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Excitable cells > lectures 13-17 > Flashcards

lectures 13-17 Flashcards

1
Q

what wavelengths of light can we see?

A

400-700nm

between UV and infrared.

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2
Q

what are the properties of light?

A

amplitude - intensity

wavelength - type of light

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3
Q

why are materials black or white?

A

black - absorb all light

white - reflect all light

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4
Q

how do you measure the reflection of light from an object?

A

spectrophotometer.

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5
Q

what is the basic molecule to detect light?

A

opsins.
present in all animals.
evolved once and has since diverged.

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6
Q

what determines development and growth of the idea?

A

pax 6, present in most

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7
Q

what is neurolation?

A

neural ectoderm foms the neural tube.

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8
Q

describe vertebrate eye development.

A

neurolation.
3 primary vesicles, the first forms the forebrain. optic vesicles come directly from the ectoderm and forebrain.

optical vesicles invert to form the retina (part of the brain), another layer forms the pigment epithelial.

surface ectoderm forms the skin - this forms the lens.

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9
Q

describe how light enters the eye.

A

light enters through the cornea (outer transparent layer), this contains the aqueous humor?
the pupil is between the iris muscles, light continous through there and the lens.

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10
Q

describe the intravitreal blood supply

A

in the vitreous humor.

fine network of capillaries, supplies nutrients in the blood to the retina.

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11
Q

what is the sclera?

A

thick outer layer.

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12
Q

what has the greatest refracting power in the eye?

A

cornea.

lens accommodates the refracting.

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13
Q

what is the structure of the retina?

A

laminar - in layers.

general structure the same for all vertebrates.

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14
Q

describe the structure of the retina.

A

light can pass through since optically clear to hit the photoreceptors at the back.

outer limiting membrane keeps PR in place.
horizontal, bipolar and amacrine cells.
ganglion cells have axons leading directly to the brain - only cell to use AP.
all kept in place by the inner limiting membrane.

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15
Q

describe the structure of the retina.

look this shit up

A

light can pass through since optically clear to hit the photoreceptors at the back.

outer limiting membrane keeps PR in place.
horizontal, bipolar and amacrine cells.
ganglion cells have axons leading directly to the brain - only cell to use AP.
all kept in place by the inner limiting membrane.

the outer nuclear layer are the nuclei of the PR.
the outer plexiform layer has connections between our PR cells and the other cells.
inner nuclear layer contains the horizontal, bipolar and amacrine cells.
inner plexiform layer has connections between ganglion cells and the other cells?

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16
Q

describe retinal pigment epithelial cells.

A

different processes wrap around the outer segments of rods and cones.

recycling retinaldehyde - essential co factor of opsins.

also important for light absorption, stop the light rebounding round the eye.

For nocturnal animals they don’t want to do this, want light rebounded to absorb it fully.

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17
Q

describe retinal pigment epithelial cells.

A

different processes wrap around the outer segments of rods and cones.

recycling and forming retinaldehyde - essential co factor of opsins.

also important for light absorption, stop the light rebounding round the eye.

For nocturnal animals they don’t want to do this, want light rebounded to absorb it fully.

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18
Q

what cells absorb or reflect light?

A

melanin granules absorb light

tapetum reflects light.

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19
Q

describe vitamin A.

A

retinaldehyde.

loss of night vision, good source in carrots.

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20
Q

describe rods and cones structure/locations

A

highly polarised.

outer segment contains lots of membranous disks containing photo pigments.
opsin is a GPCR, to get the highest number stacked in disks.

fovea is cone dominated, rest of retina cones more prevalent.

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21
Q

describe phototransduction in rods and cones.

A

rhodopsin spans the membranous disk.

high level of cyclicGMP Na channels open in the dark, influx of Na.
transducin is the G protein from rhodopsin.

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22
Q

describe phototransduction.

A

rhodopsin spans the membranous disk.

high level of cyclicGMP Na channels open in the dark, influx of Na.
transducin is the G protein from rhodopsin.

photon of light causes a conformational change in rhodopsin molecule, leads to the activation of transducin.
this hydrolysis GTP to GDP.
leads to a phosphodiesterase being activated, this changes cGMP to GMP and leads to a reduction of cGMP.
since theres less cGMP the cGMP gated Na channels close.

