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Neurobiology > Exam 5 > Flashcards

Exam 5 Flashcards

1
Q

What is the labeled line theory of sensation?

A

We know what something is based on where it goes in the brain.

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2
Q

What is transduction?

A

Translation of the environment into neural signals.

There are lots of different stimuli and there are different receptors that respond to each type of stimuli.

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3
Q

How are different intensities of signals felt?

A

There are different receptors that have different thresholds for opening.

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4
Q

What is adaptation?

A

How quickly a sensor stops responding to a stimulus.

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5
Q

What is slow adaptation?

A

Quickly responds to a signal but is slow to stop firing if the sensation persists.

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6
Q

What is rapid adaptation?

A

Quickly responds to the signal and then rapidly stops firing if the sensation persists.

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7
Q

How do habituation and sensitization change the sensation signal?

A

Habituation decreases the amount of signal sent.

Sensitization increases the amount of signal sent.

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8
Q

What is lateral inhibition?

A

When one neuron is active, it can inhibit those around it to give itself greater contrast.
Used for edge detection.

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9
Q

How does attention change our perception of sensation?

A

We only consciously perceive what we are paying attention to.

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10
Q

How does top down control change how we perceive sensations?

A

It can change our perception of the signal and turn it down or up at the CNS level.

It is used for mind over matter.

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11
Q

What are free nerve endings?

A

Polymodal nerve endings.

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12
Q

What are Merkel’s disk nerve endings?

A

Shallow
Small receptive field
Slow adapting.

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13
Q

What are Meissner corpuscle nerve endings?

A

Shallow
Small receptive field
Rapid adapting.

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14
Q

What are Pacician nerve endings?

A

Deep
Large receptive field
Rapid adapting.

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15
Q

What are Ruffini nerve endings?

A

Deep
Large receptive field
Slow adapting.

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16
Q

What is the significance of the difference in size between receptor fields?

A

Smaller receptor fields are helpful for smaller two-point discrimination. They can help you know exactly where something is.

Large receptive fields can be useful for areas that don’t need fine two-point discrimination.

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17
Q

What is the usefulness of having shallow nerve endings?

A

It is easier to activate smaller nerve endings.

Deep nerve endings can be useful to sense things that have more intensity or send signal deeper in the tissue.

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18
Q

What is rapid adapting signal useful for?

A

Rapid adapting is good for knowing when stimuli come on and off.
Know when you first grab hold of something.

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19
Q

What is slow adapting signal useful for?

A

Slow adapting is good for getting constant information.

Continues to let you know that you are holding onto something.

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20
Q

What is somatopy?

A

Map of the body for somatosensory perception.

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21
Q

What types of areas typically have more brain space dedicated to them?

A

Those with more nerve endings/receptors and those that have a more important signal.

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22
Q

What is the plasticity of somatosensory areas like?

A

When different sensory areas are lost, the brain space is reorganized so the old brain space doesn’t go to waste.

When different areas are trained and given more importance, more brain space is dedicated to them.

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23
Q

How does the sensation of phantom limbs occur?

A

Phantom limbs occur when old brain spaces dedicated to areas that no longer exist are reorganized. That are may be reorganized but the old perception pattern of thinking it is an old limb when that area is activated is still there.

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24
Q

What does area 3b do?

A

Main input for touch.

External feelings.

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25
Q

What is area 3a used for?

A

Proprioception.

Internal feelings.

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26
Q

What is area 1 used for?

A

Texture.
Takes information from are 3b.
Integrates new information with older information.
Is needed to necessitate movement.

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27
Q

What is area 2 used for?

A

Size and shape.
Takes information from are 3b.
Integrates new information with older information.
Is needed to necessitate movement.

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28
Q

How is slow adapting and fast adapting information taken in the brain?

A

For each body area, the brain has processing areas for slow adapting and rapid adapting information.

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29
Q

Which layer in the somatosensory cortex receives input from the thalamus?

A

Layer IV.

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30
Q

How are temperature receptors different than touch receptors?

A

There are different temperature receptors that open at different temperatures.

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31
Q

What is the adaptation speed of temperatures receptors?

A

They can adapt, but not as fast as rapid adapting receptors.

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32
Q

How does capsaicin in spicy foods make it feel hot?

A

Capsaicin open TRPV1 channels which are hot temperature channels.

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33
Q

How does mint make it feel cold?

A

Mint opens up cold receptors channels.

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34
Q

What is TRPV1?

A

A hot temperature receptor channel.
It is a Ca2+ channel.
The Ca2+ then opens a Cl- channel.
Cl- leaves and helps depolarize the neuron.

