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FALL 2023 > Bio Psych Exam #2 > Flashcards

Bio Psych Exam #2 Flashcards

1
Q

Sensory receptors

A

Specialized neurons that transduce some form of energy into neural activity

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2
Q

Are sensory receptors evenly spaced around the brain?

A

NO - Density and spread are different → not evenly spaced around the brain

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3
Q

Receptive fields

A

The receptor area which when stimulated results in a response of a particular sensory neuron → region of sensory space in which a stimulus modifies a receptor’s activity

  • Helps us locate events in space → receptive fields overlap
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4
Q

Goals of pathways

A

make sense of this sensory information; generally, we need to get to the cortex
Makes pitstops along the way:
At each pitstop the information is modified → gives us difference aspects of reality

-Pathways (“neural relays”) let our sensory systems interact and build upon one another

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5
Q

Afferent neuron

A

sensory neurons → impulses from sensory stimuli towards the CNS

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6
Q

Efference neuron

A

motor neuron – impulses away from CNS (usually to muscles) for responses)

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7
Q

Topographic maps

A
  • Spatially organized representation of the world
  • Maps exist all over the brain → especially prominent in primary cortical areas (V1, A1 etc.)
  • Secondary cortical areas (V2-V5) → get information after hitting the primary cortical
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8
Q

Sensation

A

registration of a physical stimulus

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9
Q

Perception

A

the subjective interpretation of sensations

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10
Q

What fills the eyeball

A

Vitreous humor (jelly-like)

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11
Q

Retina

A
  • Made up of photoreceptors; without retina, we can not see → no way to convert light into action potentials
  • At the back of the eye (has to go through many things to get here)
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12
Q

Fovea

A
  • found in the retina (it is a depression in the retina)
  • Contains a specific type of photoreceptor (rods and cones)
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13
Q

Retinal organization

A

Only the photoreceptors at the very back of the eye are stimulated by light
- contains rods and cones

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14
Q

Rods

A
  • More numerous than cones
  • Spread everywhere in the retina BUT the fovea
  • Deals with low levels of light
  • Specialty: night vision/motion
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15
Q

Cones

A
  • Less numerous than rods
  • Entirely in the fovea
  • Respond to bright lights at particular wavelengths
  • Specialty: color vision and acuity (sharp details)
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16
Q

Transduction when there is NO light

A

At baseline (in the dark): photoreceptors are depolarized → they are inhibitory
- This inhibits/hyperpolarizes the bipolar cell → it’s excitatory but currently being inhibited
- Prevents action potentials in the ganglion

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17
Q

Transduction when there is light

A

Light hyperpolarizes the photoreceptors via G-protein coupled receptors
- This reduces inhibition of the bipolar cell → bipolar cells are now excitatory and can depolarize and fire
- Can now excite the ganglion cells whose action potentials get sent to the brain

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18
Q

Types of Retinal Ganglion Cells (RGCs)

A

1) Magnocellular cells (M cells)
2) Parvocellular cells (P cells)

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19
Q

Parvocellular cells (P cells)

A
  • Smaller
  • Input mainly from cones
  • Sensitive to fine details and color
  • Found largely in the fovea
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20
Q

Magnocellular cells (M cells)

A
  • Larger
  • Input mainly from rods
  • Sensitive to low contrast and moving stimuli
  • Found throughout the retina
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21
Q

What do Retinal Ganglion Cells (RGCs) do?

A

The axons of both types of RGC cells come together to form the optic nerve
- part of the retina
- what causes a blind spot (called the optic disk)

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22
Q

Geniculostriate pathway

A
  • RGC axons from the optic nerves travel posteriorly

goes from:
1) eye
2) lateral geniculate nucleus
3) striate cortex

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23
Q

Lateral geniculate nucleus (LGN)

A
  • in the thalamus
  • formed by P cells (layers 3-6) and M cells (layers 1-2)
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24
Q

Optic chiasm

A
  • Half of the information from each eye crosses at the optic chiasm (60% cross, 40% stay)
  • “X marks the spot”
  • ventral surface of the brain
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25
Q

Optic tract

A

The bundles/visual pathway past the optic chiasm

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26
Q

Receptive fields in LGN

A

The receptive fields of many retinal ganglion cells combine to form the receptive field of a single LGN cell
- LGN receptive field is bigger

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27
Q

Primary visual cortex

A

In the occipital lobe
- Called V1 or the striate cortex
- Formed by all P cells (and some M cells)
- Striped

