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BISC 421 - Module II > STUDY GUIDE MODULE III > Flashcards

STUDY GUIDE MODULE III Flashcards

1
Q

What are the 3 hypotheses for how axons find their targets?

A
  1. Mechanical guidance
  2. Resonance
  3. Chemoaffinity
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2
Q

What is Mechanical guidance?

A

growing axons follow track

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3
Q

What is resonance?

A

growing and connecting axons induce identity of postsynaptic cell

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4
Q

What is chemoaffinity?

A

pre and post synaptic cells have ligand/receptor pair

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5
Q

Which hypothesis for how axons find their targets has the most evidence?

A

chemoaffinity

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6
Q

What are 2 points of evidence for chemoaffinity?

A
  1. taking eye out of frog + rotating it (Roger Sperry’s experiment)
  2. guidance cues that are either short or long range attraction/repulstion
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7
Q

What happens in Roger Sperry’s frog experiment?

A
  • frog sticks out the tongue when fly is in the wrong direction
  • temporal and nasal parts rotated-temporal retina still projecting to the anterior tectum
  • the nasal parts projecting to the posterior tectumï
  • shows axons already know where to go and can’t adapt
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8
Q

What interaction is coming into play in the retinal tectal system?

A

short range interactions

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9
Q

What are short range interactions?

A
  • temporal retinal axons grow only on anterior membranes (not posterior) where as nasal axons don’t discriminate
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10
Q

What experiment shows short range interactions in the retinal tectal system?

A
  • boiled membranes from anterior or posterior tectum to see which one contained the activity.
  • boiling posterior tectum membranes eliminated preference by temporal axons
  • cues were repulsive.
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11
Q

What is the cue in short range interactions in the retinal tectal system?

A

ephrin

receptor is eph

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12
Q
  1. How are neurons which are developing attracted from the roof plate to the floor plate?
A

netrin is acting as a long range attractive cue

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13
Q

How do we know that netrin acts as a long range attractive cue?

A

knock out netrin and you don’t get the attraction

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14
Q

Name the attractive and repulsive long range and short range cues

A

Attraction: Short range (collagen) and long range (netrins)

Repulsion: Short range (ephrins) and long range (slit)

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15
Q

What is required for midline crossing?

A

Slit repulsion

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16
Q

What is slit repulsion?

A
  • knock out slit and the repulsion is not turned on so

- axons stay in the midline and do not cross

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17
Q

What is required for the movement of the growth cone?

A
  • Polymerization of actin causes movement of the growth cone

- lamelapodium is tubulin rich and filopodia are actin rich

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18
Q

What regulates the dynamics of the growth cone?

A

Ca2+

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19
Q

What is the matching problem?

A
  1. Neurons require target-derived trophic factor for survival
  2. Target generates limiting quantities of factor
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20
Q

How is matching of neuron to one target (muscle) achieved?

A
  • Neurons compete

- those that get enough, survive; those that don’t die

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21
Q

What are the 2 most important events for the post synaptic changes at the NMJ?

A
  1. Immediate redistribution of ACH receptor

2. Increase in expression at synapse and decrease in expression in non synaptic regions

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22
Q

What molecules are involved in immediate redistribution of ACH receptor?

A

agrin signals through MuSK

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23
Q

What molecules are involved in the increase in expression at synapse and decrease in expression in non synaptic regions?

A

Neureglin (also called ARIA).

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24
Q

What are the four basic divisions in somatosensation?

A
  1. Touch
  2. Proprioception (not detected by the skin)
  3. Pain (nociception)
  4. Temperature
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25
Q

Where are the sensory neurons located?

A

In the Dorsal root ganglia or the trigeminal ganglion for the face

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26
Q

What is special about sensory neurons?

A

They are pseudounipolar (2 axons and no dendrite)

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27
Q

Each ganglion innervates a _______ called a ______

A
  • single region of the body

- dermatome

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28
Q

For touch, what are the four basic receptors?

