/inhibitory in muscorinic receptors.

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40
Q

What is GABA derived from?

A

Glutamate

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41
Q

What are the principle inhibitory neurotransmitters in the nervous sytem?

A

GABA and Glycine

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42
Q

What is the principle excitatory neurotransmitter in the nervous system?

A

Glutamate

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43
Q

What are the 3 Glutamate receptors that trigger cation channels?

A

AMPA
NMDA
Kainate

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44
Q

What is the name of the GCPR that Glutamate binds to?

A

mGluR (1-8)

45
Q

Histamine is a biological amine. Where is it derived from? Is it excitatory, inhibitory, or both?

A

Histidine. Both

46
Q

What is the name and type of receptors that histamine binds to?

A

H1-4. Metabotropic GCPR

47
Q

Where is the H1 receptor and what does it function in?

A

It is in the neurons of the hypothalamus. It functions in cyrcadian rhythms.

48
Q

Where is the H3 receptor, and what does it function in?

A

It is in the CNS, and it functions in inhibiting the release of ACh, dopamine, norepinephrine, 5-HT, GABA

49
Q

What type of receptor is the GABA(A) receptor, and what channel does it cause to open?

A

It is a ionotropic receptor, and it opens Cl- channels. Ethanol acts on this receptor making it more likely to be activated.

50
Q

What type of channel is the GABA(B) channel, and what kind of reaction does it cause?

A

It is a metabotropic GCPR, which eventually leads to the K+ channel activation, which causes hyperpoarization (inhibitory effects).

51
Q

What kind of receptors are GlyR receptors?

A

They bind glycine, and they are ionotropic Cl- receptors. Inhibitory.

52
Q

What kind of receptor is the AchNictonic receptor?

A

ionotropic cation channel (makes sense sense this is the receptor exclusively at the neurotransmitter)

53
Q

What kind of receptor is the AchMuscarinic?

A

Metabotropic GCPR

54
Q

Where are Ach receptors found in the parasympathetic nervous system?

A

Preganglionic neruons and post ganglionic neurons

55
Q

Where are Ach receptors found in the sympathetic nervous system?

A

pregangliotic neruons

56
Q

Where are Ach receptors located in the Adrenal Medulla?

A

Presynaptic Neurons

57
Q

What is seratonin (5HT) made from?

A

Tryptophan

58
Q

Is seratonin E/I/both?

A

Both

59
Q

Where are seratonin receptors?

A

Brain and GI

60
Q

What is the name of seratonin receptors, and what type are they?

A

5HT (1-7). They are all metabotropic GCPR, except for 5HT3, which is ionotropic cation channel.

61
Q

What is the collective name of Dopamine, Epinephrine, and Norepenphrine? What are they derived from? Are they E/I/both?What type of receptors do they have?

A

catecholamines, tyrosine, both, metabotropric GCPR

62
Q

What is the effect of Dopamine?

A

inhibit the release of prolactin

63
Q

What are the types of receptors that epenephrine and norepinephrine bind to? What are they involved in?

A

Bind to androgenic receptors (alpha 1-2 and beta 1-3), involved in stress response/fight or flight response.

64
Q

Does Nitric Oxide use receptors? How does it exert its effect?

A

It doesn’t need receptors, it just diffuses across the membrane, and causes effect in guanlyl cyclase, and it works as a vasodilator

65
Q

What are the two forms that neuropeptides can take?

A

Neurohormones-released in the bloodstream

Neuromodulators

66
Q

How can neuromodulators act?

A

Presynaptically-regulate the amount of neurotransmitter being released
Postsynaptically-cosecreted with neurotransmitters

67
Q

ATP can act with neurotransmitters? Which ones is it released with? What type of response does it elicit?

A

Noradrenaline and neuropeptide Y. Causes smooth muscle contraction. Also involved in the immune response.

68
Q

What is the cause of Parkinson’s Disease?

A

Caused by a loss of dopamine generating cells in the substantia nigra.

69
Q

How are Parkinson’s patients treated?

A

They are given derivatives of L-Dopa, which allows them to make dopamine.

70
Q

What is Resperine?