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28
Q

Layers of the primary visual cortex

A

6 layers:
- Layer 4: gets all the incoming information
- M and P RGCs are separate in the thalamus and separate in V1 (striate cortex) – ocular dominance columns

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29
Q

Optic raditaion

A

white matter highway system → how info gets to V1

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30
Q

How left and right eyes are separated in V1

A

The left eye sends things into one stripe, the right eye into the next, then left etc. → they alternate
“Occular dominance columns” (the stripes): respond preferentially to information from 1 eye

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31
Q

Blobs

A

Section of V1 that are sensitive to information about color
- input from P cells
- output to thin stripes of V2
-comes from the same region of the visual field

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32
Q

Interblobs

A

Sections of V1 that re sensitive to information about movement and form
- input form M cells
- if it is about movement, optuput to thick stripes of V2
- if it is about form: output to areas of V2 that are between thick and thin stripes
- comes from the same region of the visual field

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33
Q

The _____ sends information to a disproportionately large portion of the occipital cortex

A

Answer: Fovea → very large space in V1 for such a small region of the retina (disproportionate)

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34
Q

Out visual field compared to our eyes

A

inverted AND right-left reversed
- Inverted: The lower part of the visual field is on the upper part of the eye (If the light coming from above, hits the bottom part of the retina)

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35
Q

Decussates

A

switches side

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36
Q

ipsilateral

A

stays on the same side

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37
Q

Which portion of the visual field decussates

A

nasal fields switches sides

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38
Q

right visual cortex

A

processes left visual field

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39
Q

left visual cortex

A

processes right visual field

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40
Q

What visual deficit would you expect if you severed the optic chiasm

A

Can’t see the outer (temporal) portions of the visual fields from both eyes
Explanation: it is the nasal portion of the eyes, but the nasal portion of the eye maps to the temporal portion of the visual field

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41
Q

RCG receptive fields to LGN receptive fields

A
  • One dendrite of a LGN synapses with multiple RGCs
  • The receptive fields of many LGN cells combine to form the receptive field of a single V1 cell
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42
Q

Retinotopy

A

Receptive fields from RGCs retain thier spation relation when sent to LGN
Location information is conserved → means if we know that light coming in from one angle hits a specific portion of the retina, this same portion of V1 is activated
**V1 is mapped according to the retina

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43
Q

Retinal ganglion cell activation type

A

Can be…
1) on-centre /off-surround
2) off-center/on-surround

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44
Q

Luminance contrast

A

amount of light an object reflects relative to its surroundings

**RCGs tell the brain about the amount of light hitting a certain spot on the retina compared to the average amount of light in the surrounding retinal region

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45
Q

Retinal ganglion cells and shapes

A

Emphasizes difference in luminance along the EDGES
RCGs send information about edges
Edges ultimately form shapes

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46
Q

Orientation selectivity

A

Single V1 cell: on center, off surround (or vice versa) → but rather than a dot of light, we are working with bars of light (because receptive fields build up)
These bars are orientation-selective to the light

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47
Q

Receptive field convergence

A

Input to a V1 neuron comes from a group of RGCs that happen to be aligned in a row
That V1 neuron will be excited only when a bar of light hitting the retina strikes that particular row of RGCs
If it’s at a slightly different angle, only some will be activated and we get a weak response in the V1 neuron
- IPSP and EPSP cancel in this case

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48
Q

Ocular Dominance and Orientation columns

A

Stripes of V1 preferential to input from 1 eye
- Orientation columns form bars of light (panel A)
- Orientation columns are perpendicular to ocular dominance columns (panel B)

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49
Q

Opponent processing coding

A

There are 3 colored cones - red, blue and yellow
the combination of these being excited and inhibited is what creates colors

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50
Q

The 2 visual streams

A

1) dorsal stream
2) temporal stream

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51
Q

Dorsal stream

A

1) goes to the parietal lobe
2) how/where pathway, vision for action
3) deals with spatial orientation – visually guided reaching/grasping

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52
Q

Important Dorsal stream area

A

Area MT and Motion
- Perception of motion
- Middle temporal visual area (V5) - still dorsal stream
- Random dot motion task:
- Monkeys have to choose which way dots are moving in order to get a reward → gives insight into the perception of motion

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53
Q

Temporal Stream (vision)

A

1) temporal lobe
2) names: what pathway / vision for perception
3) deals with recognition and discrimination of visual shapes/objects