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23
Q

describe phototransduction.

A

rhodopsin spans the membranous disk.

high level of cyclicGMP Na channels open in the dark, influx of Na.
transducin is the G protein from rhodopsin.

photon of light causes a conformational change in rhodopsin molecule, leads to the activation of transducin.
this hydrolysis GTP to GDP.
leads to a phosphodiesterase being activated, this changes cGMP to GMP and leads to a reduction of cGMP.
since theres less cGMP the cGMP gated Na channels close.

this causes hyperpolarisation in the PS, this leads to glutamate release. WHY?

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24
Q

describe bipiolar, horizontal and amacrine cells.

A

they release different NT depending on the amount of glutamate present.
No AP.

“tweak” and alter signal from rods and cones to the ganglion cells.

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25
Q

describe muller cells.

A

provide nutrients.

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26
Q

describe ganglion cells.

A

fire AP down the optic nerve.
M and P type sensitive to different info from PR cells.

M - detect movement

P - colour vision

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27
Q

what is parallel processing?

A

info from M and P cells separate until higher regions of the brain.

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28
Q

Describe the visual pathway

A

from the LGN, P and M sent on different pathways.
both go to visual cortex (V1), P go to temporal cortex.
M go to dorsal pathway.

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29
Q

what is steopsis?

A

able to form 3d image in the brain.

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30
Q

what is glaucoma?

A

damage to the optic nerve

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31
Q

describe the invertebrate retina.

A

ommatidia units.

each unit has a lens/pigment cells.

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32
Q

describe phototransduction in invertebrates.

A

absorbs a photon of light, leads to change in rhodopsin, and an activation of Gq.
this activates phospholipase C, this leads to phosphoinositide hydrolysis and the opening of cation channels.

leads to depolarisation.

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33
Q

what is melanopsin?

A

5% of retinal ganglion cells.
different opsin to rods and cones.
acts in the same way as invertebrate rhodopsin.

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34
Q

what is univariance?

A

dont know what triggers a receptor

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35
Q

what type of senses do we have?

A

chemoreceptors
auditory
vision
mechanoreceptors - pressure, touch.

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36
Q

what is a somatosensory pathway?

A

activation of sensory receptor.
transmission of sensory input to the spinal cord via 1st order neuron (peripheral).
transmission of signal via ascending pathway through the thalamus (2nd order neuron) to primary sensory cortex (3rd order neuron).
processing of sensory signals in primary sensory cortex - perception.

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37
Q

describe the evolution of the ear.

A

lateral line system in fishes, senses vibration/water pressure in water.

water moves along the channel, hairs fixed in the cupula, the hairs push the cupula and mechanoreception can alert the fish.

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38
Q

describe the functions of different parts of the ear.

A

external, middle and part of inner make up the hearing.

the inner ear comprises the vestibular system (head position and movement).

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39
Q

describe hearing.

A

detecting variations in the air pressure.

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40
Q

what region can humans detect of hearing?

A

20Hz to 20,000Hz

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41
Q

what is a lower pitched sound?

A

lower frequency

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42
Q

what is a quieter sound?

A

lower intensity

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43
Q

what is infrasound?

A

below 20Hz

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44
Q

What is ultrasound?

A

more than 20,000Hz

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45
Q

what is hearing?

A

detecting variations in the air pressure.

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46
Q

Describe the process of hearing

A

sound waves are collected by auricle and conducted through the external ear.

sound waves hit the tympanic membrane and cause it to vibrate.

Vibration is transmitted and amplified through the ossicles.

vibration of the stapes causes fluid in the cochlea to vibrate.

vibrations stimulate the spiral organ (sensory receptor) which triggers action potentials in the vestibularcochlear nerve (a cranial nerve).

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47
Q

describe the endolymph

A

a high concentration of K ions, maintained by AT.

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48
Q

How do AP occur in the ear?

