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Introduction to Neuroscience > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

How do we detect stimuli?

A

receptors convert detection of stimulus into electrical signals, and brain integrates the info

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2
Q

What categories of stimuli can we detect?

A

mechanical, visual, thermal, chemical, electrical

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3
Q

What are some themes of sensory processing?

A

Sensory neurons are specialized to translate specific stimuli into electrical signals, and spatial information about the source of stimulus is preserved in the organization of the CNS

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4
Q

How is the nervous system set up for difference detection?

A

Amplification of new signals and edge detection

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5
Q

Bottom-up modification

A

As information travels up to the brain, it is processed and integrated, allowing for more complex perception

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6
Q

Top-down modification

A

Brain inhibits and prevents some signals from occurring- inhibition of pain is one such example

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7
Q

true or false: receptors only respond to a specific type of stimulus at a specific intensity

A

true

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8
Q

How is intensity of a stimulus encoded?

A

Frequency of action potentials

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9
Q

How do we distinguish different stimuli?

A

Labeled lines organization- in which sensory neurons only respond to a specific input and the brain then interprets the signal based on the wiring/source

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10
Q

What are receptor potentials?

A

Local changes in membrane potential

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11
Q

what are the steps of sensory detection?

A

sensory stimulus detected, receptor potentials, cell reaches threshold, sensory neurons fire action potentials

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12
Q

Which is sensory, the dorsal or ventral root ganglia?

A

Dorsal

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13
Q

What is a pacinian corpuscle and how is it innervated?

A

Pacinian corpuscles are what respond to vibration because their ion channels are stretch sensitive, so when stretched, the sodium enters and depolarizes the cell. They are innervated by dorsal root ganglia

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14
Q

Range fractionation

A

the term that refers to the idea that different receptors have different thresholds of firing over a range of stimulus intensities, so some receptors require a higher intensity stimulus to fire which also allows for us to determine the intensity of the stimulus- high intensity inputs cause combined responses of all three neurons

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15
Q

Sensory adaptation

A

The process by which frequency of action potentials decreases with prolonged exposure to stimuli- this is what allows for emphasis of new stimuli

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16
Q

Phasic receptors

A

Display adaptation

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17
Q

Tonic receptors

A

Little to no adaptation

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18
Q

How do we control attention to information?

A

sensory adaptation, accessory structures like eyelids, top-down processing where higher brain centers suppress some inputs and amplify others

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19
Q

Receptive field

A

The part of the body surface in which a stimulus will trigger firing of that neuron- location and size of receptive field can give information about where a stimulus came from

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20
Q

Surround inhibition

A

stimulus on outside radius of receptive field provides inhibition/prevents cell firing

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21
Q

True or false: body is mapped onto somatosensory cortex

A

true

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22
Q

pathway of sensory info

A

dorsal root ganglia to spinal cord to thalamus to primary somatosensory cortex (S1)

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23
Q

How does sensory information arrive to the brain?

A

each sensory system has its own pathway, and passes through stations during processing; most sensory pathways pass through the thalamus

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24
Q

Where do sensory pathways terminate

A

cerebral cortex

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25
Q

in the touch receptors, where does an axon from the periphery make its first synapse?

A

in the medulla, where it then crosses midline and goes to thalamus

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26
Q

does the left thalamus receive info from the right or left side of the body

A

right side

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27
Q

what are primary sensory cortical areas

A

the first cortical areas to receive sensory info

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28
Q

what are secondary sensory cortical areas

A

perform higher processing on sensory info- secondary somatosensory cortex connects sensory info to brain areas associated with learning

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29
Q

what is pain and why is it important?