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35
Q

How is pain useful?

A

Pain is useful because it tells you when you are doing something wrong.

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36
Q

What is the difference between nociception and pain?

A

Nociception is when a pain neuron fires and pain is the perception of that signal.

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37
Q

What kind of receptors do nociceptors have? What kinds of stimuli do they open to?

A

Extreme temperatures
Strong mechanical stimulation
Oxygen deprivation
H+ gated ion channels.

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38
Q

Why can it be hard to tell why something hurts?

A

Nociceptors are polymodal which means that they open due to multiple kinds of stimuli and thus, it can be hard to know why something hurts.

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39
Q

What is substance P?

A

A pain neurotransmitter.
It is a neuropeptide.
Thus it takes more energy to release substance P and you can run out of it.

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40
Q

What does substance P do?

A

Activates mast cells to release histamine.
Dilates blood vessels.
Sends a signal to the spinal cord about pain.

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41
Q

What is the role of glutamate in pain?

A

It is a pain neurotransmitter.

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42
Q

What kind of fibers are used for pain?

A

C fibers and Aδ fibers.

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43
Q

What is the difference between C fibers and Aδ fibers?

A

C fibers have a small diameter and are unmyelinated.
Easy to block.
Aδ fibers are myelinated and faster than C fibers.

44
Q

What is the gate theory of pain?

A

When touch and pain information from nearby areas come at the same time, touch information can signal an inhibitory interneuron to inhibit the pain signal.
This is why it is thought that rubbing an area near an injury decreases pain.

45
Q

What is bradykinin?

A

A cellular protease that can activate nociceptors.

46
Q

What sorts of materials from burst cells can activate nociceptors?

A

K+, ATP, various proteases, and prostaglandins.

47
Q

How does K+ activate nociceptors?

A

By increasing the extracellular concentration of K+, the equilibrium potential of K+ changes so the resting membrane potential will increase.
Also, more K+ will go through leak channels and raise the Vm.

48
Q

Where do prostaglandins come from?

A

Cell membrane lipids → arachnidoic acid → prostaglandins

Aracdniodoic acid → prostaglandins are catalyzed by cyclooxygenase (Cox).

49
Q

What do prostaglandins do?

A

Prostaglandins activate G proteins that result in phosphorylation of nociceptor cation channels.
The phosphorylation results in the channels being easier to open.

50
Q

How can inflammation activate nociceptors?

A

H+ release from high metabolic activity can change the pH.
Nociceptors can be pinched.
Inflammation can burst other cells.

51
Q

How do injured cells promote an immune response?

A

Injured cells can release chemicals that activate mast cells.
Mast cells release histamine which then helps promote an inflammation response.
Histamine also directly activates nociceptors.

52
Q

What are analegiscs?

A

Pain killers.

53
Q

What are Cox inhibitors and what are some examples?

A

Prevents the formation of prostaglandins.

Aspirin, ibuprofen, and acetaminophen, lidocaine, novocaine, and cocaine inhibit Cox

54
Q

What is substance P saporin (SP-SAP)?

A

This kills nociceptors.
It specifically kills cells that produce the substance P as it inhibits those ribosomes.
Only used in end-of-life treatment.

55
Q

What is a shot blocker? How does it help decrease pain?

A

It is a rubber material that activates touch receptors and then a shot is given.
Because the touch receptors are already activated, you are less likely to feel the pain from the shot.

56
Q

What is transcutaneous electrical nerve stimulation (TENS)? How is it a pain treatment?

A

Used for treatment for chronic pain.

Maybe be able to help through the gate theory of pain.

57
Q

How is deep brain stimulation (DBS) used as a pain treatment?

A

Deep brain stimulation (DBS) to the PAG is a treatment to lower pain.

58
Q

How are opioids a pain treatment?

A

Opioids are a pain treatment because they act like endorphins and can lower pain.

59
Q

How are antidepressants a pain treatment?

A

Antidepressants can also reduce pain by changing serotonin levels at the RNM.

60
Q

How is hypnosis a pain treatment?

A

Hypnosis reduces activity in the anterior cingulate cortex.

61
Q

What is the pathway of pain perception in the brain?

A

Dorsal horn → Raphe nucleus in the medulla → periaqueductal gray matter (PAG) in the midbrain

62
Q

What is the PAG?

A 
Periaqueductal gray matter
Midbrain. 
Uses endorphins. 
Activating the PAG reduces pain. 
This is thought to be how top-down control happens.
63
Q

What is the Raphe Nucleus Magnus (RNM)?