A

TRPA1 channels in the membrane of our hair cells, when the cell is bent the channels open. This causes an influx of K, depolarises the cell and voltage gated Ca channels to open, triggering NT release from vesicles into the synaptic cleft.

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49
Q

Describe the process of hearing

A

sound waves are collected by auricle and conducted through the external ear.

sound waves hit the tympanic membrane and cause it to vibrate.

Vibration is transmitted and amplified through the ossicles.

vibration of the stapes causes fluid in the cochlea to vibrate.

vibrations stimulate the spiral organ (sensory receptor) which triggers action potentials in the vestibularcochlear nerve (a cranial nerve).

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50
Q

How do AP occur in the ear?

A

TRPA1 channels in the membrane of our hair cells, when the cell is bent the channels open. This causes an influx of K, depolarises the cell and voltage gated Ca channels to open, triggering NT release from vesicles into the synaptic cleft.
Hair cells don’t fire AP themselves.

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51
Q

where does the AP travel to?

A

AP travels through the vestibularcochlear nerve from the chochlea to the primary auditory cortex in the temportal lobe.

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52
Q

what is tonotopy?

A

seperate parts of the auditory cortex are dedicated to particular frequencies of cells.

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53
Q

where is the primary auditory cortex located?

A

the temportal lobe.

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54
Q

what are otolith organs?

A

detect force of gravity and tilt of head.

inner ear

membrane on the bottom, microvilli (kinocilium) stuck in gelly cap. Cap is embedded with otolith crystals (CaCO3), gravity pulls the crystals to deform the cap and bend the hair cells.

Bending opens K channels –> NT release to ganglion.

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55
Q

What are semicircular canals?

A

detect head rotation.

inner ear

Hair cells in cupula, head turning causes endolymph to flow in that direction, a small delay.
This bends the cupula and can lead to NT release.

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56
Q

what are the chemical special senses?

A

smell and taste.

Both GPCRs.

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57
Q

describe the structure of the tongue.

A

papillae are projections all over the tongue, contain tastebuds.

foliate at sides, fungiform on base of tongue, vallate at top back middle.

taste cells are not neurones but can fire action potentials.

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58
Q

Who are “super tasters”?

A

people with more foliate papilae, higher no of tastebuds.

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59
Q

what food groups are dependent on GPCRs?

A

unami, bitter and sweet.

salt is Na channel.

60
Q

where is the olfactory cortex?

A

Temporal lobe

61
Q

where is the visual cortex?

A

occipital lobe

62
Q

where is the auditory cortex?

A

temporal lobe

63
Q

where is the somatosensory cortex?

A

parietal lobe

post sensory gyrus?

64
Q

what is unencapsulated and encapsulated?

A

unencapsulated - sensory nerve endings are free/not wrapped in connective tissue.

encapsulated - nerve endings are wrapped in glial cells or connective tissue. increased sensitivity.

65
Q

what are the main receptors for touch?

A

steady pressure - merkel cells and ruffini endings.

vibration- meissners and pacinian corpuscles.

all encapsulated except from merkel.

66
Q

describe receptive fields.

A

many primary neurons converging onto a single secondary neuron creates a large receptive field. Can’t perceive 2 receptors in a large field.

fewer neurones converging onto secondary neurones means the receptive fields are smaller. Can perceive 2 different stimuli better.

67
Q

what is nociception?

A

detecting damaged tissue.

Not actual perception of pain.

68
Q

describe pain.

A

first pain - myelinated axons, conducted faster. A gamma fiber

second pain - unmyelinated axons, slow.
C fiber

69
Q

describe itching

A

caused by histamines.

70
Q

describe temperate sensing.

A

Trpv1 channels are triggered at high temperatures. Capsaicin.

Trpm8 channels at cold temperates - menthol.

71
Q

what are the groups of muscle?

A

striated - skeletal, cardiac.

smooth.

72
Q

are muscles excitable?

A

yes, can generate AP.

73
Q

what are muscle fibres/myocites?

A

individual muscle cells.

multinucleus.

74
Q

how are muscle fibres arranged in skeletal muscles?