A

pain is an unpleasant experience associated with tissue damage, it helps us avoid potentially threatening situations

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30
Q

congenital insensitivity to pain

A

caused by mutation in vgnacs of nociceptive neurons- sensory neurons don’t fire action potentials so don’t communicate painful stimuli to brain

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31
Q

steps of sensory processing

A
  1. Info enters cns through brainstem or spinal cord and travels to the thalamus
  2. thalamus shares info with cerebral cortex, which directs thalamus to suppress some sensations
  3. primary sensory cortex swaps info with nonprimary sensory cortex
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32
Q

Paroxysmal Extreme Pain Disorder

A

rare inherited disorder, characterized by bouts of pain, mutation is in same gene as in cip but vgnacs are overactive

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33
Q

phantom limb pain/neuropathic pain

A

neurons that used to receive sensory input develop abberant activity in absence of normal input, often pain is from tight or clenched feeling- mirror therapy can help as it gives illusion that hand is still there so patient can unclench their hand

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34
Q

3 aspects of pain

A

sensory (throbbing, mild, shooting), cognitive (no pain, mild, excruciating), motivational (affective/emotional quality)

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35
Q

nociceptors: pain receptors

A

nociception- pain sensing, nociceptors are peripheral receptors that respond to painful stimuli, free nerve endings in dermis have specialized receptor proteins, and free nerve endings respond to temperature changes, chemicals, and pain

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36
Q

peripheral mediation of pain

A
  1. damaged cells release substances that excite free nerve endings that function as nociceptors
  2. action potentials generated in the periphery can reflexively excite blood vessels and mast cells to produce inflammation
  3. stimulated mast cells release histamine and another molecule
  4. info enters through dorsal root and synapses on neyrons in dorsal horn
  5. pain fibers release glutamate and substance p, then spinal cord sends info up to thalamus across midline
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37
Q

how is capsacin detected

A

trpv1 receptors, which are on c fibers, which are thin and unmyelinated and therefore allow for longer lasting pain

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38
Q

how is painful heat or cold detected

A

specialized receptors on sensory neurons that can also respond to chemicals

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39
Q

compare and contrast trp2 and trp1

A

trp2 detects higher temperatures, does not respond to capsaicin, and is found on a delta fibers which are myelinated and allow for quick detection of pain

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40
Q

how is cold detected?

A

cool-menthol receptor 1- responds to menthol and to cool temperatures and is located on c fibers

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41
Q

route of pain to brain

A

anterolateral or spinothalamic system transmits pain and temperature sensation; free nerve endings synapse on spinal neurons in the dorsal horn, and pain info crosses midline before moving on to thalamus

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42
Q

describe the 2 responses to pain across 2 brain regions

A

projections to motor cortex create movement, projections to limbic system assign affective aspect. anterior cingulate cortex which is responsible for things like empathy is highly stimulated by painful stimuli

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43
Q

how is analgesia (pain relief) produced?

A

analgesics like acetominophen and ibuprofen block synthesis of prostaglandins which act upon snesory nerves

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44
Q

how do local anasthetics work

A

local anasthetics like lidocaine block action potentials of sensory neurons

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45
Q

what does an epidural involve

A

injection of analgesic or anasthetic directly into spinal cord

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46
Q

analgesia vs anesthesia

A

analgesia=pain relief, anesthesia- loss of consciousness or feeling

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47
Q

top down processing of pain

A

brain can send signals to spinal cord that inhibit nociception, especially w/ release of peptide neurotransmitters like the endogenous opiates

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48
Q

PAG role in nociception

A

signals from PAG cause serotonin release in raphe nuclei, which activates opioid interneurons which inhibits ascending pathways

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49
Q

Describe the overall organization of the visual system

A

optic nerves cross over at optic chiasm and pass through the visual areas of the thalamus, where they then go to the visual cortex

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50
Q

describe the concept of binocular vision

A

info from right visual field goes down left optic tract and info from left visual field goes down right optic trac

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51
Q

does less overlap of visual field mean more or less crossing over

A

more crossing over since more info is specialized to just one field

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52
Q

accommodation

A

process of focusing the lens- lens then focuses light on retina, accommodation can also be pupil dilation to let in light

