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BIOL 373 > Sensory Systems pt 2 > Flashcards

Sensory Systems pt 2 Flashcards

1
Q

what are the different parts of chemoreception?

A 
olfaction
gustation
hearing
vision
equilibrium
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2
Q

what is the only sensory modality that doesn’t go through the thalamus?

A

olfaction

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3
Q

what is the only special sense where the primary neuron itself carries the info to the CNS

A

olfaction

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4
Q

what is the role of epithelial cells in olfaction?

A

olfactory neurons have a single dendrite that extends down from cell body to the olfactory epithelium, and a single axon that extends to the olfactory bulb

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5
Q

what types of neurons are involved in olfaction?

A

bipolar neurons

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6
Q

are olfactory neurons ever replaced?

A

yes

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7
Q

what modification allows the receptors to detect odor?

A

dendrites end in non-motile cilia that express odorant receptors proteins

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8
Q

what are the different “sheath layers” for the 1o olfactory sensory neuron

A

epithelium, cribiform plate, and bone, then they synapse w 2o neurons in the olfactory bulb

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9
Q

what are the odorant receptor proteins?

A

GPCRs

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10
Q

how many different odorant receptor proteins are there?

A

1000s, which is why our sense of smell is so good

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11
Q

how many different types of receptor proteins are there per neuron

A

one only

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12
Q

what is the relationship between odorant receptor proteins and odorants

A

each receptor can recognise more than one odorant

each odorant can stimulate more than one type of receptor

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13
Q

what is the relationship between acid and alcohol versions of a smell?

A 
acid = shitty
alcohol = litty
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14
Q

what are the five basic tastes?

A

sweet, sour, salty, bitter, umami,

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15
Q

what are the taste receptors?

A

non-neural epithelial cells

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16
Q

how are taste epithelia modified

A

with microvili for more SA

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17
Q

how is taste transmitted?

A

sweet, umami, or bitter:
1. ligand bind to GPCR, releasing Ca2+ to enter cell
2. signal cascade
3. NT or ATP is released
4. 1o sensory neuron fires and AP are released to brain
salty and sour:
-mediated by ion channels, not GPCRs

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18
Q

what’s a tongue map?

A

fakenews

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19
Q

true or false - taste bud to taste receptor is a 1:1 ratio

A

false, all taste buds will have all the different receptors.

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20
Q

what is the taste pathway in the brain?

A

taste info travels through cranial nerves to medulla –> thalamus –> gustatory cortex

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21
Q

how does signal transduction in hair cells work?

A

at rest - 10% of ion channels are open, tonic signal is sent by sensory neuron
excitation - hair cell bends and depolarizes, increases AP frequency in associated sensory neuron
inhibition - if hair cells bends in opposite direction, it hyperpolarizes, and neuron signalling decreases

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22
Q

what are the three ear bones?

A

malleus, incus, stapes (in that order)

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23
Q

what are the different fluids in the cochlea? where are they each found? what is the composition of each

A

perilymph - high Na+, low K+ (like plasma); in vestibular and tympanic ducts
endolymph - low Na+, high K+ (like ICF); in cochlear duct only

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24
Q

what does the cochlear duct contain?

A

endolymph and the organ of corti

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25
Q

what is the place coding hypothesis?

A

sound waves trigger activity along different areas of the cochlea - sounds at a lower frequency are picked up farther down the cochlea
similar to ‘labelled line coding’

26
Q

what is the temporal code hypothesis?

A

frequency of sound waves determines frequency of APs travelling along auditory nerve, perceived as pitch
low pitch = low frequency = low firing of 1o neurons

27
Q

what is the problem with temporal code hypothesis?

A

we can hear sounds up to 20k Hz but no neuron can fire at this speed

28
Q

what is the current hypothesis for pitch determination?

A

neurons work as a team, carrying temporal code - pooled neural response to pitch
place coding DOES play a role
low pitches –> temporal code
high pitches –> place code

29
Q

what are the different types of hearing loss?

A

conductive
sensorineural
central

30
Q

what is conductive hearing loss?

A

problem in outer and middle ear (earwax or fluid)

solvable issue

31
Q

central hearing loss

A

damage to neural pathway between ear and cerebral cortex (uncommon)

32
Q

sensorineural hearing loss

A

damage to structures of inner ear (eg death of hair cells bc of loud noises, or bacterial infection)

33
Q

can mammalian cells regenerate?