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54
Q

Important temporal stream area

A

Fusiform face area (FFA)
- Part of the inferior temporal cortex
- Particularly important for processing faces
Not only faces; expertise hypothesis – helpful for discriminating very similar objects
- In experts: humans are experts at faces and experts at other things

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55
Q

Prosopagnosia

A

face blindness
- Ventral stream problem

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56
Q

General Sensory Processing

A

1) Sense organs only process a narrow range of relevant stimuli
2) Physical stimuli have to be transformed into neural activity
3) Perception is the interpretation of what is sensed

57
Q

Sound waves

A

Displacement of molecules into compression or rarefication which moves through something

58
Q

Frequency

A
  • how many waves you can get in a specific period of time → controls low or high-pitch
    Ex: if the frequency is doubled but the amplitude stays constant there is a higher pitch
59
Q

Amplitude

A

height of the waves → controls volume
- Ex: if the amplitude is doubled but the frequency is the same, the sound is louder

60
Q

External ear

A

1) Pinna: collects sound waves
- Think of it like a funnel
2) Ear canal: amplification of sound waves directed at the eardrum
3) Tympanic membrane (aka ear drum): when a sound wave hits it, it vibrates
- Particularity sensitive to 2000-5000hz frequency range → range of human language

61
Q

Middle ear

A

1) 3 ossicles (bones): connect the eardrum to the oval window
2) Oval window
3) Round window: opposes the oval window; As the oval window pushes in, the round window pushes out (and vice versa)
- Allows the fluid of the inner ear to move → backbone of transduction

62
Q

Ossicle parts

A

Mallus: hammer
Incus: anvil
Stapes: stirrup
- Flat part (base): presses on the oval window → transmits movements to the oval window

63
Q

Fluid and air in middle ear

A
  • The external and middle ears are filled with air BUT the inner ear is filled with fluid
  • The goal of the middle ear is to match up this discrepancy → needs to boost pressure
  • Think about underwater: can’t hear when in fluid → have to boost pressure
64
Q

Inner ear

A

1) Cochlea (snail shape)
2) Scala = fluid
3) Semicircular canals (don’t need to know): tell us when we are upright → vestibular system (balance)

65
Q

Parts of the cochlea

A

1) Basilar membrane: where hair cells sit
2) hair cells (outer and inner)

66
Q

Inner hair cells

A

actual auditory receptors (equivalent of photoreceptors in vision)

67
Q

Outer hair cells

A

1) Not auditory receptions
2) Sharpen cochlea’s resolving power by changing the stiffness of the tectorial membrane at specific locations → makes sure loud noises don’t damage the inner ear
3) Amplify low-level sounds

68
Q

Auditory nerve

A

How we get from the ear into the brain (similar to the optic nerve)
- formed by bundles of the spiral ganglion cells (analogous to the RGCs)

69
Q

Auditory Transduction steps

A

Step 1: the pinna catches sound waves and deflects them into the external ear canal
Step 2: waves are amplified and directed to the eardrum causing it to vibrate
Step 3: vibrations cause ossicles to vibrate
Step 4: ossicles amplify and convey vibrations to the oval window
Step 5: vibration of the oval window sends waves through cochlear fluid
Step 6: waves cause the basilar and tectorial membranes to bend
Step 7: the bending of the membranes causes the cilia of inner hair cells to bend → bending generates neural activity in hair cells

70
Q

Tip links

A

connect the cilia of the inner hair cells

71
Q

Depolarization of hair cells

A

Movement in the same direction as the tallest cilia: tip links are stretched and ion channels open → more + ions enter the cell (depolarizing)
- When you move in the direction of the peak (the tallest cilia) and the rope (link) gets taut → physically opens the ion channel

72
Q

Hyperpolarization of hair cells

A

Movement in the opposite direction of the tallest cilia: tip links are compressed so ion channels are closed (hyperpolarizing)

73
Q

Hair cells after being depolarized

A

There are voltage-gated Ca2+ channels along the hair cells:
When hair cells become depolarized, Ca2+ enters → neurotransmitter release onto the auditory nerve

74
Q

Auditory pathways

A

1) Ears: very close to the neck → auditory nerve enters the brain at the level of the brainstem (medulla); very low
2) Information decussates at the medulla → crosses
3) Move superiorly through the midbrain
4) Info goes to the medial geniculate nucleus (in the thalamus) - pitstop
5) Then goes to A1: primary auditory cortex in the temporal lobe

75
Q

what is one of the similarities between the geniculostriate pathway and the auditory pathway