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53
Q

how is light entering the eye controlled

A

controlled by the pupil dilating or contracting

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54
Q

what is the optic disc

A

where optic nerve leaves the eye

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55
Q

layers of the retina

A

from bottom to top

  1. pigmented epithelium
  2. rods and cones
  3. bipolar cell layer
  4. ganglion cell layer- their axons form the optic nerve
  5. optic nerve
56
Q

cell types in retina

A

interneurons- horizontal (associated with photoreceptors) and amacrine cells (associated with bipolar cells) form lateral contacts and facilitate lateral inhibition

57
Q

compare rods vs cones

A

rods- activate in dim light, cones- associated w/ color - have lots of membrane space called photoreceptor disks that provide a large surface area for rhodopsin and the ion channel

58
Q

fovea

A

center of where light focuses on retina- least cell density, only cones, highest visual acuity

59
Q

blind spot

A

optic disc where optic nerve leaves

60
Q

what is the largest portion of our visual cortex devoted to

A

processing info from the fovea

61
Q

why are our eyes so sensitive to light?

A

amplification of signals downstream of photopigments- photopigments like rhodopsin capture photons

62
Q

what are the two parts of rhodopsin?

A

retinal and opsin, which is a gpcr; when light activates rhodopsin, retinal dissociates and opsin is activated; retinal changes conformation when coming in contact with light

63
Q

steps of signal amplification

A
  1. light changes retinal’s shape
  2. rhodopsin deformed to activate 500 molecules of g protein transducin
  3. gtp replaces a GDP bound to transducin, activating PDE, which reduces cgmp concentration
  4. this causes closure of vgnac’s and hyperpolarization of receptor, so one photon can block a million Na ions
64
Q

how does the visual system deal with a wide range of light?

A

adjusting pupil size, range fractionation, adaptation

65
Q

how does the visual system emphasize edges and change?

A

center-surround organization emphasizes edges and change- number and sensitivity of photoreceptor input onto ganglion cells is the receptive field of that ganglion cell and input to ganglion cell is moderated by bipolar cells and horizontal interneurons; receptor fields have center-surround organization, so the maximum action potentials are released when there is contrast in receptive field- edge detection is also facilitated as there is a different amount of action potentials for different stimuli

66
Q

Effect of light on center and surround of receptive field

A

depending on how photoreceptors are hooked up light may inhibit or excite ganglion cells- in on center, light in center excites, and in off-center, light in center provides inhibition of ganglion cells

67
Q

what is lateral inhibition?

A

excited neurons prevent excitation of other lateral neurons so the cells know exactly where the stimulus is instead of everything becoming excited

Light receptors receiving input from the lighter side of the edges produce a stronger visual response than receptors receiving input from the darker side. This action serves to enhance contrast at the borders making the edges more pronounced.

68
Q

how many of each color cone do we have?

A

more l than m, fewest s (corresponding to wavelengths of light)

69
Q

describe color receptive fields

A

opposing colors can have different affects on receptive field so red off center, green on surround- allow for increased color discrimination and contrast through lateral inhibition

70
Q

what causes color blindness?

A 
loss of functional cones
dichromacy: one type gone
- red: protanopia
- green: deuteranopia
- blue: tritanopia
monochromacy:
- missing 2
achromatopsia
- missing all 3
71
Q

what is retinotropic mapping

A

idea that spatial organization of info from each eye is preserved

72
Q

Laterate geniculate nucleus

A

info from left and right visual field get sent to right and left lgn respectively, info from same part of visual field gets sent to adjacent parts of lgn in the thalamus; axons project back and forth between lgn and striate cortex

73
Q

hemispatial neglect

A

damage to visual cortex or parietal lobe, patient ignores half of stimuli in one visual field

74
Q

where does mixing of two visual pathways first occur

A

striate cortex

75
Q

what parameters does the visual cortex use

A

orientation, movement, frequency

76
Q

what does a simple cortical cell respond to

A

bars of specific orientation; complex cortical cells also respond to movement

77
Q

organization of receptive fields

A

circular receptive fields can combine to form rod shaped receptive fields

78
Q

what is v1

A

primary visual cortex

79
Q

what is v2

A

detects shapes and contours, more complex relationships

80
Q

v4

A

neurons responsive to particular increasingly complex shapes

81
Q

what two processing streams originate in the primary visual cortex?

