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Neurobio I > Exam 3: Lectures 11-15 (+ olfaction) > Flashcards

Exam 3: Lectures 11-15 (+ olfaction) Flashcards

1
Q

there are two broad categories of sense

A

specific and somatic senses

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2
Q

specific senses

A

vision, hearing, taste, smell, equilibrium

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3
Q

somatic senses

A

touch, temperature, pain, itch, proprioception (sense of body position and movement)

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4
Q

pathway of sensory transduction

A

stimulus → transduction (convert stimulus energy into ΔVm) → central processing resulting in sensation

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5
Q

sensory physiology

A

detection

(transduction → central processing resulting in sensation)

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6
Q

psychophysics

A

perception (how people experience physical stimuli)

(stimulus → central processing resulting in sensation)

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7
Q

goal of sensory transduction

A

to get from sensation to perception

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8
Q

there is a _____ between sensory physiology and psychophysics

A

correlation

  • psychophysics studies the relationship between physical stimuli and subjective sensory experiences, while sensory physiology investigates the physiological mechanisms underlying how sensory receptors detect and transmit those stimuli, essentially bridging the gap between the physical world and our perception of it
  • didn’t know about correlation until studies were done
  • w/ sensory physiology: showed the greater the stimulus, the more identification (higher spikes)
  • second graph w/ psychophysics looked similar
  • if there is a mass deviation from the curve, can tell a doctor that something is wrong
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9
Q

organization of the retina

A

outside → in (light goes to back of eye, where photosensation occurs)

  • RGC (retinal ganglion cells) transmit from eye to brain
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10
Q

photoreceptor cells

A

rods and cones

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11
Q

rods

A

detect changes in scenes

  • nighttime only (night vision)
  • more photo-pigment
  • highly convergent (many rods synapse onto a single bipolar cell)
  • sensitive to light (need just 1 photon)
  • slow response
  • low acuity (poor visual detail)
  • monochromatic
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12
Q

cones

A

detect colors

  • daytime only (day vision)
  • less photo-pigment
  • less convergent (a few cones synapse on a single bipolar cell)
  • less sensitive to light (need 10s-100s of photons)
  • fast response
  • high acuity (high visual detail)
  • color vision
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13
Q

phototransduction in retina

A

when light is applied, the cell is hyperpolarized, and the starting voltage is at -40 mV (more depolarized than in standard neuron)

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14
Q

atypical feature of the cells in retina

A

hyperpolarization is the activating signal in these cells

  • leads to less glutamate being released
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15
Q

in the dark, cells are …

A

.. constantly depolarized (slightly depolarized)

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16
Q

organization of the somatosensory system

A
  • chief cells are dorsal root ganglion neurons (DRG) (sensory neurons activated by sensory stimuli that transmit sensory information from the peripheral nervous system to the central nervous system)
  • has neurons that are heavily myelinated, lightly myelinated, and unmyelinated
  • spinal cord is the relay station that integrates signals before they go to the brain
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17
Q

discovery of receptors in skin led to …

A

… mechanotransduction

  • the ability of a cell to actively sense, integrate, and convert mechanical stimuli into biochemical signals that result in intracellular changes
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18
Q

TRPV1

A

heat-activated ion channel in pain pathway (detects pain from heat/temperature)

  • Julius and colleagues found that this gene for VR1 was responsible for response to capsaicin, figured out that applying capsaicin and heat are essentially the same
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19
Q

Piezo1 and Piezo2

A

mechano-sensitive channels that respond to mechanotransduction

  • Artem used physiology and took a cell line that was mechano-sensitive, knocked out genes until they found the gene that caused the inward current to be lost
  • 71st gene: lost mechanosensory current when this gene was knocked out, this gene became the mechanosensor
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20
Q

Piezo2 mutations alter …

A

… limb positioning and gait

  • no Piezo in mouse’s sensory neurons mean their limbs will flail in all directions, have trouble walking (can’t walk in straight line)
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21
Q

Trpv1 receptor responds to capsaicin and heat. If Trpv1 is misexpressed on sensory neurons that do not normally express this receptor, will those cells now be activated by capsaicin and heat and trigger noxious heat sensation? What experiment could prove your thinking?

A
  • In mice, knock out Trpv1 in neurons, add them to itch neurons
  • Capsaicin is normally painful in mice, causes wiping: no Trpv1, no wiping, if you misexpress Trpv1 onto itch neurons you will still get no wiping, but you WILL get scratching
  • Will still have the endogenous function of the neuron it was added to (activated scratch neurons w/ heat receptor, so still get scratching when added to itch neurons)
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22
Q

general anatomical pathways of sensory systems

A

Stimulus → sensory receptors (signal transducers) → primary sensory neurons → secondary sensory neurons in CNS → cortex

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23
Q

When APs are more or less the same, how can our brain perceive a particular stimulus?

