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Sensory systems > Weeks 1-3 > Flashcards

Weeks 1-3 Flashcards

1
Q

What is the role of Wernickes area?

A

language comprehension

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2
Q

What is the role of Brocas area?

A

speech formation

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3
Q

what are the 5 taste groups?

A

sweet, sour, bitter, salty, unami

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4
Q

what are the two types of sensory systems?

A

sensing internal environment and the external environment.

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5
Q

what is the job of the vagus nerve?

A

sensing the internal environment.

goes round lungs, liver, intestines etc everywhere

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6
Q

what is proprioception?

A

the body’s ability to sense movement within joints and joint position. This ability enables us to know where our limbs are in space without having to look.

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7
Q

what is the law of specific nerve energies?

A

Receptors are (usually) specific to a particular modality.

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8
Q

what does adequate stimulus mean?

A

The modality to which a receptor responds best.

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9
Q

what is transduction?

A

Conversion of physical energy to a receptor potential in the receptor neuron

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10
Q

meissner corpuscle?

A

?

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11
Q

pacinian corpuscle?

A

?

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12
Q

ruffini’s corpuscles?

A

?

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13
Q

Merkel’s disks?

A

?

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14
Q

what is an afferent neuron?

A

A neuron in the peripheral nervous system that conducts action potentials to the central nervous system

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15
Q

cortexs n stuff diagram

A

lecture 2 diagram.

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16
Q

what is a somatotopic map?

A

touch, areas allocated based on where they receive info from.

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17
Q

how does a cochlear implant work?

A

microphone implanted behind ear, includes amplifier and freq splitter.
wires carrying different freq come out the wire, freq are split.

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18
Q

patient GO?

A

darts player, got bad, problems with sensory peripheral nerves in hand, motor nerves fine.

stimulated finger, recorded at elbow. APs reached wrist, but not elbow.

Stereognosia

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19
Q

what is stereognosia?

A

unable to perceive and recognize the form of an object in the absence of visual and auditory information by using tactile information.

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20
Q

describe sea squirts.

A

no need for sensory info for adult sea squirt, since it sits on a rock.
senses guide action in environment, they have no need for it.

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21
Q

role of microvilli on taste cells?

A

increase surface area.

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22
Q

what cranial nerves are involved in the taste pathway?

A

Three cranial nerves involved (VII, facial; IX, glossopharyngeal; X, vagus)

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23
Q

where do taste axons go?

A

All taste axons enter the brainstem and together enter the gustatory nucleus (also known as solitary nuclues), where they form synapses with other neurones which continue in different directions, including the thalamus (projections from which project to primary gustatory cortex), amygdala and hypothalamus

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24
Q

how many tastes do receptor cells taste for?

A

Distinct receptor cells express receptors for one single taste

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25
Q

describe the response of taste cells.

A

graded changes in polarisation and NT release, not APs.

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26
Q

describe the resting potential of taste cells.

A

Resting potential

Sodium/potassium exchanger ensures high intracellular [K+] and high extracellular [Na+]

Leakage K+ channels allow K+ to leave the cell, establish potential

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27
Q

describe how we taste salt

A

High extracellular Na+ enter cell at microvilli through Na-selective ion channel or open Na-regulated cation channels. leads to vesicles fusing and NT release.

Depolarisation

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28
Q

describe how we taste sour

A

Proton donors (ie acids), H+ open cation channels in microvilli or carry charge directly into cell.

Depolarisation

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29
Q

how do we taste umami?

A

Amino acids, in humans especially glutamate.

heteromer GPCR, T1R1:T1R3

GBy activates PLC, makes IP3 causes release of Ca from intracellular stores.
activates cation channels which depolarises the cell.

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30
Q

how do we taste sweet?

A

A large number of natural (eg sucrose, fructose, amino acids) and synthetic (eg saccharin) compounds.

heteromer GPCR: T1R2:T1R3

same as umami,
GBy, PLC, IP3, Ca, cation

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31
Q

how do we taste bitter?

A

A wide variety of natural and synthetic compounds

Large family (30) TAS2R genes, GPCR. highly selective.

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32
Q

why do we have more bitter taste receptors?

A

ability to taste toxins.

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33
Q

what is Gustducin?

A

a G protein associated with taste and the gustatory system, found in some taste receptor cells. Research on the discovery and isolation of gustaducin is recent. It is known to play a large role in the transduction of bitter, sweet and umami stimuli.