A

Both systems make a pitstop in the thalamus
vision: in the lateral geniculate nucleus
audition: medial geniculate nucleus

76
Q

Pitch perception

A

If we unroll the basil membrane there are peaks in different locations along the basilar membrane for different frequencies → where there is a spike tells you the pitch

77
Q

Tonotopy

A

Higher and lower-pitched tones are in different regions of A1 → different parts of A1 correspond to different frequencies; what gives us pitch perception

78
Q

Loudness perception

A

1) Firing rate
2) number of neurons
Both of these work in conjunction to perceive loudness

79
Q

Firing rate and loudness

A

Steps: Louder noise → more intense vibrations of eardrum and ossicles → greater displacement of the basilar membrane; hair cells bend more → more NT released → greater firing rate of the auditory nerve
How we can perceive loudness by physically moving a hair cell more when sounds are louder (higher amplitude)

80
Q

number of neurons and loudness

A

Steps: Louder noise → more intense vibrations of eardrum and ossicles → broader region of basilar membrane displace; more hair cells bend → more neurons firing
Recruiting more hair cells: bigger waves will move more hair cells
The more intense the vibration, the more hair cells will move

81
Q

Location of sound

A

**Arrival time difference: aka interaural time difference (ITD) **
We can detect the amount of time it takes sound to reach the eardrum
- ITD works primarily in the lateral plane (left or right) → what about elevation? – The pinna is bumpy: sound waves will hit this at different points and reflect into the ear canal
Can determine elevation by how the sound waves hit the pinna

82
Q

Coincidence detectors

A

cells in the hindbrain that allow us to localize sound (based on the difference in time)
**The difference in time between ears tells us where the sound is coming from → if a sound hits the right ear first, coincidence detectors tell us this and thus we know the angle of the sound

83
Q

Auditory dorsal stream

A

1) where pathway
2) sound localization
3) audition for action
**if someone calls your name, how you move towards them

84
Q

Auditory ventral stream

A

1) what pathway
2) identifying objects by sound characteristics
3) auditory object recognition
4) audition for perception

**if you hear two different people talking → how do you tell who is talking (distinguish sounds)

85
Q

Hearing and aging

A

Older adults lose their ability to hear high frequencies

86
Q

Why do older adults lose their hearing?

A

1) Tympanic membrane stiffens: doesn’t vibrate as much
2) Ossicles: don’t move as much (also stiffen)
3) Thickening of the basilar membrane
4) Damage to neurons: loud music, sounds etc.

87
Q

Theories on why hearing declines with age

A

Cognitive decline: people with hearing loss have more cognitive decline
**Cognitive load model:
Age → sensory decreases → increased attention and effort → cognitive performance decreases (limited capacity)

88
Q

Common motor behavior systems

A

1) Repeated sequences (walking, running, chewing)
2) Learned sequences (typing, playing music)
3) Coordinated actions (lifting, throwing jumping)
4) Fine-grained movements (manipulation with hands, writing)
5) Accurate movements (reaching, aiming)
6) Sustained actions (gripping, squeezing, carrying)
7) Reaction (catching, ducking, withdrawal)

89
Q

Cortical motor areas

A

1) primary motor cortex (M1) - to the left of the central sulcus
2) premotor area
3) supplementary motor area
*go to notes for a diagram

90
Q

Premotor Area (PMA)

A

Organizes movement sequence
- Ex: if you want your water, you have to walk, reach, grab
- Movement guided by sensory information
- Important in planning → firing when reaching for the button but not actually pressing

91
Q

Supplemental motor area (SMA)

A

1) Complex sequences; especially bimanual movement (both hands)
2) Anticipation of a movement

92
Q

Somatotopy

A

If you take an electrode and stimulate different parts of M1, different body parts will move

93
Q

Big parts of somatotopy

A

1) Big hands: use hands the most, need more area dedicated to it
2) Big mouth: language → takes fine motor movements of lips and tongue to produce specific sounds
3) Tiny torso: not a lot to move → if you move your leg, the torso moves with it

94
Q

Force

A

Also coded in M1
- The more planning you are able to do, you can anticipate the force needed and recruit more neural activity

95
Q

Direction

A

Monkey moves a joystick
Neural mapping: this is right before you move
**The firing rate of any particular neuron can help decode which direction you are moving in

96
Q

Basal Ganglia parts

A

Caudate nucleus
Putamen
Globus pallidus
- Internal and external

97
Q

Direct pathway controlling movement

A
  • SN has excitatory effect, disinhibits GPi output
  • Positive feedback loop: start with excitation and end at the cortex with even more excitation **MORE MOVEMENT

1) Cortex: excites the caudate and the putamen
2) Caudate putamen sends out inhibitory information to the globus pallidus (it wants inhibitory information so when it is excited, it is less powerful)
3) Global pallidus sends out inhibitory information to the thalamus but it itself is inhibited → because it is being inhibited, it does not get to send as much inhibitory information
4) The thalamus is less inhibited (see above) so is excited and sends excitatory information to the motor cortex

98
Q

Is the motor cortex excitatory or inhibitory?