A

The main area for serotonin production.
Decreases attention to stimuli.
Inhibits nociceptors at the spine.

64
Q

What is the anterior cingulate cortex? What does it do?

A

Controls the unpleasantness of pain.

65
Q

After going from a very cold environment to a warm environment, why can cold water feel warm?

A

Temperature receptors desensitize meaning that they don’t open as easily. Temperature is perceived as a ratio between cold and hot receptors opening so if you run your cold hands under cold water, the cold receptors won’t open but some hot ones will. So you will perceive the water as much more hot than it actually is.

66
Q

What are some possible individual differences that can change pain perception?

A

Pain can have individual differences based on past environmental experiences, genetic differences, age, sleep, serotonin levels, sex, and more.

67
Q

What are the symptoms of depression?

A 
Changes in sleep. 
Changes in appetite
Apathy 
Lack of motivation
Anger
Shows more in males. 
Persistent negative thoughts
Feelings of worthlessness or guilt
A diminished ability to concentrate
Recurrent thoughts of death
Memory problems
The hippocampus is definitely involved in depression. 
Many depression symptoms present as ‘sick’ symptoms. Stuff you could see with a sick animal. 
This is some of the reasoning behind the cytokine hypothesis.
68
Q

What are some social reasons that women may be diagnosed more with depression?

A

Women are socialized to talk more about their feelings than men.
Women have a lot more expectations with emotionally exhausting roles such as child-rearing.
Women tend to worry more often. This could be evolutionarily or by culture.
Could be increasing their cortisol levels.

69
Q

What are some social reasons that men may not be as diagnosed as often with depression?

A

Men are socialized to not share their feelings and have control over their life.
Men are more likely to self-treat in other ways such as alcohol and drugs.
There is a lack of social support for men.

70
Q

What are some biological reasons that women are diagnosed with depression more often than men?

A

Females tend to present with more ‘classic’ depression with a lower mood and sadness while males may present more uncommon presentations such as increased anger.
Women tend to have MAO.
MAO is coded for on the X chromosome.
The bed nucleus of the stria terminalis (BNST), an area near the hypothalamus, is different between men and women.
This area is sexually dimorphic.
This area also releases CRH.
Females tend to have more methylation of genes.

71
Q

What are some biological reasons that men are not diagnosed with depression as often?

A

Men synthesize serotonin 52% faster.

They may be less likely to run low on serotonin.

72
Q

What are some links between depression and alcoholism?

A

Alcohol increases serotonin production.
Alcohol is used as a self-treatment for depression.
Alcohol decreases CRH levels.
Depression drugs that target CRH and serotonin can help alcoholics as well.

73
Q

What is the first part of the cortisol pathway?

A

Hypothalamus makes cortisol releasing hormone (CRH)

CRH is also sometimes called CRF for factor instead of the hormone.

74
Q

What does CRH stimulate in the cortisol pathway?

A

CRH stimulates the anterior pituitary to make an adrenal corticotropic hormone (ACTH).

75
Q

What does ACTH stimulate in the cortisol pathway?

A

ACTH stimulates the adrenal glands to produce cortisol.

76
Q

What does cortisol do?

A

Cortisol is a stress hormone that increases the stress response.

77
Q

What does the normal stress response consist of?

A

Increased respiration.
Increased heartbeat.
Slower digestion.

78
Q

What the negative feedback for the cortisol pathway?

A

Cortisol is also used for negative feedback of the cortisol pathway.
It inhibits the anterior pituitary, hypothalamus, and it activates the hippocampus.
Each of these areas has glucocorticoid receptors that bind to cortisol.

79
Q

What is the positive regulator for the cortisol pathway?

A

The amygdala.

80
Q

What is the monoamine hypothesis?

A

The monoamine hypothesis says that differences in monoamines such as serotonin, norepinephrine, and dopamine cause depression.

81
Q

What are SSRIs?

A

Selective Serotonin Reuptake Inhibitors (SSRIs)=blocks the reuptake of serotonin.
SSRIs are selective to some serotonin receptors but there are other reuptake inhibitors that inhibit the reuptake of other monoamines as well.

82
Q

What are MAOIs?

A

Monoamine oxidase inhibitors (MAOIs)=block MAOs from working which degrade monoamines in the synaptic cleft.

83
Q

What are tricyclics?

A

Tricyclics=reuptake inhibitor for serotonin and norepinephrine.
Not specific.
Also affects muscarinic, CNS acetylcholine, histamine, and epinephrine.
Has more side effects.

84
Q

What are tetracyclics?

A

Tetracyclics=reuptake inhibitor for serotonin and norepinephrine.
Widespread.