A
  1. Merkel Receptors
  2. Messiner receptors
  3. Ruffini
  4. Pacinian
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29
Q

What are Merkel Receptors?

A

small receptive field, slow adapting, medium threshold for mechanical stretch, edges and points and fine texture, braille

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30
Q

What are Messiner receptors?

A

medium receptive field, rapid adapting, small threshold for mechanical stretch, motion and grip

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31
Q

What are Ruffini receptors?

A

large receptive field size, slowly adapting, very large threshold for mechanical stretch, skin stretch and finger position

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32
Q

What are Pacinian receptors?

A

large (entire finger) receptive field size, rapidly adapting, and very small threshold for mechanical stretch, vibration and grasping

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33
Q

What are the 4 somatosensory response characterizations?

A
  1. Speed of conduction
  2. Adapting or non adapting
  3. Receptive field size
  4. Threshold of activation
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34
Q

Where in the body is the best two-point discrimination? (smallest receptive field size)

A

In the fingers

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35
Q

How do we respond to mechanical deformations?

A
  • At level of nerve endings there are ion channels that exist in the closed state prior to the mechanical change and then
  • when stretched Na+ is allowed in
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36
Q

What is an example of a mechanical deformation?

A

piezo1 and piezo2 are essential components of distinct mechanically activated cation channels

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37
Q

What is the general pathway for touch sensation?

A

ascend ipsilaterally and don’t synapse until the brainstem

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38
Q

What is the pathway for touch sensation?

A
  1. Mechanosensory input ascends ipsilaterally through the dorsal columns
  2. synapse and cross at the midline near the brain
  3. (gracile and cuneate nucleus extends through the medial lemniscus to the thalamus and then the cortex)
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39
Q

What do proprioceptors detect?

A
  • change in muscle length

- tension in on the muscle to detect body positioning

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40
Q

Proprioceptors are part of _______

A

local circuit in the spinal cord that underlies the knee jerk reflex

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41
Q

Why should you practice the piano?

A

Expansion of a cortical representation by a repetitive behavioral task

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42
Q

The cells that mediate pain and temperature are cells that terminate in what?

A

Free nerve endings

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43
Q

What is congenital insensitivity to pain and what is happening in individuals who have this disorder?

A

-Individuals with this disorder cannot feel pain but can feel normal touch

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44
Q

What is the cause of congenital insensitivity to pain?

A

-Due to a mutation in a Na+ channel that is specific to nociceptors

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45
Q

What are the 2 types of nerve fibers that detect pain and what kind of pain?

A

Alpha delta = sharp pain

C fibers = slow dull pain

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46
Q

Which afferents are the slowest for pain nerve fibers?

A

skinniest afferents are the slowest

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47
Q

What are the 3 molecules of temperature and pain?

A
  1. TRPV1- heat and chili peppers
  2. TRPM8- cold and menthol
  3. TRPA1-pain and mustard
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48
Q

What was the experimental method for isolating the TRPV1 or capsaicin receptor?

A
  • Used cloning:
  • isolated total mRNA from DRG
  • introduced to tissue culture that don’t normally respond to capsaicin
  • measured influx of calcium with intracellular calcium imaging
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49
Q

What can an isolated single mRNA generate?

A

-response to capsaicin (calcium ion channel) and determine receptor amino acid sequence

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50
Q

What is the TRPV1 receptor opened by?

A

This receptor is opened by heat, capsaicin, and acidification

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51
Q

What does knocking out TRPV1 do?

A

causes inability to taste chili peppers and less sensitive to hot temperatures

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52
Q

What happens with a knockout of TRPA1?

A
  • injecting formalin into the paw of a mouse
  • measuring the time spent licking the paw,
  • see that with knockout all phases of the pain response are decreased.
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53
Q

What else does TRPA1 also respond to?

A

carbonation

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54
Q

What happens in an inflammatory reaction?