A
  • location of the stimulus
  • which type of receptors are activated
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24
Q

stimuli have 4 attributes that we register

A

modality (type), intensity, location, timing

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25
Q

modality

A

quality: the type (nature) of stimulus, submodality

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26
Q

intensity

A

lux, decibel, psi, etc.

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27
Q

location

A

part of body touched, part of retina stimulated, etc.

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28
Q

timing

A

start, end, duration, speed of intensity change

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29
Q

encoding of modality

A

types of receptor stimulated: sub-modalities (e.g. taste), stimulus has to be adequate, stimulus has to be threshold, receptor tuning curve

neural pathway stimulated (each is specified)

labeled line coding

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30
Q

vision receptor tuning curve

A

light: shows that each color has ideal wavelength that activates it (at the max of each curve)

  • dif. receptors are activated at each dif. wavelength, dif. combos of colors produce dif. overall color
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31
Q

auditory receptor tuning curve

A

dif. parts of ears sense dif. volumes of sounds (have dif. tuning frequencies)

  • dif. combos have dif. perceptions
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32
Q

encoding of timing is done by …

A

… tonic and phasic receptors

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33
Q

tonic receptors

A

slowly adapting, will fire as long as stimulus and the appropriate neurons are there

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34
Q

phasic receptors

A

fast adapting, some will only fire after the stimulus is removed (unlike tonic)

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35
Q

receptive field

A

where a neuron is active (where stimulus can be applied that will activate the neuron)

  • encoding of location: each neuron has a domain (location) where it can be activated
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36
Q

if you have increased spatial resolution, you will need …

A

… more neurons to transmit the info

(i.e. more neurons produce a better picture)

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37
Q

sensory homunculus

A

shows how much of cortex is dedicated to each sense

  • brain dedicates a lot of neural space to touch
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38
Q

somatosensory neurons

A

large = touch neurons (b/c heavily myelinated for faster transmission)

small = temperature neurons

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39
Q

somatosensation

A

lots of dif. feelings due to lots of dif. pathways

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40
Q

DRG

A

dorsal root ganglion neurons; the primary somatosensory neurons that are activated by sensory stimuli that transmit sensory information from the peripheral nervous system to the central nervous system

  • each is a collection of ~15,000 somatosensory neurons
  • no organization by submodality (function): some sense temperature, some sense touch, etc., but they all intersperse together
  • amongst the longest cells in the body, send large projections
  • interacts w/ muscle, other cell types: all have receptors for things that are secreted by DRG
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41
Q

touch is mediated by 4 types of mechanoreceptor neurons in the skin

A

Meissner corpuscle, Merkel cells, Pacinian corpuscle, Ruffini endings

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42
Q

Merkel cell

A

a sensory complex (many neurons have many branches on a Merkel cell)

  • is NOT a neuron, is an epithelial cell (act together as one unit, as a mechanoreceptor neuron)
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43
Q

qualities of mechanoreceptor neurons in skin

A
  • tighter vs. more disperse receptor fields (more precise detection vs. fewer cells in skin, activated by stimuli across skin surface, cannot localize signal)
  • some cells only fire at beginning (onset) and end (offset), some cells activate throughout
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44
Q

mechanoreceptive complex for touch: Pacinian corpuscles

A

detect vibrations between 20-2,000 Hz; corpuscle structure is necessary for detection and adaptation (neurons fire @ beginning and end b/c have fluid-filled sac, squeezed when stimulus enters, released when stimulus released)

  • not sure why mice and other animals have these in their joints, maybe can explain why animals can detect vibrations in earth b/c of earthquakes better than us
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45
Q

Merkel cell complex sensory signaling

A

there is a chemical synapse between Merkel cells and sensory neurons, activated through addition of norepinephrine (NOT glutamate)

  • Piezo2 is not just expressed on neurons, but also on epithelial cells
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46
Q

proprioception

A

limb position in space, signal to spinal cord to signal how much tension is on your muscles

  • sensory spindle wrapped around muscle
  • Piezo channel opened when muscle is pulled or stretched
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47
Q

molecular subtypes of somatosensory neurons

A

can categorize somatosensory neurons through which genes they express after they are in a mature functional state (undifferentiated state → mature functional state)

  • single-cell RNA sensory in DRG neurons
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48
Q

optogenetics

A

using blue light to activate neurons through channelrhodopsin proteins (ChR2)

  • ChR2 used to activate cells, opens when hit by blue light, allows cations to enter cell which activates the neurons
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49
Q

sensory transduction of touch

A
  • Piezo opens, allows ions to follow through (Na+ and other things flood into neuron)
  • strong enough stimulus = spike, neuron fires
  • mechanisms of action are still being discovered through high resolution biophysics
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50
Q

Piezo channels respond to …

A

… touch (pressure, suction, shear stress)