A

Reserpine was a commonly prescribed drug for hypertension. However, it is rarely used now due to its severe side effect of catecholamine depletion from
neurotransmitter vesicles, leading to prolonged neurotransmitter vesicles leading to prolonged
and severe depression.

71
Q

How are pre-synaptic vesicles released?

A

When an action potential travels down an axon, it causes calcium gated channels to open, and this causes the intracellular concentration of calcium to rise up to 1000x, which then causes presynaptic vesicles with neurotransmitters to fusion and be released into the synapse.

72
Q

What is Lambert‐Eaton myasthenic syndrome (LEMS) ?

A

a rare neuromuscular autoimmune disorder that occurs as a result of self‐antibodies against voltage‐gated calcium channels in the self antibodies against voltage gated calcium channels in the
presynaptic nerve terminal at the NMJ.

73
Q

What is Synaptotagmin?

A

is believed to be the calcium sensor that links calcium channel activation to vesicle fusion

74
Q

What is the zipper model for synaptic fusion?

A

There are SNARE proteins that bind, which causes fusion

75
Q

How does botox work?

A

SNARE proteins are cleaved by Botulinum toxin and Tetanus toxin, which allows muscle to relax.

76
Q

What does Acetylcholinesterase (AchE) do?

A

It degrades Ach in the synapse

77
Q

What do some of the drugs (Rivastigmine and Donepezil) to treat dementia in Alzhiemer’s target?

A

They target AchE

78
Q

What is Neostigmine? What does it target? What disease is it used for?

A

It blocks AChE, and it is used to increase muscle tone for people with Myasthenia Gravis

79
Q

What is Sarin, and how does it work?

A

Sarin is a nerve gas(organophosphate), and it works by inhibiting AchE, which causes Ach to build up at the neuromuscular junction, causing muscular paralysis (intermittent contractions), and leads to asphyxiation.

80
Q

Is Ach E/I/B? is this intrinsic of the neurotransmitter?

A

It is both excitatory and Inhibitory. This is not intrinsic tot eh neurotransmitter, it depends on the post-synaptic neuron it is stimulating.

81
Q

What happens when a neurotransmitter binds to a post-synaptic receptor?

A

It directly or indirectly causes an ion channel to open

82
Q

Describe the nAch receptor at the NMJ. How many Ach need to bind to it?

A

It is made up of 5 subunits. 2 alpha, 1 beta, 1 gamma, and 1 delta. Two Ach will bind to the alpha subunits, which causes the ion channel to open, which allows movement of Na+ and K+, causing depolarization

83
Q

How much Ach is in one quantum?

A

a vesicles worth

84
Q

What is a miniature end plate potential?

A

Ach vesicles will fuse and be released from the presynaptic membrane even without an action potential. These will cause very small depolarizations in the post-synaptic terminal. Each MEPP, is caused by one quantum of Ach.

85
Q

Does an action potential from a nerve at the NMJ usually lead to a response in the post synaptic cell?

A

Yes! An AP from a nerve leads to muscle response almost 100% of the time.

86
Q

In the CNS is one symaptic inut enough to trigger a post synaptic AP?

A

No, one is usually not sufficient. Usually requires many/

87
Q

What are the two agonists of the nACh receptor? (open the receptor)

A

Acetylcholine and Nicotine

88
Q

What are the 3 antagonist of nAchR? (inhibit the receptor)

A

Curare (used by natives on darts), Hexamethonium, Pancoronium

89
Q

What causes Myasthemia Gravis?

A

It is an autoimmune disease which binds to nicotinic acetylcholine receptors, which doesn’t allow muscles to be stimulated.

90
Q

What are some symptoms of Myasthemia Gravis?

A

Muscle weakness/Fatigue, especially after muscle activity. Usually weakness in the eye muscle. Double vision and drooping of eye lid.

91
Q

How is myasthenia gravis treated?

A

With AchE inhibitors (Neostigmine), as well as immunosuppressants such as Corticosteriods

92
Q

What is a Myasthenia Crisis?

A

When there is a failure of muscles that are required for breathing. This may require a respirator.

93
Q

What makes Nicotine so addictive?