A
  • Inflammatory mediators (NGF) up regulates TRPV1 activity causing channels to open at lower temperature
  • cells fire at lower temp
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55
Q

What are inflammatory mediator cells?

A

NGF

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56
Q

What is the result/example of an inflammatory reaction?

A

warm shower feels hot

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57
Q

What tract do nociceptor afferents ascend through?

A

-anteriolateral tract

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58
Q

Where does the anteriolateral tract cross?

A

-crosses at same level of spinal cord where axons enter

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59
Q

What happens when you have a lesion of the spinal cord?

A
  • won’t feel pain on opposite side of body

- won’t feel touch on same side of body in regions lower than region

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60
Q

What do we mean by saying that pain has descending control?

A
  • descending fibers synapse on pain afferents

- block incoming pain signals

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61
Q

What are the 3 chemical senses?

A
  1. smell
  2. taste
  3. vomeronasal (not in humans)
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62
Q

There are odor primaries (T/F)

A

False

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63
Q

What is the general pathway for olfaction?

A
  1. Olfactory sensory neurons in the olfactory epithelium send axons that pass through the cribiform plate to the olfactory bulb
  2. Odorants are detected on sensory cilia that project into the olfactory mucosa
  3. sensory response initiates in cilia
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64
Q

What kind of current is the olfaction sensory response?

A
  • inward current

- action potential depolarizaiton

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65
Q

3 reasons why humans have lower ability to smell than other animals

A
  1. humans have fewer receptor neurons than dogs
  2. humans have fewer receptor genes than mice
  3. humans have ~300 genes each encoding different receptor, mice have ~1000
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66
Q

What is the olfactory sensory transduction pathway? (5)

A
  1. Receptor binds ligand
  2. G protein exchanges GDP for GTP
  3. Adenylate cyclase makes cAMP from ATP
  4. cAMP opens a CNG (cyclic-nucleotide gated) ion channel
  5. Na+ and Ca2+ comes into cell causing depolarization
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67
Q

What is the olfactory sensory transduction pathway? (5)

A
  1. Receptor binds ligand
  2. G protein exchanges GDP for GTP
  3. Adenylate cyclase makes cAMP from ATP
  4. cAMP opens a CNG (cyclic-nucleotide gated) ion channel
  5. Na+ and Ca2+ comes into cell causing depolarization
68
Q

What provides specificity in the olfactory system?

A

Each receptor binds a different constellation of odorants

69
Q

What are 4 characterisits of odorant receptors?

A
  1. They are -7 TM G protein coupled
  2. encoded in intronless genes
  3. scattered throughout the genome
  4. number in the hundreds (we have 388 functional receptors)
70
Q

How many genes for odorant receptors?

A

hundreds

71
Q

How many receptors per neuron/

A

1 receptor/neuron

72
Q

What kind of distribution of olfactory sensory neurons?

A

random distribution in olfactory epithelium

73
Q

Each neuron responds to _______ and each odorant activates _______

A

subset of odorants, several receptors

74
Q

________ in olfactory bulb of axons from olfactory sensory neurons that express same receptor

A

convergence

75
Q

What are our five tastes?

A
  1. Bitter: toxins (from plants) aversive
  2. Sweet: nutritious (can detect at only high concentrations)
  3. Umami: amino acids
  4. Sour: protons, citrus.
  5. Salty: NaCl
76
Q

How are different tastes detected?

A
  • specific receptors detect tastants

- specific subsets of cells respond to each class of tastants

77
Q

What was the experiment used to identify the sweet receptor?

A
  • cloned from mouse based on identification of mouse that cannot taste sweet
  • respond to sweet using calcium imaging
78
Q

In the mouse used to identify sweet receptor, what was the role of calcium?

A

Ca2+ elevation in response to sweet

79
Q

What are the 2 sweet response receptors?

A

T1R2 and T1R3 coupled to PLCB2 and TRPM5

80
Q

What is the umami receptor composed of?