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34
Q

PTC?

A

The PTC taster/non-taster polymorphism has evolved at least twice in primate evolution

PTC non-tasters do not ‘lack’ TAS2R38

Could the non-PTC sensitive TAS2R38 alleles detect other bitter compounds?

Heterozygote advantage

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35
Q

flavour?

A

olfaction, temp, texture etcetc.

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36
Q

what is a learned negative?

A

seasick and eat shellfish, seasick made you ill but you associate with shellfish.
can’t eat again.

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37
Q

describe odorants.

A

volatile, hydrophobic, lipophylic and organic molecules (carbon based).

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38
Q

describe the olfactory epithelium

A

olfactory sensory neurones:
cilia in mucus.
axons go directly to the olfactory bulb in brain.

fire AP in response to odorants.

basal cells regenerate olfactory sensory neurones if they die

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39
Q

mucus is aqueous, odorants are hydrophobic, howwut?

A

binding proteins for odorants, hydrophobic core and hydrophilic outside.
forms a complex and presents to receptors on the cilia.

proteins produced by the lateral nasal gland.
what is the protein?

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40
Q

describe the receptors on the cilia.

A

GPCR.

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41
Q

how do GPCR work?

A

extra and intra domains.
Ga, B & y subunits.

Ga separates from B and y subunits.

what does what?

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42
Q

describe the mechanism of olfaction

A 
binds to GPCR, 
Golf activates adenylate cyclase,
this produces cAMP (2nd messenger),
cAMP gated cation channels,
depolarizing,
primarily Na and Ca, 
Ca activated Cl channels open, Cl leaves the cell (depolarizing)

calcium calmodulin binds calcium, activates cAMP phosphodiesterase, breaks down cAMP.

43
Q

how many smells can receptors recognise?

A

GPCRs are not that specific,
Each receptor detects multiple odorants,
Most odorants excite several receptors

44
Q

How does the brain ‘keep track’ of which receptor proteins have been activated?

A

axons of receptors go to olfactory bulb, tiny just above the nose.

45
Q

why are we so shit are smelling?

A

tiny olfactory bulb.

46
Q

describe the transgenic lac z reporter mice

A

genetically modify the coding seq of a protein youre interested in to a reporter protein.
lac z encodes b galactosidase, which metabolises coulourless sugar x gal to form a blue pigment

soak in xgal and look for blue pigments, thats where gene is expressed

47
Q

describe the olfactory sensory neurones distribution in da brain n stuff?
is dis mice or human idk

A

The 10k olfactory sensory neurones expressing a given olfactory receptor are distributed across the nasal epithelium.

Their axons converge on just 2 specific locations (glomeruli) in the olfactory bulb

2k glomeruli in the olfactory bulb

An odour is translated into 1.) a pattern of olfactory receptor activations, becomes 2.) a spatial pattern of activity in the olfactory bulb

48
Q

after olfactory bulb what happens yo?

A

olfactory tract takes to olfactory cortex, from there can go to lots of different areas like thalamus/hypo/hippo

49
Q

where do pheromones originate from?

A

vomeronasal organ

50
Q

why does flehming occur?

A

draw air across gums to detect pheromones.

51
Q

pathway of pheromones?

A

starts at vomeronasal organ, vomeronasal nerves take to accessory olfactory bulb and then goes to the hypothalamus.

52
Q

describe pheromone receptors.

A

GPCR,
2 evolutionarily distinct families.

V1r (about 150 genes; v high interspecific variation; mostly pseudogenes in primates).

V2r

53
Q

mechanism for pheromones?

A

Vomeronasal sensory neurones are GPCR,
activates PLC
IP3 and DAG produced, IP3 releases intracellular Ca stores and activates TRP2 cation channels.

what does DAG do?

54
Q

do all organisms that have photopigments have photoreceptors/eyes?

A

noooooooo

55
Q

describe a pigmented pit

A

Pigmented pit:
Limits the range of directions from which light can reach each photoreceptor

-ve phototaxis

56
Q

what is a planarian eye cup?

A

simple eye/pigmented pit.

eyes have PR cells with photopigments in pits, there is a screening pigment.

cant respond to light from below, directional.
the pit is curved and creates directional preference.

