stimulus and responce Flashcards

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1
Q

taxis

A

-a simple respite whose direction is determined by the direction of the stimulus

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2
Q

positive taxis

A

-if the movement is towards the stimulus

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3
Q

negative taxis

A

-if the movement is away from the taxis

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4
Q

why is taxis advantageous?

A

-it increases the chance of survival as an organism will move to its favoured conditions (towards or away)

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5
Q

kinesis

A

-a response where an organism doesn’t move to or away from a stimulus
-it just changes speed and rate of direction change (it has no specific direction)
-stimuli = humidity and temperature

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6
Q

IAA

A

-movement is caused by a plant hormone (auxins)
-IAA is a specific auxin
-there is a particular distribution of IAA around a plant, causing movement or bending

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7
Q

IAA affect on shoots

A

-IAA is produced in the top
-IAA diffuses down the shoot
-if light is at one side, it diffuses down and accumulates on the shaded side
-this leads to cell elongation on the shaded side
-this means that the shoot will elongate/ bend towards the light

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8
Q

IAA affect on roots

A

-IAA is produced in the tip
-IAA diffuses down the root
-IAA accumulates art the base of the root due to gravity
-IAA inhibits elongation in the root
-the root elongates downwards
-as the cells elongate at the top, making it bend and grow downwards

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9
Q

pacinian corpuscle

A

-pressure is applied and the lamellae is deformed
-the stretch mediated Na+ channel opens
-Na+ diffuses into the axon
-this leads to depolarisation and an action potential if the threshold is exceeded
-a pacinian corpuscle is a sensory receptor found deep in the sink that detects changes in pressure

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10
Q

myelin sheath

A

-myelin sheaths insulate the axon (ions can’t move in or out)
-the impulse must jump from node to node
-this speeds up the transmission of an action potential
-this is called salary conduction

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11
Q

visual acuity

A

-the ability to tell objects apart and see fine detail

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12
Q

convergence

A

-the ability to tell objects apart and see fine detail

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13
Q

rod cells

A

-rods are found around the outside of the retina, away from the fovea
-light stimulus triggers depolarisation in the rod cells
-many rods converge and are connected to a single sensory neurone
-depolarisation undergoes (spatial) summation to trigger an action potential
-in low light there is enough light to lead to an action potential, however this reduced visual acuity

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14
Q

cone cells

A

-cone cells are located in the fovea (behind the retina to maximise light stimulus)
-every cone cell is connected to a single sensory neurone (no convergence)
-each cone cell sends a single impulse to the brain
-with high visual acuity
-three types of cones detect three different wavelengths of light

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15
Q

control of heart rate

A

-the SA (sino atrial) node initiates a wave of electrical impulses across both atria causing them to connect
-non-conductive tissue prevents impulse from going straight into the ventricle
-AV (atrio ventricular) node delays impulses so the ventricles can fill
-AV node sends a wave of electrical impulses down the Bundle of His
-the ventricles contract from the bottom up

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16
Q

response to CO2 increasing

A

-pH in the blood lowers
chemoreceptors detect it
-CO2 needs to be removed
-sensory neurone takes more impulses to the medulla
-the medulla sends more impulses along the sympathetic nerve
-the sympathetic nerve cause SAN to increase
-heart rate increases
-(opposite occurs for decreasing CO2)

17
Q

response to blood pressure increasing

A

-baroreceptors detect the pressure increase
-too high pressure can cause damage to the artery walls, so it needs to be restored
-the sensory neurone takes more impulses to the medulla
-the medulla sends more impulses along the parasympathetic nerve
-the parasympathetic nerve causes SAN to decrease
-heat rate decreases
-(opposite occurs for decreasing blood pressure)

18
Q

normal and hormonal communication

A

-nervous is fast
-response is short lived
-requires neurone, neurotransmitters and nervous impulses

-hormonal is slow
-response is long lasting
-hormones are produced in glands, travel in the blood to an organ/ tissue with a target receptor

19
Q

resting potential

A

-Na+/ K+ pumps 3 Na+ out of the axon and 2 K+ into the axon using ATP
-membrane is more permeable to K+ so K+ moves out through channels and less permeable to Na+
-axon has a more negative potential difference inside

20
Q

refractory period

A

-the period between firing of one action potential and the next
-the axon is hyperpolarised (very negative) on the inside
-the refractory period ensures that:
-action potentials occur in one direction
-limits the number of action potentials
-keeps action potentials separated

21
Q

action potential

A

-Na+ ions enter the axon
-the axon membrane is depolarised
-the potential difference across the axon becomes. ore positive
-the potential difference will reach threshold, triggering an action potential
-voltage gated Na+ channels will open
-Na+ moves into the axon by facilitated diffusion
-Na+ channels close, K+ channels open
-K+ leaves the icon by facilitated diffusion (the axon is repolarised)
-the axon membrane becomes hyper polarised in the refractory period
-Na+/K+ pump restores resting potential

22
Q

synapse

A

-action potential arrives ay the pre-synaptic neurone
-Ca2+ channels open in the pre-synaptic membrane
-Ca2+ flood into the pre-synaptic end of the axon
-this sudden increase in Ca2+ causes the synaptic vesicles to fuse with the pre-synaptic membrane
-this releases the acetylcholine into the synaptic clef
-it diffuses across the gap
-acetylcholine then binds to the receptor molecules on the post-synaptic membrane
-the channel opens in response to this and Na+ diffuses into the post-synaptic membrane
-an influx of Na+ propagates a new action potential in the neurone
-an enzyme (acteylcholinesterase) exists in the synapse
-it’s job is to break down ACh into acetic acid and choline
-this stops the action potential from being constantly generated

23
Q

NMJ

A

-vesicles of neurotransmitter fuse with the pre-synaptic membrane
-neurotransmitter e.g. acetylcholine diffuses across the neuromuscular junction
-neurotransmitter binds to the Na+ receptors causing Na+ to enter the sarcolemma (muscle tissue), depolarising it
-depolarisation is transmitted through the T-tubules causing Ca2+ to be released from the sarcoplasmic reticulum
-Ca2+ binds to tropomyosin in the leading to muscle contraction

24
Q

muscle contraction

A

-Ca2+ diffuse into the myofibrils from the sarcoplasmic reticulum
-Ca2+ binds to tropomyosin, changing its shape
-this exposes the myosin binding sites on the actin
-myosin ‘heads’ bind to the actin, forming a cross bridge
-Ca2+ activates ATPase, which hydrolyses ATP
-the myosin ‘heads’ tilt in a rowing motion, pulling the actin molecules
-ATP can now bind to the myosin head, changing the shape and breaking the cross bridge
-ATP is hydrolysed by the head, providing energy for the head to flip back
-ADP and Pi remains on the head