A

excitatory

99
Q

is the caudate putamen excitatory or inhibitory?

A

inhibitory

100
Q

is the globus pallidus (internal) excitatory or inhibitory?

A

inhibitory

101
Q

is the thalamus excitatory or inhibitory?

A

excitatory

102
Q

is the motor cortex excitatory or inhibitory?

A

excitatory

103
Q

Indirect Pathway WITHOUT SN

A

**less movement (reduced activity in the motor cortex
**negative feedback loop
1) Cuadate putamen → goes to globus palliduas external
2) Extra inhibiting the global pallidus external
3) Likes to inhibit but because it is being inhibited, we have less inhibition of subthalamic nuclei (nuclei under the thalamus)
4) Subthalamic nucleus: not being inhibited and it likes to excite → excites the globus pallidus internal segment
5) Globus pallidus internal inhibits the thalamus –the thalamus likes to be excited so it does not send excitation to the motor cortex
Overall: less motor initiation

104
Q

Indirect Pathway WITH SN

A

SN = flips the circuits → leads to more motor initiation
SN Inhibits in the indirect pathway
Overall: more motor inhibition
**inhibits the caudate putamen

105
Q

Descending motor tracts

A

Limbs and digits: decussate at brainstem
Trunk, shoulders: no decussation

106
Q

if you damage the right corticospinal tract superior to the brainstem what deficit would you expect

A

Issues with the left limbs and right side of the torso

107
Q

Parkinson’s disease

A

Loss of dopaminergic neurons in the substantia nigra
- harder to initate motor movements
- inhibiting the direct pathway

108
Q

Symptoms of parkinsons

A

1) Slowness/absence of movement (bradykinesia/akinesia)
2) Rigidity (stiff walking, posture, no arm swinging)
3) Resting tremor
4) Patients have difficulty initiating movements and once initiated the movements are abnormally slow

109
Q

Treatment of parkinsons

A

Low dopamine → give people more dopamine
- Drugs to increase L-dopa (levodopa)
Many side effects:
- Too much dopamine: psychosis (positive symptoms)
Deep brain stimulation (DBS): place electrode into the basal ganglia → globus pallidus internal segment

110
Q

What is huntington’s disease

A

Rare, inherited neurodegenerative disease
Due to caudate putamen problems:
- Direct pathway: understimualte motor cortex → hard to execute planned movements
- Indirect pathway: unwanted movements; overstimulating motor cortex

111
Q

Huntington’s Disease symptoms

A

1) Involuntary jerking/writhing movements (chorea)
2) Muscle problems (rigidity)
slow/abnormal

112
Q

Cerebellum damage

A

1) Intention tremors
2) Dysmentia: overestimating or underestimating the range of motion needed to place limbs correctly during movement
3) Difficult performing rapid alternating movements
4) Difficult with balance
5) Difficulty walking

113
Q

What is different between smell/taste and other senses

A

instead of physical stimuli, these are chemical stimuli

114
Q

Functions of smell

A

Identification
- Friend or foe
- Is something food / fresh food

Survival
- Avoiding predators
- Locating food
- Finding mates (pheromones)

115
Q

Characteristics of smell

A

1) Difficult to verbalize and describe smells
2) Difficult to classify smells into categories
3) Smell has the peculiar ability to evoke strong memories

116
Q

Olfactory receptor neurons

A

In the skin lining the air passages (at the epithelium)
- Cell bodies are in the skin
Have protrusions (cilia) that stick out → when you breathe in, the smell molecules (odorants) touch the cilia and physically bind to receptors there
- Channels open and transduction occurs

117
Q

The olfactory bulb contains…

A

Glomeruli and mitral cells

118
Q

Transduction of smell

A
  • Olfactory cilia stimulated by molecules of odorants
  • When odorants bind to receptors, it sets of g-protein-coupled receptors
119
Q

does smell decussate

A
  • stays ipsilateral
    Smells coming in from the right nostril will activate the right side of the brain and vice versa with the left
120
Q