  • when Piezo ablated in sensory neurons, mice lose response to touch
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51
Q

Piezo1 channels are inherently …

A

… mechanosensitive

  • Piezo channels reconstituted in liposomes can be directly activated by mechanical force
  • opening channel causes transduction
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52
Q

Piezo1 transduces _____ in mice

A

mechanical itch

  • paper used 3 dif. genotypes, wild type, knockout, and heterozygous (heterozygous is needed b/c for some genes, allele levels matter, so there could be a dif. b/c of dif. allele levels)
  • Piezo1 would be sufficient to drive mechanical itch if itch still happens when all other channels except Piezo1 are blocked (can also put ChR2 into neurons and simulate it and see if itch still happens, or upregulate Piezo1)
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53
Q

thermosensation

A

heat stimulus provided, response recorded

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54
Q

TRPV1 is a _____

A

“hot” channel (intrinsically a heat-sensitive channel)

  • hotter = more current flowing through channel
  • some respond to capsaicin, some respond to heat
  • other things that activate the channel too, like acid
  • TRPV1 receptors expressed on broader pain neurons
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55
Q

TRPV1 variations account for …

A

… varying heat tolerance

  • heat tolerance of ground squirrels and camels is due to a dramatic reduction of the temp. sensitivity in TRPV1 channels (dif. in channels lies in a single amino acid), vs. heat-sensitive rats and mice
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56
Q

TRPM8

A

activated by cooling compounds, e.g. menthol and eucalyptus, and cool temperature (analogous to TRPV1)

  • inward currents happen when cooling compound/temperature applied, later activates TRPM8
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57
Q

sensory neurons for thermosensation

A

Peripheral sensory tissues are innervated by two largely non-overlapping populations of neurons, those expressing Trpv1 (red) and those expressing Trpm8 (blue)

  • A small number of Trpv1+/Trpm8+ neurons exists (purple), but their response characteristics are not known
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58
Q

TRPV1+ neurons

A

heat neurons + nociceptors and warm neurons

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59
Q

TRPM8+ neurons

A

Type 1, 2, and 3

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60
Q

TRP channels are important for …

A

.. thermosensation

  • so much so that TRP channels are highly conserved across evolution
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61
Q

enduring cold temperatures involves TRPM8 channel adaptations

A

experiments showed a single point mutation (one singular mutation) in TRPM8 channels mean that cold temperatures are no longer sensed

  • fixing this mutation causes cold temperatures to be sensed again
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62
Q

looking at pain-sensing neurons and itch-sensing neurons shows that …

A

… itch is a dif. modality than pain

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63
Q

pain serves an important biological purpose

A

there are hazards of growing up painlessly: we don’t do certain things b/c it hurts, this protects us from tissue damage

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64
Q

pain is an enormous health burden

A

while acute pain serves an important biological role, nearly 40 million adults have acute pain that becomes long-lasting

  • # 1 reason why people seek medical attention and why people call out of work
  • $635 billion/year spent on chronic pain (treatment and missed labor)
  • very limited treatment options (opioid epidemic)
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65
Q

neuroanatomy of the pain/somatosensory system

A

neurons just end freely in skin

  • spinal cord → (mechanosensory afferent fiber, pain and temperature afferent fiber) → DRG neurons → receptor endings
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66
Q

afferent neurons

A

info from outside, moves inwards (sensory receptors to CNS); sensory neurons

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67
Q

efferent neurons

A

info is descending (carry motor info from CNS to muscles/glands); motor neurons

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68
Q

nociceptor

A

a pain transduction neuron

  • thermal
  • mechanical
  • polymodal
  • silent
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69
Q

silent receptors

A

start firing after injury or nerve damage

  • might be responsible for chronic pain
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70
Q

A-delta fibers

A

a nociceptor responsible for initial pain: sharp, well-localized pain

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71
Q

C fibers

A

a nociceptor responsible for second pain: dull, lingering pain

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72
Q

proof of nociceptor

A

Edward Pearl used two recording electrodes in the same neuron for speed, neurons fired when given painful (noxious) stimulus

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73
Q

spatial transcriptomics of DRG identifies …

A

… molecular signatures of human nociceptors

  • human nociceptors are very similar to those of mice
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74
Q

mechanisms for tissue injury causing pain

A

if you injure skin, there are immune cells and molecules that infiltrate that area, ATP then releases

  • many of the immune molecules are localized to site of injury
  • there are receptors on these sites (on the sensory neurons) that activate pain neurons
  • medications like tylenol block glandin
75
Q

ion channels involved in pain

A
  • voltage-gated Na+ channels
  • DRG neurons and pain neurons
  • many channels can activate receptor
  • high enough receptor potentials will lead to AP
76
Q

Paper: “An SCN9A channelopathy causes congenital inability to experience pain”