57
Q

describe the insect compound eye

A

thousands of ommatidia, a column.

in the middle are PR cells, at the top is a cornea and crystalline cone (makes a lens together)

pigmented cells cover the PS in a tube, gives directionality to the light.
responsive to only a very specific direction.

58
Q

what is acuity?

A

capacity for seeing distinctly the details of an object.

High acuity requires an array of ‘pixels’ each receiving light from a restricted range of points in visual space.

59
Q

describe mirror eyes.

A

scallop has it.
reflective surface at the back, and arrray of PR in between.
light falls on the concave mirror, focused on the PRs.

directional.
REFLECTION

60
Q

describe the relationship between acuity and distance for a compound eye.

A

collecting area of ommitidium is limited as you get closer, you can see specific details more.

closer = higher acuity.

61
Q

describe the relationship between acuity and distance for a mirror eye

A

rays are closer together closer to an object, more separated when far away.

from a distance the image is in focus, when close the rays are divergent.
REFLECTION

62
Q

describe lens eyes.

A

Very high acuity:

Light focused on the retina by refraction

In theory each photoreceptor receives light from a different point in visual space – becomes an independent ‘pixel’

refracted onto a point on the retina.

63
Q

describe the relationship between acuity and distance for a lens eye.

A

The degree of refraction required depends on distance from object.
The refraction provided by cornea is constant, therefore any adjustment originates with the lens.

64
Q

what is refraction?

A

Refraction: focusing divergent rays from a point in visual space into a single point on the retinal surface

65
Q

lens eye, distant object how is the lens?

A

Distant objects:
Light rays near parallel, require little refraction to focus.
Lens thin and low refractive power.

ciliary muscles relax, suspensory ligaments taught, lens pulled thin

66
Q

lens eye, close object how is the lens?

A

Close objects:
Light rays diverging, require greater refraction to focus.
Lens thick and has high refractive power.

ciliary muscles contract, suspensory ligaments loose, lens small and thick (refractive power increases), pupils constrict

67
Q

what is accommodation?

A

Changing focus close/far.

68
Q

where do refractive errors arise from?

A

problems with corneal or lens refraction.

69
Q

what is myopia?

A

eye too deep, refractive power of cornea too great.
distance out of focus.

light falls in front of retina

a diverging concave lens corrects this.

70
Q

what is hyperopia/hypermetropia?

A

eye too shallow, effective refractive power of cornea too small.
can’t see close.

light falls beyond retina

converging convex lens corrects this.

71
Q

how do opsin absorb light?

A

changes from cis to trans isoform when absorbs a photon.

all trans is agonist.
11-cis inverse agonist?
activates GPCR

72
Q

why do PRs have envaginations in the plasma membrane.

A

increase surface area so can fit more opsin molecules (cos dey r GPCR)

73
Q

describe opsin.

A

GPCR, 7 TMD

they bind retinaldehyde/retinal, derivative of b carotene.
comes in isoforms 11-cis / all-trans retinaldehyde, 11/12 carbon.

74
Q

describe the phototransduction cascade.

A

photon changes rhodopsin to active state, binds transducin (GPCR).
a subunit activates cAMP phosphodiesterase, which then hydrolyses cGMP reducing its conc.
cGMP cation channels, less cGMP closes the channels. less cations entering cell.
hyperpolarised

effector enzyme - cAMP phosphodiesterase
second messenger - cGMP

PRs release glutamate in the dark when depolarised, when exposed to light they hyperpolarise and release less glutamate.

75
Q

rods v cones?

A

rods higher sensitivity, capture more photons, bigger so capture more light.

cones better at adjusting sensitivity.
higher acuity.
colour vision.
fovea is all cones.

76
Q

functions of the retina?

A

Translate light into a biological signal
Photoreceptors

Transmit that information to the brain
Optic nerve

Early visual processing
Contrast detection
Colour
Movement

77
Q

describe bipolar cells

A

after PRs, second order neurones,
get info from cones.
graded change in membrane potential.

two types: ON or OFF bipolar cells
same signal but respond differently.

78
Q

describe how off cells respond to glutamate.

A

depolarise in the presence of Glu (dark),
have ionotropic receptors, glu gated ion channel

hyperpolarise to light

when the light is off the cell depolarises.

79
Q

describe how on cells respond to glutamate.

A

hyperpolarise in the presence of glutamate (dark), have GPCR, metabotropic glu receptors

depolarise to light

when the light is on the cell depolarises.

80
Q

describe retinal ganglion cells.