Three pathways of smell

A

All: axons of mitral cells in the olfactory bulb

1) Pyriform cortex (primary olfactory cortex) → thalamus → hypothalamus → OFC (orbital frontal cortex)
- Can go through the thalamus but do not have to → different from vision and audition
2) Amygdala → hypothalamus (regulation of behavior)
3) Entorhinal cortex → hippocampus (memory)

121
Q

Where is the OFC

A

OFC: close to the eyes on the ventral surface of the brain

122
Q

Perception: Olfaction coding

A

400 different types of olfactory receptors
Cilia of each olfactory neuron constraints only 1 type of receptors
Each glomerulus received info from 2000 ORNs but only received information from the same type of ORN → about 400 types of glomeruli as well

123
Q

Combinatorial coding

A

A particular odorant binds to more than 1 receptor (based on orientation etc)
Different odorants produce patterns of activity in glomeruli
Chemical recognition → spatial recognition
- If we know which pattern of receptors is activated, we know which odorant is present
-Not quite known how we decode the patterns

124
Q

Olfactotopic

A

Particular glomeruli send information to specific regions of the olfactory cortex
Different smells map onto a different region in space

**Discontinuous/discrete map
You can not have an in-between smell → not on a scale, not linear

125
Q

Smell and taste: their connection

A

Odorants enter the nose AND the mouth
- The mouth and nose have an airway passage that connects them
- Odorants entering the mouth (from food) can travel upward and stimulate olfactory receptor neurons

126
Q

Why smell is unique

A

1) Stimulus is chemical not physical
2) We can not easily describe smells (not like movement, seeing or hearing)
3) No decussation – ipsilateral cortex
4) Pathways in the brain do not need to stop at the thalamus before reaching the primary cortex → no pitstop at the relay station
5) Topographic map is discrete, not continuous
6) ORNs constantly die and are replaced → one of the very few populations of neurons that regenerate

127
Q

What are problems with smell called

A

Called anosmia and hyposmia

128
Q

How can we get smell damage?

A

Damage/inflammation:
- To nose = cold
- To brain = TBI
Congenital anosmia: usually genetic
Covid (pre-delta strain)
Early signal of something worse (Alzheimers and Parkinsons)
Zinc gluconate, a homeopathic “remedy” to prevent colds → can cause permanent anosmia

129
Q

Receptor types in gustation

A

1) Bitter
2) Sweet
3) Sour
4) Umami (responds to glutamate → protein ish)
5) Salt

130
Q

Mapping of tongue

A

Taste buds contain several if not all receptor types (tongue is NOT mapped by receptor type)

131
Q

Transduction of taste

A
  • Food interacts with microvilli to open ion channels → leads to changes in membrane potential
  • Connects the branches of three different cranial nerves
132
Q

Gustation pathways

A

1) Enters the brain at the level of the midbrain
2) Three branches form the solitary tract
3) No decussation
4) Makes a pitstop at the thalamus
5) Primary gustatory cortex = taste (the insula)
6) S1 (primary somatosensory cortex) = tactile information; texture/mouth-feel
7) The primary gustatory cortex projects to the orbitofrontal cortex (OFC)
– Smell and taste are very linked

133
Q

Specialist taste bud cells

A

Sweet
Bitter
Salty

134
Q

Generalist taste bud cells:

A

Sour
- mix of many things: a bitter chemical could still activate a sour taste receptor

Once you get to the hindbrain: there is lots of nuance
**You might have a neuron that prefers specific tastes

135
Q

Gustatopic map

A

1) 1 region per “taste” → a type of map
2) But not just salt in one place or umami in another → not sure exactly what is being mapped
3) Discrete map (not linear)

136
Q

Taste avoidence

A
  • You can avoid a taste or smell you have had a bad experience with → can change your brain to send a signal that this food is “bad”
  • Receptors replaced every 7-10 years → Previous things you might not have liked you might like now
137
Q

Perception of flavor

A

Mixture of gustatory and olfactory input gives us “flavor”
- insula/gustation cortex → identifies nature and intensity of flavor
- OFC = tells us the affective properties of taste (emotions, smell integration)

138
Q

Spice and gustation

A

Spicy is not a taste
- Triggers pain and heat receptors in mouth, lips, and tongue

139
Q

possible 6th flavor

A

Salt licorice → sour receptors might also respond to ammonium chloride

FALL 2023 (5 decks)

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