A
  • individuals didn’t feel pain, at any time, in any part of their body, though they were constantly experiencing pain (had scars)
  • reason the families didn’t feel any pain: single point mutation in a single gene (Nav1.7, a voltage-gated Na+ channel, which is almost exclusively expressed in pain neurons)
77
Q

erythromelalgia

A

patients have spontaneous sharp, burning pain for life

  • found patients w/ disease all mapped to same gene (Nav1.7)
  • a gain of function (not a loss of mutation)
  • in periphery (not connected to brain), so if channel blocked, unlikely to see addiction to pain meds
78
Q

lose Nav1.7

A

no pain

79
Q

too much Nav1.7

A

too much pain

  • a drug that targets Nav1.7 will block pain
80
Q

pain and itch are mediated by …

A

… neurons w/ free nerve terminal endings in the skin

  • itch is its own sensory modality (not sensed by pain neurons)
  • some neurons only express histamine receptors, showing that they only respond to itch
81
Q

Paper: “Sensory neuron-specific GPCR Mrgprs are itch receptors mediating chloroquine-induced pruritus”

A

wildtype: mice respond to chloroquine

when single receptor is knocked out, no more chloroquine response

82
Q

modulation of pain

A

anterior cingulate cortex, insula, amygdala

  • pain can be modulated through many dif. circuits in brain
83
Q

Paper: “Opiate Agonists and Antagonists Discriminated by Receptor Binding in Brain”

A

found which cells opioids act on in the brain by finding evidence of opioid receptor binding in brain (opioids have a sedative effect)

  • one of the endogenous pain inhibition systems in the brain
84
Q

Paper: “Analgesia from Electrical Stimulation in the Brainstem of the Rat”

A
  • in rats, if you electrically stimulate certain areas, it leads to pain (descending inhibition system)
  • BUT, stimulating a certain area causes pain RELIEVEMENT
  • another one the endogenous pain inhibition systems in the brain
85
Q

projections from brain to spinal cord

A

descending; composed of excitatory and inhibitory projections, these projections go down to spinal cord and prevent ascending pain

  • whole process is opioid-dependent (opioids work through these descending inhibition pathways)
  • another one the endogenous pain inhibition systems in the brain
86
Q

effects of opiates and opioids on nociceptor signal transmission

A

opioid receptors are everywhere, broadly expressed throughout brain, also expressed on nociceptors and projection neurons on spinal cord

  • pain projection neuron activated through sensory input alone: glutamate and neuropeptides released, enkephalin NOT released
  • sensory input + opiates/opioids: when morphine is added, cell is not as active (seen w/ decreased voltage); opioids can have presynaptic effects or downstream effects on postsynaptic neuron; enkephalin (local to the cell), is released from cell
  • shows that opiates/opioids cause enkephalin to be released (acts like endogenous opiates/opioid), which greatly inhibits nociceptor signal transmission, thus decreasing release of neurotransmitters from the primary afferent nociceptive neurons (by not allowing Ca2+ to come into cell), which reduces the perception of pain
87
Q

DRG neurons transmit information to dorsal spinal cord in …

A

… specific regions

  • spinal cord has dif. lamina, pain innervates upper layers of spinal cord (if innervates deeper neurons, typically touch neurons)
  • lots of local interneurons that don’t project past spinal cord
88
Q

pain innervates the _____ of spinal cord

A

upper layers

89
Q

Paper: “The Cellular and Synaptic Architecture of the Mechanosensory Dorsal Horn”

A

separated neurons based on expression of two proteins, excitatory (glutamate) and inhibitory (GABA)

  • found that excitatory neurons depolarize, inhibitory neurons hyperpolarize
90
Q

Gate Control Theory of Pain

A

Melzack and Wall found that gating of pain occurs in the spinal cord (gate can either open or close to allow or block pain signals from reaching brain)

  • normally have C fiber neurons (nociceptive = pain) that activate pain
  • can have non-nociceptive neurons (non-pain neurons = Aβ fiber) that can activate inhibitory interneuron, forming a gate that blocks pain message
  • Aβ fibers show how non-painful sensations can reduce pain
91
Q

evidence for the Gate Control Theory

A

showed that there is a population of neurons in the spinal cord that express genes called RET, these genes are inhibitory, can do experiments where these neurons can be ablated, a lot more pain behavior w/o the gating neurons in the spinal cord

92
Q

the brain processes _____ and _____

A

sensation, emotion

  • there are dif. pathways for sensation (actually feeling it) and emotion (what the sensation causes you to feel)
93
Q

Paper: “An amygdalar neural ensemble that encodes the unpleasantness of pain”

A

Give painful stimuli to animals, as increase to pain, animal will move paw away at higher rate (more stimulation, more withdrawal)

  • when silence amygdala, response is still there, animal still wants to withdraw paw, BUT behavior changes
  • behavior is lost of silencing, mouse will still withdraw paw, but won’t care anymore
  • shows that amygdala is responsible for emotion, NOT for sensation
94
Q

How can chronic pain cause touch hypersensitivity w/o touch neurons?