A

T1R1 + T1R3

81
Q

What are the bitter receptors?

A

-T2Rs

82
Q

What are 2 qualities of bitter receptors?

A
  1. family of 30 GPCRs-all expressed in same cells

2. cannot distinguish different bitter tastes

83
Q

What is the transduction pathway for bitter taste?

A
  1. T2R/T1R receptors are GPCRs, activate G protein, which is coupled to PLCB2
  2. PLCB2 breaks down PIP2 to generate IP3
  3. IP3 binds to IP3 receptors to release intracellular stores Ca2+
  4. open a Ca2+ gated TRPM5 channel
84
Q

Can TPRM5 and PLCB2 Knockouts taste bitter or sweet taste?

A

no

85
Q

What determines whether something tastes good or bad?

A

-Cell type, not receptor

86
Q

What experiment showed what determines whether something tastes good/bad?

A
  • inserted unnatural receptor (RASSL) into T2R expressing cells
  • animals avoid agonist
87
Q

What happens when human specific bitter receptor is put into T2R cell?

A

-animal avoid biter agonist

88
Q

What happens if human bitter receptor in T1R cell?

A

-animal attracted to bitter

89
Q

How are genetic changes made?

A

promoters

90
Q

What is the T1R1 promoter?

A

-T1R1 promoter directs gene to be expressed in umami cell

91
Q

What is the T1R2 promoter?

A

-directs gene to be expressed in sweet cell

92
Q

What is the T2R promoter?

A

-directs genes to be expressed in bitter cell

93
Q

What is so interesting about PTC?

A

-There is polymorphism of whether or not people can taste it.

94
Q

Where is the variation for PTC?

A

• Tas2R38 gene (PAV is taster and AV1 is non taster)

95
Q

What is evidence for balancing selection?

A
  • both tasters and nontasters are found in equal proportions in the populations
  • both alleles must have some selective advantage
96
Q

Why can’t cats taste sweet?

A

-T1R2 is a pseudogene in cats meaning it contains inactivating mutations
EX: cats are obligate carnivores

97
Q

What are sour and salty receptors?

A
  • Both are ion channels

- do not use PLCB2 or TRPM5.

98
Q

What are pheromones?

A
  • chemicals released by animals

- elicit stereotyped behavioral/endocrine response in another animal of same species

99
Q

What do pheromones involve?

A

-vomeronasal system (no cortical representation)

100
Q

How many types of VNO receptors are there?

A

-2 V1Rs have about 200 members and V2Rs have about 70

101
Q

What is the transduction pathway for pheromones?

A
  1. The VNO receptor interacts with PLC through a G protein coupled receptor
  2. TRPC2 channel (express in VNO microvilli) opens
102
Q
  1. What knockout eliminates electrical response to pheromones?
A

TRPC2 knock out-responsible for response of neurons to pheromones

103
Q

What happens when the VNO is silenced in males? (normal/castrated)

A
  • male mouse (intruder) introduced to established mouse, resident attacks intruder (normal)
  • attacks occur less frequently (castrated)
104
Q

What happens is castrated intruder is swabbed with pheromones from urine?

A

-he will again be attacked by resident

105
Q

Do TRPC2 KO mice attack intruders? why/why not?

A
  • no

- consistent with the idea that they cannot sense the pheromones on the intruders

106
Q

What do TRPC2 KO do?

A

-mate with intruders

107
Q

Why do TRPC2 KO try to mate with intruders?

A
  • detection of pheromones by the VNO is necessary to allow male mice to discriminate gender
  • in the absence of this information the default is to mate
108
Q

What do female TRPC2 KO show?

A
  • male typical mating behavior

- seems like the lack of inputs somehow “masculinizes the brain.”

109
Q

Why don’t humans have pheromones?

A

-TRPC2 in humans is a pseudogene probably lost when trichromacy appeared

110
Q

What experiment figured out that we must have a central circadian clock?