A

after bipolar cells,
send AP through axons via optic nerve.

OFF and ON types.

Ganglion cells monitor relatively large patches of retina encompassing many photoreceptors

81
Q

what are parallel pos/neg visualisations?

A

piccy wic.

82
Q

what is a receptive field?

A

Receptive field

Area over which stimuli elicit a change in activity of a neuron

83
Q

where is the receptive field of retinal ganglion cells?

A

The receptive field of retinal ganglion cells extends beyond the photoreceptors immediately above them in the retina.

gets info from cones directly above and also above and to the side.

84
Q

what are amacrine cells?

A

synapse between bipolar cells and ganglion cells.

responsible for lateral communication.

85
Q

whole map of retina and cells n stuff.

A

idk find a pic or summin m8

86
Q

centre on surround off? ON cells

A

slideywide.

centre is hyperpolarised cos in light.
horizontal cells are depolarised when in dark, it send inhibitory signals to the centre cone making it more hyperpolarised.

87
Q

centre off surround on? ON cells

A

centre cone depolarised, surround cells hyperpolarised.

horizontal cell hyperpolarised, no inhibitory signals to centre cone.

no AP

88
Q

centre on surround on? ON cells

A

all cells hyperpolarised, no inhibitory signals from horizontal.

nothing happens ???

89
Q

why does centre/surround on work like it does?

A

to map edges of objects with high resolution.

90
Q

describe centre on surround off? OFF cells

A

centre hyperpolarised, releasing less glutamate, hyperpolarising ganglion cell.

stop firing AP.

91
Q

describe centre off surround on? OFF cells

A

centre depolarised, ganglion cell fires AP.

92
Q

describe order of cells.

A 
PRs
horizontal
bipolar
amacrine cells
ganglion cells
optic nerve fibres
93
Q

how are ganglion cells direction selective?

A

slides.

amacrine cells inhibit signal.

94
Q

rods v cones?

A

rods more sensitive than cones, in low light rely on rods.

95
Q

what are rods called when fully hyper polarised?

A

saturated in light.

96
Q

how can you alter the sensitivity of a PR, cascade cycle.

A

change rate at which cGMP is made.
guanylate cyclase makes cGMP from GTP.

Ca inhibits GCAP (guanylate cyclase activating protein) which regulates guanylate cyclase.

in the light ca can’t enter the cell, GCAP free and cGMP made which blocks cation channels.

97
Q

describe light adaptation.

A

Changes the relationship between light intensity and photoreceptor polarisation:

Under dark adapted conditions, even relatively dim light drives full hyperpolarisation

Under light adapted conditions, photoreceptor can be partly depolarised even under much brighter light

98
Q

describe mimosa plants.

A

Wilt at night or at ‘subjective night’

An internal ‘circadian’ clock that is set to local time by light from the sun.

99
Q

effect of light on rodent clock?

A

changing the time you produce light changes the rodents internal clock, takes a few days to adjust.
measure when it runs on wheel.

100
Q

bilateral enucleation on house sparrow?

A

no eyes, PRs elsewhere.
extra retinal photoreception.

black dye injected under the skull. fucked up their pattern yo.

101
Q

bilteral enucleation in mammals?

A

Bilateral enucleation abolishes all responses to light in mammals
‘Time of day’ responses also originate in the retina

102
Q

time of day signal comes from where in mammals? experiment with mice?

A

other PRs in retina, not rod/cone.
few retinal ganglion cells.

mice modified with no rod/cones, pupils still responded to light.
Inject dye into the hypothalamus which is transported (retrograde) down axons of retinal ganglion cells
…. labels >1% of all ganglion cells

103
Q

describe the RGCs that project to the hypothalamus.

A

The Retinal Ganglion Cells that project to the hypothalamus are themselves photoreceptors.

Depolarise to light, fire APs. responds even when seperated from retina, intrinsic ability to respond to light.

> 1% of all ganglion cells

melanopsin responsible.
can make non light sensitive cells sensitive when added.
don’t work if removed.

104
Q

describe melanopsin phototransuction.

A

G protein - Gq/11
effector enzyme - phospholipase C
second messengers - IP3 & DAG

Gq/11 activates PLC, PLC metabolises PIP2 to DAG/IP3.
that opens TRPC cation channels, depolarise cell.

same cascade as flies, not melanopsin tho.

Sensory systems (3 decks)

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