85
Q

How does the Raphe Nucelus Magnus support the monoamine hypothesis?

A

People with depression tend to cite pain and it is known the Raphe Nucleus Magnus produces serotonin. If it makes less serotonin it may not be as active with pain perception.

86
Q

How do monoamine drugs support the monoamine hypothesis?

A

Drugs like SSRIs, MAOIs, and more that target monoamines do help some people.

87
Q

What role does tryptophan play in the monoamine hypothesis?

A

Increasing tryptophan levels, a serotonin precursor, in some populations alieves depression symptoms.

Mutations that decrease the efficiency of tryptophan hydroxylase-2 make people susceptible to having depression.

88
Q

What role does MOA-A play in depression?

A

People that have the high activity allele of MOA-A are more likely to have depression.

89
Q

What is evidence against the monoamine hypothesis?

A

Monoamine drugs don’t work for 40% of people and if they do they take weeks to work.
Neurogenesis or some other compensatory mechanism may be happening with monoamine drugs to resolve depression symptoms.
The serotonin reuptake gene plays a role but it doesn’t fit the monoamine hypothesis as having less of it doesn’t result in less susceptibility to depression.

90
Q

What is the diathesis-stress hypothesis?

A

This hypothesis states that having early life stressors can make you susceptible to depression by lowering the efficiency of the negative feedback of the cortisol pathway.

91
Q

What is diathesis?

A

Diathesis=predisposition.

92
Q

What parts of the cortisol pathway are altered in people with depression?

A

More cortisol, more CRH, shorter/altered cortisol cycle, more ACTH (though not all cases with increased ACTH lead to depression) and fewer glucocorticoid receptors.

93
Q

What did the experiment with dexmethasone show?

A

Experiments with dexamethasone, which mimics cortisol, showed only a temporary decrease in cortisol levels.

94
Q

How is the hippocampus involved in depression?

A

People with depression tend to have a smaller hippocampus.
People with depression tend to have memory problems.
Antidepressants increase hippocampus size.
In mice, antidepressants lead to hippocampal neurogenesis.

95
Q

Why would people with depression have a smaller hippocampus?

A

Due to higher levels of stress hormones, the hippocampal neurons can die if they are overstimulated with cortisol.

96
Q

What is the link between serotonin and the hippocampus?

A

Serotonergic neurons in the hippocampus are affected by serotonin depression drugs and the increased serotonin levels may increase hippocampal growth and possibly neurogenesis.

97
Q

What evidence was found in animals with early life stress?

A

Rodents and birds that were stressed early on had stronger stress responses later in life.

98
Q

What role does epigenetics play in depression?

A

Epigenetics plays a role with more methylation of NR3C1, a glucocorticoid receptor, occurring during stressful situations.
Methylation makes transcription harder to occur.

People who died by suicide and had a history of child abuse had more methylation and less expression of NR3C1 receptors.

99
Q

What evidence did the Dutch Hunger Winter show?

A

Analyses of people who were fetuses during the Dutch Hunger Winter showed a higher risk of having mood disorders.

100
Q

What is some evidence against the diathesis-stress hypothesis?

A

It is hard to know exactly what role stress plays in depression in humans because there are so many factors for both and then there are individual differences in how people handle the situation.
Not everyone who undergoes early-life stress develops depression.
They could be using different compensatory mechanisms.

101
Q

What is the cytokine hypothesis?

A

This hypothesis states that background inflammation due to an increased presence of cytokines can cause depression.

102
Q

How is being depressed similar to being sick?

A

People who are depressed have similar behaviors to a sick animal with decreased social interaction and pleasure-seeking activities.

103
Q

What evidence did bone marrow transplants show for the cytokine hypothesis?

A

Bone marrow transplant from susceptible depression animals to control animals resulted in the control animals presenting depression symptoms.

104
Q

What shows some possible comorbidity between depression and inflammation?

A

Individuals with long-term or temporary inflammation have high rates of depression.
Drugs that lower inflammation can help treat depression.
Depression can be harder to treat if someone has an inflammatory disease.
Both may be helped if the inflammation is treated first.

105
Q

What is evidence against the cytokine hypothesis?

A

Some pieces are more correlational such as adding the IL-6 antibodies leading to fewer depression symptoms.

106
Q

What areas does the Raphe Nucleus Magnus innervate?

A

Amygdala.
Hypothalamus.
Hippocampus.
Cortical areas responsible for cognition.
Areas that control norepinephrine which is involved in attention.

107
Q

What has a negative input to the cortisol pathway?

A

Cortisol and the hippocampus.

Neurobiology (5 decks)

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