A

muscle fibres surrounded by connective tissue called the endomysium.

muscle fibres are bundled into a fascicle, fascicles are surrounded by the connective tissue called perimysium.

the muscle is a block of fascicles surrounded by the epimysium.
most are bound to bones by tendons.

75
Q

how are muscle fibres arranged in skeletal muscles?

A

muscle fibres surrounded by connective tissue called the endomysium.

muscle fibres are bundled into a fascicle, fascicles are surrounded by the connective tissue called perimysium.

the muscle is a block of fascicles surrounded by the epimysium.
most are bound to bones by tendons.

76
Q

what is a fascicle?

A

bundle/”strength through unity”.

muscle fibres are bundled into a fascicle, fascicles are surrounded by the connective tissue called perimysium.

77
Q

describe the structure of skeletal muscle fibres.

A

composed of myofibrils surrounded by a membrane called the sarcolemma.
The

78
Q

describe the structure of skeletal muscle fibres.

A

composed of myofibrils surrounded by a membrane called the sarcolemma.
The sarcoplasmic reticulum is the muscle equivalent of the Endoplasmic reticulum.

Terminal cisterna are part of sarcoplasmic reticulum.
interaction of a T tubule and 2 terminal cisterna - triad

79
Q

describe the structure of sarcolemma

A

repeating units of sarcomere, its what gives the stripes to striated muscles.

sarcomere is between the z lines.
H zone A band Z line M line I band all that shit.

optimum overlapping.

80
Q

why do sarcomere have stripes?

A

actin and myosin, pattern of overlap changes as muscles contracts.
sliding filament model.

81
Q

describe titin.

A

a structural protein that gives the muscle elasticity.

very big - hence titan

82
Q

what is the frank stalin curve?

A

as you push blood back to the heart cardiac muscle fibres become stretched, the degree of contraction increases, then it starts to come down again.

??

83
Q

describe myosin.

A

its a hexoamer.
2 heavy chains and 4 light chains, heavy chains are tails coiled around each other.

head has ATPase activity.

84
Q

describe myosin.

A

its a hexoamer.
2 heavy chains with heads on them and 4 light chains, heavy chains are tails coiled around each other.

head has ATPase binding sites and can hydrolyse ATP, power source for muscle contraction.

skeletal muscle myosin is myosin type II.
other types of type II in cardiac/smooth muscle.

85
Q

describe Actin.

A

Globular (G) actin.
Filament (F) actin.

G actin collect to make F actin in a helical form, F actin is present in muscle.

86
Q

describe tropomyosin and troponin

A

tropomyosin - really long, 1 for every 7 actin monomers.

troponin

  • troponin T interacts with tropomyosin
  • troponin C binds to calcium
  • troponin I inhibits shit?
87
Q

describe the contraction cycle.

A

myosin heads bind ATP.
causes the conformation of the myosin head to change, it loses the bind to actin

hydrolysis of the ATP, myosin head changes to a “cocked” state (it swings).

myosin can now reinteract with myosin, it happens 2 monomers further down the chain due to movement.

phosphate dissociates from myosin head, myosin head moves back to original conformation (power stroke).

ADP dissociates, back to where we started but interaction is 2 monomers further down.

88
Q

what does Troponin I do?

A

covers myosin binding site.

Troponin C iniates a conformational change and exposes myosin binding site when bound to calcium.

89
Q

what is a triad?

A

2 terminal cisternae around 1 T tubule.

90
Q

what do T tubules do?

A

allow the AP to spread all the way into the muscle fibre, a bigger surface area.

91
Q

what do T tubules do?

A

allow the AP to spread all the way into the muscle fibre, a bigger surface area.

92
Q

describe the calcium distribution in muscle cells.

A

high conc outside muscle cells, low in cytoplasm, high in sarcoplasmic reticulum (inside).

2 big ass pools of calcium, very low in cytoplasm.

93
Q

describe the calcium distribution in muscle cells.

A

high conc outside muscle cells, low in cytoplasm, high in sarcoplasmic reticulum (inside).

2 big ass pools of calcium, very low in cytoplasm.