A

what (ventral, identifying objects) and where (dorsal, assessing location) damage to ventral causes agnosia where u cant name objects, ataxia causes difficulty in using vision to reach for objects

82
Q

prosopagnosia

A

facial fusiform gyrus is in ventral stream, causes face blindness

83
Q

pareidolia

A

perceiving patterns/faces where there is none

84
Q

how do we perceive sound?

A

amplitude=loudness, frequency is pitch

85
Q

which part of ear converts sound into neural activity?

A

inner ear

86
Q

describe the cochlea

A

fluid-filled, a spiral structure with base and apex, 3 cavities, middle of which converts sound into action potentials (organ of corti)- sound vibrations cause basilar membrane of cochlea to oscillate, different parts respond to different frequencies so low frequency displaces lower floppier apex

87
Q

3 main structures of organ of corti

A

sensory/hair cells with stereocillia, basilar membrane, and framework of supporting cells

88
Q

how are cilia activated

A

vibration makes cilia sway, causing ion channels to open and ca2+ influx causes nt release at base of cell

89
Q

where is sound processed?

A

info transmitted from cochlea to brain by vestibulocochlear nerve (cranial nerve viii)

90
Q

what receives bilateral input (imporant for locating sound)

A

superior olivary nuclei- intensity and latency differences that by the duplex theory facilitate location of sound

91
Q

inferior colliculi

A

in the midbrain, which then send output to medial gen nuclei in thalamus

92
Q

where is primary auditory cortex located

A

temporal lobe

93
Q

where is tonotopic organization reflected

A

cochlea, primary auditory cortex, inferior colliculus

94
Q

conduction deafness

A

a middle ear problem that blocks sound vibrations from reaching the inner ear

95
Q

sensorineural deafness

A

problems w/ structures like cochlea that convert sound to neural activity

96
Q

central deafness

A

damage to auditory brain structures

97
Q

what streams are in the auditory cortex

A

dorsal stream- in parietal lobe, associated with spatial location
ventral stream- in temporal lobe, associated with components of sound including processing of language

98
Q

is language lateralized

A

yes it is processed in left temporal lobe mainly

99
Q

language and the split brain patient

A

since info in left visual field goes to right visual cortex there is no crossover into left side so they can’t identify the object

100
Q

right ear advantage

A

right eared person recognizes right ear stimuli first

101
Q

right hemisphere auditory responsibilities

A

lots of music processing and emotional tone of voice

102
Q

inability to understand speech

A

agnosia

103
Q

inability to produce speech

A

aphasia- symptoms include paraphasia (substituting words for other words), neologisms, and nonfluent speech

104
Q

types of aphasia

A

nonfluent/broca’s aphasia- difficulty producing speech but comprehension good, fluent or wernicke’s aphasia- can make speech sounds but difficulty in comprehension, global aphasia- deficits in both speech production and comprehension

105
Q

discovery of brocas area

A

partient had nonfluent aphasia, led paul broca to find area specialized for speech

106
Q

wernicke’s area

A

posterior regions of left superior temporal gyrus and part of adjacent parietal cortex, involved in perception and production of speech

107
Q

What is the neuromuscular junction

A

where motor neuron terminal and nerve fiber meet

108
Q

is the nmj effective

A

yes, almost every AP initiates a contraction

109
Q

motor unit

A

motor neuron’s axon and all of its target fibers

110
Q

spinal motor neurons

A

send axons out the ventral roots to the periphery, and each collateral innervates a different muscle fiber within the muscle

111
Q

what is the neurotransmitter at the nmj

A

acetylcholine, which causes depolarization

112
Q

myasthenia gravis

A

attacks ach receptors at nmj, characterized by muscle weakness that worsens with use, drugs that inhibit ach breakdown can help