A

no, but they’re working on it

34
Q

what is the vestibular apparatus? two components?

A

maintains equilibrium (balance); movement through space + position of head

35
Q

true/false - vestibular apparatus functions all on its own

A

No, it’s integrated w information from muscles (proprioception) and visual info

36
Q

how do vestibular apparatus operate?

A

detected by hair-cells in fluid filled chambers

  • otolith organs (in the utricle, saccule) for LINEAR ACCELERATION
  • semicircular canals for ROTATIONAL ACCELERATION
37
Q

how do hair cells detect spin?

A

hair cells in the semicircular canals are pushed on by the cupula and activated

38
Q

how do hair cells detect linear acceleration?

A

otoliths move in response to gravitational forces, perched on the otolith membrane above hair cells that are grouped in maculae, within utricles and saccules

39
Q

what is the role of utricles?

A

backward/forward acceleration

40
Q

what is the role of saccules?

A

vertical acceleration

41
Q

what are the neural pathways for equilibrium?

A

cranial nerve –>
1. cerebrum
OR
2. vestibular nuclei (medulla) –>
THEN EITHER
2a. somatic motor neurons controlling eye movements
2b. reticular formation –> thalamus –> cerebral cortex

42
Q

canal of schlemm

A

circular canal that drains fluid from aqueous humor, similar to choroid plexus in that it maintains the composition and environment of your eye

43
Q

fovea

A

special place that allows for fine vision (eg reading)

44
Q

what is the neural pathway?

A

optical nerve –> optical chiasm –> optical tract –> thalamus –> visual cortex (in occipital lobe)

45
Q

what is the autonomic ‘reflex’ pathway for pupillary light?

A

detector: photoreceptors in retina
afferent: optic nerve
intergrating centre: thalamus/brainstem = midbrain
efferent: motor neurons travelling along oculator nerve
effectors: smooth muscle regulating pupil diameter

46
Q

what is the sympathetic response in regulating pupil diamater? parasympathetic?

A

dilating, constricting

47
Q

how does phototransduction happen?

A

conversion of light into changes in the membrane potential by photoreceptor cells in the retina

48
Q

what are the photoreceptors?

A

rods and cones

49
Q

what is the role of modified ganglion cells?

A

mediate pupillary light reflex, circadian rhythms, other non-visual responses to light

50
Q

what is the cellular organization of retina?

A

ganglion cells attached to bipolar cells attached to rod or cone attached to pigment epithelium
horizontal cells that integrate info
amacrine cells

51
Q

cone

A

colour vision - only red, green, blue

52
Q

rod

A

b&w vision

53
Q

path of light in retina

A

pigment epi –> rod/cone –> bipolar cell –> ganglion cell –> optic nerve

54
Q

where is AP generated in retina

A

ganglion

55
Q

what is fovea composed of; what does it need to work;

A

only cones - this is where you focus for high res vision, and you NEED bright light for it
small receptive field
minimal convergence

56
Q

convergence in the retina

A

multiple rods to a single bipolar cell, multiple bipolar cells to a single ganglion

57
Q

rods and cones structure

A

have disks with lots of membrane area with transmembrane proteins (opsin), and a vitamin that interacts w opsin called RETINAL
outer segment with a tip that touches the pigment epi of retina + inner segment that contains cell nucleus and organelles for ATP and protein synthesis + basal segment with synaptic terminal that releases glutamate to bipolar cells

58
Q

rhodopsin

A

opsin (protein) + retinal (vitamin)

59
Q

phototransduction

A

in light:

  • retinal looses affinity for opsin, and is released
  • G protein = phosphodiesterase decreases [] of cGMP, closing channels (cation Na+ and Ca2+ influx stops, K+ efflux continues so hyperpolarization)
  • glutamate decreases release to bipolar cells (proportional to brightness of light)
  • action potential generated in ganglion cells - they determine receptive fields on retina
  • retinal slowly returns n is reunited w opsin
60
Q

rod and cone function in darkness

A
  • high cGMP
  • constant release of glutamate to bipolar cells (dark current)
  • Na+ and Ca2+ influx is greater than K+ efflux, so rod is depolarized slightly (-40mV)
61
Q

retinal formations and when

A 
cis-retinal = light
trans-retinal = dark
62
Q

why do rods and cones respond to different things

A

they have different opsin proteins that respond to different proteins

BIOL 373 (8 decks)

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