SERCA is an ATPase puts Ca into sarcoplasmic reticulum against it’s conc gradient.

94
Q

how does an AP get created in muscle cells?

A

influx of Ca in the cytoplasm from the sarcoplasmic reticulum, Ca from outside not needed.

95
Q

how does an AP get created in muscle cells?

A

influx of Ca in the cytoplasm from the sarcoplasmic reticulum, Ca from outside not needed.

ryanodine receptors on sarcoplasmic reticulum, it’s coupled to voltage sensitive Ca channels on T tubules.

AP from T tubule opens voltage sensitive Ca channels on sarcoplasmic reticulum.
“L type voltage sensitive Ca channel”
“di-hydro pirodine receptor”

96
Q

how does an AP get created in muscle cells?

A

influx of Ca in the cytoplasm from the sarcoplasmic reticulum, Ca from outside not needed.

ryanodine receptors on sarcoplasmic reticulum, it’s coupled to voltage sensitive Ca channels on T tubules.

AP from T tubule opens voltage sensitive Ca channels on sarcoplasmic reticulum.
“L type voltage sensitive Ca channel”
“di-hydro pirodine receptor”

97
Q

describe the dihydro pirodine receptors.

A

4 DHP (tetrad) in the T tubule membrane linked to one single ryanodine receptor in the sarcoplasmic reticulum.

98
Q

how is calcium removed from the cytoplasm?

A

SERCA burns ATP and pumps Ca back into the sarcoplasmic reticulum.

99
Q

summarise the nerve to muscle action potential

A

Acetylcholine released by motor neurone.

Activates nACh receptors.

Sarcolemma depolarised, action potential triggered and spreads to T tubules.

DHP receptor activated. Triggers ryanodine receptor.

Calcium ions released from sarcoplasmic reticulum.

Troponin C binds Ca2+ and is activated.

Muscle contraction initiated.

Calcium ions pumped back into SR.

100
Q

need to read -

A

muscle spindles
myotactic reflexes
gamma motor neurones

BEAR CHAPTER 13 PROPRIOCEPTION

101
Q

how can you contract constantly when action potentials only last 2ms?

A

calcium not reuptaken from the cytoplasm immediately, it can hang around y0.

102
Q

what happens when you contract individually rapidly one after the other?

A 
they summate (increase) and fuse into one single contraction. 
You get fused tetanus (maximally contracted muscle).
103
Q

what is tetanus?

A

maximally contracted muscle.

104
Q

what is henneman’s size principle?

A

the size of the cell body of the motor neurones that leave the spinal cord and go to the muscle, bigger contains more muscle fibres.

105
Q

what is henneman’s size principle?

A

the size of the cell body of the motor neurones that leave the spinal cord and go to the muscle, bigger contains more muscle fibres.

a small AP only triggers the smallest neuron, this triggers a bigger one, etc etc.
allows control??

106
Q

what are the types of skeletal muscle?

A

fast twitch glycolytic
fast twitch oxidative
slow twitch oxidative

107
Q

describe fast fibres.

A

Type IIa, IIb.
fast myosin isoform (different myosin type),
Ca released fast due to highly efficient Ca pumps.

allows rapid contraction but at high energy cost, ATP hydrolysed quickly.

108
Q

Describe slow fibres.

A

Type I.
posture maintenance.
have myoglobin as oxygen store, many mitochondria, good capillary supply.

109
Q

describe fast fibres glycolytic.

A

Type IIa, IIb.
fast myosin isoform (different myosin type),
Ca released fast due to highly efficient Ca pumps.

allows rapid contraction but at high energy cost, ATP hydrolysed quickly.

110
Q

Describe slow fibres oxidative.

A

Type I.
posture maintenance.
have myoglobin as oxygen store, many mitochondria, good capillary supply.

111
Q

describe the problem with fast twitch glycolytic fibres.

A

lactate accumulation due to not going through the full Krebs cycle, causes acidosis and can cause cramping.

112
Q

describe fast twitch oxidative fibres.