A

in an experimental model, cut pain and touch neurons: over course of 42 weeks, pain neurons have regrown, touch neurons have not regrown, but animals still have touch sensitivity (very sensitive to touch) despite touch neurons not being there

  • during regrow, pain neurons grow into areas where touch neurons are located, so the area is still wired to pain, but activated by vibrations (touch/pain hybrid circuit area)
95
Q

hearing

A

the neural perception of sound energy

96
Q

properties of sound

A
  • pitch or tone (determined by frequency) (babies can hear 20-20,000 Hz, adults can hear 1000-4000 Hz)
  • intensity or loudness (measured in decibels, dB)
97
Q

sound frequency

A

frequency (Hz) = waves/sec

  • human range is from 20-20,000 Hz
  • hearing test is administered at birth
98
Q

steps in transduction of sound

A
  • air wave
  • mechanical vibration of ear bones
  • fluid vibration in cochlea
  • shearing movement between tectorial and basilar membranes
  • receptor potential in inner hair cells
  • AP firing in auditory nerve
99
Q

hair cells can be …

A

… permanently lost

  • have about 16,000 hair cells, once you lose them that’s it
  • loud sounds, multiple infections, and drugs can all kill hair cells
100
Q

structure inside cochlea

A

three bones (malleus, incus, stapes) will rattle and shake, which pushes air through fluid-filled canal, hair cells detect the fluid movement

101
Q

the 3 fluid-filled compartments in the cochlea

A

scala vestibuli, scala media, and scala tympani

  • scala vestibuli and scala tympani contain perilymph
  • scala media contains endolymph
102
Q

endolymph

A

like intracellular fluid, what hair cells are bathing in

  • high K+ concentration inside (outside of hair cells)
103
Q

perilymph

A

like extracellular fluid

104
Q

Organ of Corti

A

16,000 hair cells are innervated by 30,000 afferents

  • basilar membrane and hair cells have tonotopic arrangement (arranged by frequency) in cochlea
105
Q

outer and inner hair cells

A

have 3 rows in V-shape formation

106
Q

outer hair cells

A

innervated by efferent neuron

  • neuron goes away from cell, come from brain to system, silencing out hair cells
  • feedback to outer hair cells from brain
  • amplify vibrations to improve cochlea sensitivity and frequency selectivity
107
Q

inner hair cells

A

innervated by afferent neuron

  • inner hair cells send info to brain for processing
108
Q

hair cells transform …

A

… mechanical energy into neural signals

  • imaging of bullfrog (an ideal system) shows that hair cells are mechanically activated
  • if you deflect cilia on hair cells, get AP in hair cells (when deflected towards the highest cilia, get activation)
109
Q

deflection to the right on a hair cell is …

A

… depolarization (increased firing)

  • this is deflection to the highest cilia (direction from shortest to tallest)
  • more NT release
110
Q

deflection to the left on a hair cell is …

A

… hyperpolarization (less firing)

  • deflection from tallest cilia to shortest
  • less NT release
111
Q

tip-link

A

acts as springs, connected to machinery (connects one hair cell to another, shorter to taller)

  • needs the right orientation for transduction, can be destroyed by calcium chelator (abolishes transduction)
112
Q

How do sound waves depolarize hair cells?

A

through the mechano-senstive ion channel, TMC1

  • opening of TMC1 channels by tension in the tip-link during hair bundle deflection → TMC1 channels are localized @ tips of shorter stereocilia near the lower end of the tip-link → once activated, channel pore carries K+ and Ca2+ ions from outside to inside the stereocilia, leading to depolarization of hair cells
113
Q

Tip-links are made up of …

A

… a pair of cadherin 23 and a pair of protocadherin 15

  • if we don’t have a normal tip-link, can’t go from sound waves to sensory detection
  • absolutely crtical for perception
114
Q

TMC1 is the _____ channel

A

mechanotransduction (MT)

  • mutations in TMC1 causes deafness in mice
  • TMC1 is expressed at right time (acquisition of hearing) and in the right place (cochlear hair cells)
  • knockout of TMC1 abolishes MT currents
115
Q

auditory pathway from periphery to brain

A
  • sensory axons from cochlear ganglion terminate in cochlear nucleus in brainstem
  • axons from the neurons in the cochlear nucleus project to other brainstem nuclei or to inferior colliculus
  • axons from inferior colliculus project to thalamus
  • thalamic neurons project to the auditory cortex
  • cortex is where perception occurs
116
Q

hair cells are bathed in _____, separated by ____

A

endolymph, perilymph

  • outside environment (endolymph) is where mechanosensory channels are, has a very high potential (due to K+)
  • inside environment has a very negative potential
  • there is an electrical difference present (between endolymph and hair cell)
117
Q

endocochlear potential

A

the voltage difference between endolymph and perilymph

  • creates an electrical drive when the channels are open (NOT chemical)
  • K+ in endolymph wants to move down electrical gradient, which is what pushes K+ into the hair cell
118
Q

What is the driver in auditory systems?