A
  • Had people sleep with and without cues a
  • found that in the absence of cues humans still showed a sleep wake cycle, but the cycle was more than 24 hours (about 25 hrs)
111
Q
  1. What other daily cycles do we have besides sleep/wake? (3)
A
  1. Melatonin levels
  2. Body temp
  3. Serum control
112
Q

Where is the central clock?

A

-In the SCN (suprachiasmatic nucleus)

113
Q

How do we know where central clock is?

A
  • neurons in the SCN fire action potentials in a 24 hour rhythm
  • isolated SCN neurons continue to keep this rhythm
114
Q

What happens during ablation of SCN?

A

disrupts wake/sleep cycle in mice

115
Q

What happens if SCN is transplanted?

A

transplanted SCN confers time keeping of host to recipient

116
Q

What is per?

A

-central component of the clock, which when mutated leads to altered circadian rhythms

117
Q

How do per mRNA and protein cycle?

A

with a 24 hour rhythm

118
Q

per is a ______ factor which means that it controls _______

A
  • transcription

- expression of other genes

119
Q

What do per and cry form? What is the function?

A
  • heterodimer

- together they inhibit their own expression

120
Q

What are per and cry turned on by?

A
  • Bmal

- Clk

121
Q

How is the central clock maintained?

A

a ~24 hr of cycle of per transcription, translation, degradation
-controlled by negative feedback of per on its own expression

122
Q

What is the non-visual input to the SCN?

A

-retinal ganglion cells that express the visual pigment melanopsin can detect light (even in the absence of photoreceptor input)

123
Q

What are the cells of the non-visual input to the SCN?

A
  • intrinsically photosensitive RGCs

- (ipRGCs)

124
Q

Where do Melanopsin cells/ipRGCs project? How is this determined?

A
  • SCN

- by expressing lacZ gene

125
Q

What does the lacZ gene generate?

A

-blue color under melanopsin promoter

126
Q

What happens when you genetically kill melanopsin cells?

A

-animals lose entrainment to light

127
Q

Does melanopsin KO produce the same results as genetically killing melanopsin cells?

A
  • no

- ipRGC can also receive input from photoreceptors in abscence of melanopsin

128
Q

What kind of cells are essential for circadian entrainment?

A

ipRGCs(melanopsin cells)

129
Q

ipRGCs(melanopsin cells) are essential for ________

A

circadium entrainment

130
Q

What is familial advanced sleep phase syndrome?

A

-people go to sleep very early and wake very early

131
Q

What is familial advanced sleep phase syndrome associated with?

A
  • associated with mutation in the per gene
  • causes it to accumulate more quickly
  • shortening the clock
132
Q

What is the definition of sleep? (4)

A
  1. naturally recurring state
  2. reduced/absent consciousness
  3. relatively suspended sensory activity
  4. inactivity of nearly all voluntary muscles
133
Q

What is the pattern of sleep cycle?

A
  • Sleep cycle is about 90 minutes

- Each cycle has longer REM stages

134
Q

How many sleep stages?

A

5

135
Q

What is REM?

A
  • rapid eye movements

- dreaming, muscle paralysis

136
Q

What is stage 4 of sleep?

A
  • deepest sleep

- most restful (2 per night)

137
Q

How was it shown that sleep is essential?

A
  • take 2 rats and allow one to fall asleep and not the other

- The one that isn’t allowed to sleep dies and loses body weight

138
Q

What is the sleep center and how is it activated and inactivated?

A
  • If you stimulate the Reticular activating system the animal is awakened
  • If you stimulate the thalamus the animal falls asleep.
139
Q

What is the effect of antihistamines on sleep?

A
  • cause sleepiness
  • histamine is used as a neurotransmitter by a brain area that promotes arousal (TMN)
  • if this is inhibited, sleep is promoted
140
Q

What are 3 sleep disorders?