A

in between fast twitch glycolytic and slow twitch oxidative.

use oxygen and glycogen.

113
Q

describe duchenne muscular dystrophy

A

X linked. 1:3600 births.
problem in structure of muscle, fibres arent linked to extracellular matrix properly.

excess calcium enters and muscle fibres die.
muscle weakness.
25-30yr life expectancy.

114
Q

what happens in a myosin statin defect?

A

doesn’t inhibit muscle growth.

115
Q

Describe cardiac muscle.

A

sliding filament and regulation of calcium is the same as skeletal.

cells aren’t fused together, they are linked together through intercalated discs.
gap junctions mean cardiac muscle cells are electrically connected to each other.

116
Q

Describe cardiac muscle.

A

sliding filament and regulation of calcium is the same as skeletal.

cells aren’t fused together, they are linked together through intercalated discs.
gap junctions mean cardiac muscle cells are electrically connected to each other.

joined by intercalated discs into a branced syncytium.

not stimulated to contract by neurons, self stimulating.

117
Q

describe the cardiac muscle action potential.

A

upspike followed by a plateau, it’s longer lasting - 200ms compared to 2-5ms.

plateau due to Ca influx.

118
Q

describe the cardiac muscle action potential.

A

upspike followed by a plateau, it’s longer lasting - 200ms compared to 2-5ms.

plateau due to Ca influx.

119
Q

describe calcium induced calcium release.

A

most Ca comes from sarcoplasmic reticulum through ryanodine receptors.

ryanodine receptors are stimulated to open by calcium entry through L type calcium channels.

120
Q

describe myogenic properties of cardiac muscle.

A

some muscle cells can spontaneously create an AP - sinal atrial node.

pacemaker current, slowly depolarise until they reach a threshold to create an AP.

121
Q

describe myogenic properties of cardiac muscle.

A

some muscle cells can spontaneously create an AP - sinal atrial node.

pacemaker current, slowly depolarise until they reach a threshold to create an AP.

122
Q

what is a pacemaker potential?

A

If (funny)

123
Q

how does the nervous system influence the heart rate?

A

doesnt create them, alters their speed.

changes the slope of AP, speed it up (sympathetic), slows down (parasympathetic).

124
Q

how does the nervous system influence the heart rate?

A

doesnt create them, alters their speed.

changes the slope of AP, speed it up (sympathetic), slows down (parasympathetic).
changes concentration of cytoplasmic Ca.

125
Q

how does the cardiac muscle power itself?

A

oxidative metabolism, needs a good blood supply.

takes blood from seperate capillaries and arteries, not the blood it’s pumping.

126
Q

describe that smooth muscle y0

A

no striations.
no t tubules.
small spindle shaped cells.

sliding filament broadly the same.

if coupled by gap junctions - unitary, act as a single unit.
if not act independently - multiunit.

127
Q

describe that smooth muscle y0

A

propel contents or to regulate flow

controlled by autonomic nervous system.

no striations.
no t tubules.
small spindle shaped cells.

sliding filament broadly the same.

if coupled by gap junctions - unitary, act as a single unit.
if not act independently - multiunit.

128
Q

where is smooth muscle found?

A 
blood vessels
guy
bladder
uterus
bronchi
129
Q

describe that smooth muscle y0

A

propel contents or to regulate flow. contracts slowly for long periods of time, more energy efficient.

controlled by autonomic nervous system.

no striations.
no t tubules.
small spindle shaped cells.

sliding filament broadly the same.

if coupled by gap junctions - unitary, act as a single unit.
if not act independently - multiunit.

130
Q

describe excitation-contraction in smooth muscle.

A

no troponin.
AP not always required to contract.
more Ca comes from extracellular.

release from SR via ryanodine receptors and IP3 (GPCR activated).

131
Q

describe excitation-contraction in smooth muscle.

A

no troponin.
AP not always required to contract.
more Ca comes from extracellular.

release from SR via ryanodine receptors and IP3 (GPCR activated).

store operated calcium release.

132
Q

sources of calcium for smooth muscle?

A

L type calcium channel can act on ryanodine receptors.