A

K+

  • depolarization (shortest to tallest cilia) is what opens channel, allows K+ to flow into cell
  • very sensitive response (0.3 nm, just a bit bigger than diameter of K+ ion)
  • very fast response speed (~10 micros)
119
Q

Paper: “The frequency selectivity of auditory nerve fibres and hair cells in the cochlea of the turtle”

A

half-head of a turtle used, the electrical responses of single auditory nerve fibers or cochlear hair cells were recorded in the isolated half-head of the turtle Pseudemys scripta elegant

  • if record from hair cells all along basal membrane, there is frequency selectivity: tonotopic (high frequencies at base, low frequencies at apex), hair cells are tuned (placement in membrane are tuned towards certain frequency)
120
Q

efferent input to outer hair cells from brain

A

prestin is the motor protein of cochlear outer hair cells

  • hair cells can move, this is what generates amplification of signal
121
Q

motor function of outer hair cells amplify auditory signals

A

don’t know exactly how this happens, but know that movement increases dynamic range of system, which allows you to respond to higher frequency stimulation

122
Q

prestin

A

a transducer of electromotility required for auditory signals

  • gives cell the ability to respond to high frequencies
  • in prestin knockout mouse, mouse no longer responds to high frequencies (unlike wild type)
123
Q

vision

A

the predominant sense, the way we communicate w/ one another (in most mammals)

124
Q

3 steps of vision

A
  • light → eye → focused on the retina
  • phototransduction: light stimulus → electrical signal
  • processing of visual information by retina and brain
125
Q

in the eye, transduction occurs at …

A

… the back of the eye

  • signal then goes back to the brain
126
Q

organization of the retina and photoreceptors

A
  • whatever doesn’t need to be transduced is picked up by pigment cells (prevents excess light)
  • transduction w/ rods and cones
  • signal then synapses onto bipolar cell, then amacrine, then retinal ganglion cell (RGC), then to optic nerve to brain
127
Q

photoreceptor cells

A

rods and cones

  • both have outer segments where rhodopsin are, this is where most of the action happens
128
Q

rhodopsin

A

detects light and initiates a biochemical cascade

129
Q

ratio of rods to cones

A

20:1

130
Q

a rod can respond to just …

A

… a single photon of light

  • in a setup in a frog, hit w/ singular photons of light and did recordings, saw outward currents (light HYPERPOLARIZES neurons)
  • most of the time, no responses, but still had some responses, which shows that system is very finely-tuned, down to one photon
131
Q

light _____ the photoreceptor membrane potential, produces _____ current

A

hyperpolarizes, outward

  • when light comes into the cell, Na+ channels are closed, and way less glutamate is released
  • each photon of light blocks inward flow of 10,000,000 Na+ ions
132
Q

basal state

A

lots of glutamate released, Na+ channels open

  • happens in the dark
133
Q

neural signaling in the dark

A

rhodopsin inactive, Na+ channels open, cell depolarized, glutamate released (basal state)

134
Q

neural signaling in the presence of light

A

rhodopsin active, Na+ channels closed, cell hyperpolarized (light hits hair cells shortest to longest), glutamate release reduced

135
Q

the location of photoreceptor is …

A

… NOT uniform across the retina

  • there is an area of the retina where the cones are localized, and an area outside of that were the rods are
  • also optic disk (no rods or cones)
136
Q

optic disk

A

area where there are no rods or cones, if light hits this region there will be no response

137
Q

fovea

A

a dense area of cone photoreceptors where our center of gaze focuses light on

  • focusing light towards fovea increases visual acuity
  • no multiple layers (unlike other parts of retina), means that light can get there easier (lower impedance to light)
  • more cones are why we can see when it’s light outside
138
Q

blind spot

A

located in optic disk (where optic nerve connects to retina), has no light-sensitive cells

139
Q

3 steps of phototransduction

A
  • activation of visual pigment by light
  • reduction of cGMP
  • closure of cGMP-gated channels → membrane hyperpolarization
140
Q

What does light do?