113
Q

proprioception

A

knowing where we are- collection of info about body movements and positions- sensory neurons in muscles give feedback about muscle tension with stretch sensitive nerve endings

114
Q

2 kinds of proprioceptive nerve receptors

A

muscle spindles and golgi tendon organs

115
Q

what are reflexes and how do they happen

A

spinal connections between dorsal and ventral roots

116
Q

describe steps of knee jerk response

A

hammer tap stretches tendon which stretches sensory receptors in leg extensor muscle, sensory neuron excites interneuron and motor neuron in spinal cord, interneuron inhibits motor neuron to flexor muscles, motor neuron conducts ap to synapse on extensor muscle fibers, causing contraction, , flexor muscles relax, causing leg to extend

117
Q

what does the primary motor cortex do

A

initiates commands for action, nonprimary motor cortex provide an additional source of motor commands, cerebellum, and basal ganglia modulate activities of these control systems, sometimes via thalamus in a loop back to cortex

118
Q

hierarchy of motor control systems

A

brainstem integrates motor commands, spinal cord controls skeletal muscles, skeletal system allows for movement

119
Q

where are skeletal muscles innervated from

A

mainly from spinal cord, but muscles of head and neck also innervated by cranial motor nuclei in brainstem

120
Q

2 major pathways of commands to muscles

A

pyramidal (originate from neurons in primary motor cortex, axons pass through brainstem to spinal cord)
extrapyramidal: modulatory role in motor learning+motor coordination

121
Q

nonprimary cortical areas

A

in front of m1, include premotor and supplementary motor area

122
Q

SMA function

A

receives info from basal ganglia, involved in rehearsal of actions

123
Q

premotor cortex

A

broca’s area partly involved, has to do w/ control in speech- important for motor sequences externally guided so this is where mirror neurons are

124
Q

mirror neurons

A

active when an individual makes a movement, important in understanding+imitating others

125
Q

ALS

A

lower motor neurons and m1 cortex degenerate, leading to muscle atrophy

126
Q

extrapyramidal system

A

include basal ganglia and cerebellum, basal ganglia have a collection of circuits initiating and inhibiting motion

127
Q

parts of basal ganglia

A

caudate nucleus, putamen, globus pallidus, (substantia niagra and subthalamic nuclei are associated structures)

128
Q

Functions of basal ganglia

A

amplitude, direction, initiation of movement, esp/ w movement influenced by memory, also modulate other circuits like motor pathways of motor cortex, bidirectionally modulate voluntary movement

129
Q

huntingtons

A

degenerative disorder involving cell loss in striatum and cortex, degeneration of neurons in striatum leads to involuntary movement since bj modlates movement, 36 CAG lead to HD, more repeats is earlier onset

130
Q

function of cerebellum

A

cerebellar cortex has purkinje muscles which send inhibitory muscles, loss of cerebellum results in ataxia esp w/jerky movements, tremors, etc

131
Q

wernicke’s area

A

perception and production of speech, damage results in fluent aphasia- complex verbal output with unintelligible speech, difficulty understanding language, word deafness or blindness can indicate site of lesion

132
Q

global aphasia

A

total loss of ability to understand or produce language, results from large left hemisphere regions

133
Q

arcuate fasciculus

A

connects brocas and wernickes areas- lesions produce conduction aphasia- connectionist model may be too simplistic

134
Q

deep dyslexia

A

word interpreted as different word, acquired after brain injury

135
Q

surface dyslexia

A

rely on rules to pronounce words

136
Q

developmental dyslexia

A

struggle w/ reading, may be genetic, associated w/ ectopic cell clusters and micropolygria

137
Q

songbirds common model of language acquisition

A

refining song based on hearing others, critical period for learning, but not really language similar to primates and alex the parrot because innate, not learned,

Introduction to Neuroscience (3 decks)

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