GPCR produce IP3 which acts on a IP3 receptor on the Ca channel.

133
Q

sources of calcium for smooth muscle?

A

L type calcium channel can act on ryanodine receptors.

GPCR produce IP3 which acts on a IP3 receptor on the Ca channel.

when SR has used all the Ca, signals sent to store operated Ca channels which allows more Ca to enter the cell.

134
Q

describe myosin in smooth muscle.

A

in smooth muscle the heads have much lower ATPase activity and the role of calcium is to increase this ATPase activity.

135
Q

describe myosin in smooth muscle.

A

in smooth muscle the heads have much lower ATPase activity and the role of calcium is to increase this ATPase activity.
Only activate when light chains are phosphorylated.

calcium binds to calmodulin, binds 4 Ca ions.
activates myosin light chain kinase (MLCK), [kinase phosphorylate things] this phosphorylates the light chain and ATP production increases, allowing cross bridges to form.

136
Q

differences between all muscle types.

A

last slide on lecture 16

137
Q

why do plants need rapid movements?

A

external stimuli:
protection from damage
prey capture

spreading pollen and seeds

138
Q

describe mimosa pudica.

A

“sensitive plant”

Rapid response to touch, light, vibration, temperature
Leaflets fold up to avoid damage and at night
Apparent ‘wilting’ exposes thorny stems and deters herbivores and pests

139
Q

describe dionea muscipula.

A

venus fly trap.

sensitive hairs within trap that snaps shut to catch the prey.

140
Q

describe paramecium.

A

protist.

Single celled organism – 100-200 µm long.
Purposeful swimming locomotion.
Swims by coordinated beating of cilia.
Rapidly changes direction to avoid obstacles and predators.
Behavioural mutants.

Stimulus → receptor potential → Ca2+-based action potential → increased intracellular Ca2+ → reversal of ciliary beat

Stimulus = chemical, heat, touch, light

Receptor potential graded to stimulus intensity – allows for decision-making

Mutants without action potentials can move but show impaired responses to stimuli – locomotion no longer purposeful

141
Q

how do action potentials come from cilia?

A

Ca channels are located on cilia membrane,
K channels located on cell body membrane
(Other conductances also present).

142
Q

How do cilia move?

A

Whip-like movements of cilia coordinated into a wave.
‘9 + 2’ arrangement of microtubules to create axoneme.

Protein crosslinks stabilise the microtubules in the axoneme.
Bending caused by crosslinks of dynein ‘walking’ along the microtubule – cf. muscle sliding filament.
Increased intracellular Ca2+ causes reversal of ciliary beat.

????

143
Q

what are the mutants of paramecium?

A

Pawn: no V-gated Ca current – cannot generate APs and cannot reverse direction of locomotion

Dancer: enhanced Ca current – reverses in response to much weaker stimulation

Pantophobiac: reduced V-gated K current – prolonged depolarisation and therefore swims backwards for longer

144
Q

what is didinium nasutum?

A

ciliate protozoan.

A voracious predator of paramecium.
Both predator and prey show fast, directed movements using beating cilia.
Didinium ‘captures’ paramecium and then engulfs it.

145
Q

how do Cl- ion based action potentials cause cell shrinkage?

A 
Cl- ion efflux
K+ follows
H2O follows by osmosis
- Sudden loss of turgor
- Ions and H2O pumped back in
146
Q

how does the mimosa leaflet move?

A

Pulvinus attaches leaflet to stem.
Cells on upper surface have thick walls and cannot shrink.
Cell on lower surface shrink causing bending of pulivus.

147
Q

how does the venus flytrap work?

A

Resting membrane potential of sensory cells and other tissue cells is -150 mV.
All cells can generate APs, which are 1-3 sec duration and 150 mV amplitude.
APs are Ca2+-based.

Cell to cell AP transmission is electrotonic via ‘plasmodesmata’ (= cytoplasmic links between cells).
Mechanism of trap closure is uncertain, but probably involves changes in turgor of cells in midrib and trap lobes. Lobes ‘flip’ from convex to concave.

Excitable cells (6 decks)

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