A
  • activates rhodopsin (the -opsin molecules in rods)
  • activates 11-cis retinal, which undergoes a conformational change into all-trans retinal
  • need vitamin A in order to synthesize retinal (vitamin A is covalently attached to K296 of opsin)
141
Q

opsin molecule

A

a protein that acts as a light-sensitive receptor, found in the eyes of animals

142
Q

rhodopsin absorption spectrum matches psychophysical (figuring out threshold) measurements

A

there is a 1:1 response of how rhodopsin is absorbed and how humans detect dim light

143
Q

molecular processes in phototransduction: dark

A

cell is depolarized in the dark b/c of a high concentration of cGMP

  • cGMP binds to intracellular surface of cGMP-gated Na+ channel, opens channel, lets Na+ and Ca2+ flood into neuron
  • Na+ influx depolarizes cell, leads to the continuous release of glutamate at synapse
144
Q

cGMP

A

directly activates a cation channel

  • when performing patch-clamp recordings (recording from a single ion channel in rod membrane), can see that more [cGMP] causes more channel openings
145
Q

Molecular processes in phototransduction: light

A
  • light activates rhodopsin, which then activates transducin (the G protein)
  • activated transducin activates phosphodiesterase (PDE), which breaks down cGMP
  • less [cGMP] means Na+ channels can’t be opened; this reduced Na+ influx hyperpolarizes the cell
  • why mutations in CNG (the cGMP-gated Na+ channels) channels can cause blindness
146
Q

amplification in phototransduction

A

a small input (e.g. a single photon of light) can be very amplified (10,000 fold amplification)

  • absorption of 1 photon of light leads to closure of ~200 CNG channels and 1 mV of hyperpolarization
147
Q

color vision

A

3 types of detecting cells (unlike just one for rods)

  • short-wave cone = blue
  • middle-wave cone = green
  • long-wave cone = red
148
Q

tuning curves for rhodopsin and the 3 photopsins

A

shows spectral absorption curves of the short, medium, and long wavelength pigments in human cones, and the absorption curve for rod pigment

  • shows the ideal wavelength of light that each opsin is activated at (max of curve is max activation)
  • in order of shortest to longest wavelength: short (blue), rods, medium (green), long (red)
149
Q

comparison of human opsin genes

A
  • in blue vs. rhodopsin and green vs. rhodopsin, shows that they have lots of dif. amino acids between the two sequences (not a lot of similarities)
  • in red vs. green pigments, lots of similarities (can see that sequences of red and green pigments are highly similar): this is why red-green color blindness is most common
  • animals that can see more colors have more sequences of pigments
150
Q

distribution of red, blue, and green cones in a living retina

A
  • red and green cones predominate, only 5-10% are blue cones
  • ratio of green:red varies from 1:1 to 4:1, but does not seem to affect color perception
151
Q

red-green color blindness is most common in …

A

… males, b/c on X gene

152
Q

the chemical senses

A
  • olfaction
  • gustation
  • trigeminal
  • vomeronasal
153
Q

vomeronasal

A

we have vomeronasal organ during fetal development, but it is gone by birth

  • receptors are still in our genome
154
Q

purpose of the nose

A
  • food and flavoring (nutrition, palatability)
  • sense environmental dangers (like gas leaks)
  • industrial odor control
  • perfumes and fragrances
  • “green” pest control
155
Q

aspects of a model neural system

A
  • molecular recognition
  • signal transduction
  • regulation of gene expression
  • axon guidance
  • stimulus coding
  • regeneration and proliferation
156
Q

flavor

A

a hedonic sense, consists of taste and olfaction

  • olfaction is very important in sense of flavor and taste
  • in people w/ COVID, they did not lose sense of taste, but DID lose sense of flavor
157
Q

mammalian olfactory

A
  • nasal cavity: a hole in the nose that is primarily empty
  • set of turbinates: have a thin olfactory epithelium, where odors are captured
  • 2 synapses to cortex (from outside world to cortical tissue) (when there is a synapse in the olfactory bulb, there is a synapse to the cortex once you get to the PCX)
158
Q

turbinates

A

have a thin olfactory epithelium, where odors are captured

  • have a mechanism for increasing surface area that comes into contact w/ odors
  • sends axons to olfactory bulb and make second order neurons reach the cortex
159
Q

Ramon y Cajal olfactory discoveries

A
  • olfactory sensory neurons in the nose send thin axons to olfactory bulb
  • second order cells send dendrites and synapses w/ primary receptors; their axons bundle together and go back to the cortex, where they synapse w/ pyramidal cells in the cortex
  • 2 synapses to the cortex: local inhibitory interneuron
160
Q

main epithelium

A

tissue in the nose, supporting cells, basal cells

161
Q

tissue in the nose

A
  • olfactory sensory neurons (similar to primary neurons in eye) have a long axon that goes to olfactory bulb, cell body, and single dendrite that goes to top of tissue and ends up in dendritic knob
  • anywhere from a few to a couple of fine cilia, increasing surface area
  • from cilia, you find receptors
162
Q

supporting cells

A

epithelial type of cells that provide trophic (structural and nutritional) support to neurons