A

Its addictive properties are mediated through nAChR actions in the mesolimbic reward neural pathways in the forebrain.
Nicotine facilitates the release of dopamine from ventral tegmental area neurons to nucleus accumbens targets.

94
Q

How do post-synaptic alpha androgenic receptors work? They are metabotropic.

A

They are mostly excitatory, and they work through GCPR, which activate Gq, activating phospholipase C, causing DAG and IP3 to be released, and this causes an increase in calcium, which activates PKC, which phosphorylates things, and opens ion channels.

95
Q

What ligands activate alpha-1- androgenic receptors?

A

They are activated by large quantities of catecholamines, at the synapse. However, they are NOT activated by epinephrine and norepinephrine in the blood stream.

96
Q

In what tissues are alpha-1- androgenic receptors expressed? What does the activation of alpha androgenic receptors cause in these tissues?

A

They are expressed in smooth muscle of the skin, skeletal muscle, splanchnic region, spincter of GI tract/bladder, and iris of the eye

Activation of these receptors causes contraction

97
Q

Where are alpha-2-androgenic receptors found? Are they pre/post synaptic? Are they E/I/B?

A

CNS. Pre and Post synaptic. Inhibitory.

98
Q

Which GPCR does alpha-2-androgenic receptor activate?

A

It activates the Gi, which causes an inhibitory effect on adenyl cyclase, lowering the concentration cAMP.

99
Q

How to alpha-2-androgenic rceptors act in pre-synaptic and post synaptic ways?

A

Pre-synaptic, they act as autoreceptors, and inhibit the release of neurotransmitters.

Post synaptic, they act as heteroreceptors, and inhibit an action potential from happening in that cell.

100
Q

Which GCPR do B-androgenic receptors activate?

A

They activate the Gs system, which activates adenyl cyclase, which then causes an increase in cAMP, which activates PKA. BUT B-2 receptors can activate the Gi pathway.

101
Q

Where are B-1 receptors mostly found? What is their function there?

A

They are prominent in the heart.

1) Increased heart rate in the SA node
2) Increased conduction velocity in the AV node
3) Increased contractility in ventricular muscle

These are important in the fight or flight response

102
Q

Where are B-2 androgenic receptors found?

A

They are found in skeletal muscle, smooth muscle in the wall of GI/bladder, and brionchioles.

103
Q

What preferentially binds to B-2 receptors?

A

Epinephrine. In general, a lower concentration of catecholamines is necessary to bind to Beta receptors than alpha receptors.

104
Q

How many synapses in the CNS?

A

hundred billion

105
Q

What the difference between NMJ innervation and CNS innervation in terms of number of neurons?

A

In muscle, you have a one nerve to one muscle fiber innervation, that is always excitatory with Ach. In the CNS, you may have a neuron getting thousands of stimuations, and also branching out and stimulating thousands of other cells. These innervations may be excitatory or inhibitory, and they integrate, and the cell responds if the threshold for AP has been achieved.

106
Q

What are type 1 synapses in the brain?

A

They are often Glutamatergic and therefore excitatory.

107
Q

What are type 2 synapses in the brain?

A

they are often GABA-ergic, and thus inhibitory

108
Q

What’s an example of a neurotransmitter that can excite two different receptors?

A

Glutamate can excite both AMPA and NMDA receptors

109
Q

How is Glutamate exciticity involved in ischemic stroke?

A

When there is a lack of blood going to neurons, this puts the astrocytes in an energetic crisis, which then disables them from removing Glutamate from the extracellular space in the brain, which leads to prolonged excitement, and calcium mediated cell death.

110
Q

What is the only FDA approved drug for someone with an ischemic stroke due to thrombosis?

A

TPA (tissue plasminogen activator), it will dissolve the clot. However, this would be very bad to give to a patient with a hemorrhage.

111
Q

What are Selective Seratonin Reuptake Inhibitors (SSRIs)? Name 3 of them. What conditions is it used for?

A

They block seratonin from being taken back up by the pre synaptic neuron. Zoloft, Prozac, Paxil. Depression, Anxiety, OCD, chronic pain.

Physio Neurons (1 decks)

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