A
  1. Narcolepsy
  2. Sleep apnea
  3. Delayed sleep phase syndrome
141
Q

What is narcolepsy?

A
  • recurring short episodes of sleep accompanied by cataplexy-mutation in orexin receptor gene leads to narcolepsy in mice and dogs
  • in humans it is thought to be an autoimmune response that leads to loss of orexin neurons
142
Q

What is sleep apnea

A

obstruction of upper airways due to loss of muscle tones leads to frequent awakening

143
Q

What are the 3 association areas?

A
  1. Anterior or prefrontal involved in planning motor output
  2. Posterior links information from several sensory modalities for perception and language
  3. Limbic emotion and memory
144
Q

What are the two major language areas?

A
  1. Brocas

2. Wernicke’s

145
Q

What is Broca’s area?

A
  • left frontal lobe (posterior inferior frontal gyrus)

- known as motor or expressive aphasia cant get the words out

146
Q

What is Wernicke’s area?

A
  • left superior temporal gyrus where temporal and parietal lobes meet
  • Sensory or receptive asphasia-problem in language comprehension so speech is meaningless
147
Q

What does it mean to say we are split brained?

A
  • Different brain functions are localized to different sides of the brain
  • Each hemibrain can operate independently despite fragmented system for processing information
148
Q

What are the 2 theories of emotion?

A
  • James Lange theory

- Cannon-bard Theory

149
Q

What is the James Lange theory of emotion?

A

-physiological response to a perceived threat precedes and causes an emotional response

150
Q

What is are 4 pieces of evidence of the James lange Theory?

A
  1. Subjects given muscle instructions for facial expression without being told what emotion they are imitating show a change in automatic response appropriate to that expression
  2. Paraplegics show lessoned emotion responses
  3. Adrenaline injection produces fear sensation
  4. Block facial expression, reduced emotion response
151
Q

What is the cannon-bard theory?

A
  • physiological and emotional response occur simultaneously
  • sensory information travels both to the cortex where we have a conscious subjective experience of the emotion and to the hypothalamus which then triggers visceral responses and facial expressions
152
Q

What brain centers control emotion? How do we know?

A
  • hypothalamus
  • if cortex is removed + leave posterior hypothalamus, animals act enraged
  • cortex not necessary for emotional response
153
Q

What is Kluver Bucy syndrome?

A
  • Removal of medial temporal lobes (including limbic lobes) from monkey
  • found that the monkey became tame.
154
Q

How can Kluver Bucy syndrome be observed in humans?

A
  • temporal lobectomy

- see similar changes with removal of amygdala alone

155
Q

What is wrong with patient SM?

A
  • genetic mutation that leads to calcification of bilateral amygdala
  • cannot recognize facial expression of fear, but recognize other emotions
  • fearless
156
Q

What region of the brain is involved with perceptual awareness and attention?

A

-posterior parietal cortex

157
Q

What does the posterior association cortex do?

A

-links information from several sensory modalities for perception + language

158
Q

What is the temporal region used for?

A

face recognition

159
Q

What is a problem associated with unilateral lobe lesions?

A

Contralateral neglect syndrome (lesions on right side neglect left side)

160
Q

What are the 2 types of memory?

A
  1. declarative - what you know

2. non declarative - what you do

161
Q

What are the 2 parts of declarative memory?

A
  1. Long term storage- not well understood

2. Short term memories-hippocampus

162
Q

What are 3 parts of non declarative memory?

A
  1. Procedural memory doesn’t require hippocampus- HM can do procedural memories
  2. Long term storage- not known
  3. Short term- widespread
163
Q

What are the two types of amnesia?

A
  1. Anterograde

2. Retrograde

164
Q

What is anterograde amnesia? What portion of the brain is affected?

A
  • inability to establish new memories

- HM-hippocampal damage and medial temporal lobe

165
Q

What is retrograde amnesia?

A

-difficulty retrieving memories established beforehand

BISC 421 - Module II (14 decks)

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