163
Q

basal cells

A

at base of main epithelium

164
Q

olfactory cells can_____ when necessary

A

regenerate at a rapid rate

165
Q

components of cilia

A
  • hundreds of GPCRs
  • Ca2+-activated chloride channel
  • numerous pathways of desensitization that depends on Ca2+; increasing Ca2+ opens more Cl- channels, which increases the electrical activity of the cell
166
Q

GPCR in cilia

A
  • G protein receptor binds to ligand, which changes GDP to GTP
  • GTP binds adenylyl cyclase, which activates cAMP
  • CNG channel allows positive ions to come through, one of which is Ca2+; this activates Cl- channel
167
Q

Ca2+- activated Cl- channel

A

olfactory system has high intracellular chloride concentration, so when channels open, Cl- leaves cell, which further depolarizes the cell

  • Cl- leaving leaves behind positive charges, which amplifies the signal
168
Q

olfactory receptor

A

has significant amplification: when voltage increases, [Ca2+] increases significantly

  • transduction pathway opens two channels
169
Q

What is an odor?

A
  • all kinds of dif. functional groups
  • odor discrimination
  • if it binds to an odor receptor
170
Q

the dif. functional groups in odors

A
  • primary organic compounds
  • low molecular weight (<350 Daltons)
  • volatile
  • aromatic and aliphatic
  • alkanes, aldehydes, alcohols, ketones, esters, formates, acids, halides, etc.
171
Q

odor discrimination

A

very dif. molecules can have the same small

  • e.g. two molecules can both smell like sandalwood, show that there is excellent reciprocal cross-adaptation to deal w/ very difficult discrimination

dif. concentrations can also have dif. smells

  • e.g. w/ indole and skatole, low concentration smells like grapefruit, and high concentration smells like shit
172
Q

odor receptors

A

the molecular logic of smell (a molecular basis for odor recognition)

  • Class A GPCRs (proteins); the largest family of GPCRs
  • 1 gene = 1 protein (a single coding exon)
  • contains conserved and variable regions
173
Q

each odor sensory neuron expresses …

A

… only ONE odor receptor gene

174
Q

number of odor receptors _____ compute to how good of a sense of smell you have

A

DON’T

  • e.g. dogs have a better sense of smell than mice, but have 300 less receptors (800 as opposed to 1100 in mice)
175
Q

Is there a code in the nose (a code as there is in color vision)?

A

there is a discrete, high-dimensional, non-linear code

  • as opposed to a continuous, low-dimensional code in vision that is additive
176
Q

olfactory code: receptors

A

the code is COMBINATORIAL (400 ORs in unique combos of 5 = 8.3 x 10^10 dif. codes)

  • HOWEVER, a matrix of chemicals vs. receptors will not reveal the olfactory code
  • in any mixture of volatiles compounds, even those that don’t have a perceivable odor may act as antagonists or enhancers, which can alter the aroma of the blend
177
Q

the combinatorial olfactory code is _____

A

reciprocal (neurons influence each other)

  • dif. odor molecules activate unique combinations of olfactory receptors (same neurons can participate in dif. combos to encode various stimuli)
  • a single odorant receptor can be part of the code for multiple dif. odorants, allowing for a vast range of smells to be detected w/ a relatively limited number of receptors
178
Q

complexity of the olfactory world

A

we don’t smell singular odors: most naturally occurring smells are odor mixtures, which can be made up of hundreds of aroma chemicals

  • 1 → 5 receptors, blend of 10 = 50 receptors
179
Q

Paper: “The Capacity of Humans to Identify Odors in Mixtures”

A

humans can identify singular odors up to 3 in a mixture, but after 4 odors, will smell something completely dif. (will smell a new odor that is the combination of the 4 odors, won’t be able to tell odors apart from each other)

  • smell isn’t additive
  • some odors will activate one receptor, but suppress the activity of another receptor (some odors can be excitatory, some inhibitory, which makes sense b/c it is a GPCR)
180
Q

Is there an olfactory code (map) in the brain?

A
  • single odorant receptor type in each sensory neuron
  • all neurons w/ the same receptor send axons to the same glomerulus
  • synaptic connectivity from olfactory epithelium to olfactory bulb
  • each glomerulus is innervated by 10-25 mitral cells that send their axons to the piriform cortex
181
Q

glomerulus

A

the basic unit in the olfactory bulb

  • each odor activates a dif. pattern of glomeruli, analyzing dif. sets of activated glomeruli could decode identity of odor
  • connected to piriform cortex via mitral cells
182
Q

mitral cells

A

connect single glomerulus to several areas of the cortex (piriform cortex)

  • project widely
  • why we don’t have additive mechanism
183
Q

synaptic connectivity from the olfactory epithelium to the olfactory bulb is …

A

… “mapped”

  • each glomerulus collects the inputs from the same receptor

Neurobio I (4 decks)

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