MODULE 5 SECTION 3 - ANIMAL RESPONSES Flashcards

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1
Q

Why do animals respond to changes in their external and internal environment?

A
  • to increase their chances of survival.

- to ensure optimal conditions for metabolism.

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2
Q

What is a stimulus?

A

A stimulus is any change in the internal or external environment.

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3
Q

Receptors?

A

Receptors detect stimuli.

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4
Q

Effectors?

A

Effectors bring about a response to a stimulus.

Includes:

  • muscle cells
  • cells found in glands
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5
Q

How is the nervous system split up?

A

Nervous system split into:

  • CNS (brain and spinal cord)
  • Peripheral nervous system (all the neurones that connect the CNS to the rest of the body.
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6
Q

How is the peripheral nervous system split up?

A

Split into:

  • Somatic nervous system (controls conscious activities such as running, playing games).
  • Autonomic nervous system (controls unconscious activities such as digestion and heart rate).
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7
Q

How is the autonomic nervous system split up?

A

Split into:

  • Sympathetic nervous system (‘fight or flight’ system that gets the body ready for action. Sympathetic neurones release noradrenaline).
  • Parasympathetic nervous system (‘rest and digest’ system that calms the body down, parasympathetic neurones release acetylcholine).
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8
Q

Cerebrum

A
  • Largest part of the brain
  • Divided into 2 cerebral hemispheres
  • thin outer layer called cerebral cortex, highly folded (to increase surface area).
  • Involved in vision, hearing, learning, thinking.
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9
Q

Hypothalamus

A
  • Found just underneath the middle part of the brain.
  • Automatically maintains body temperature at the normal level.
  • Produces hormones that control the pituitary gland.
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10
Q

Medulla oblongata

A
  • Found at the base of the brain, top of spinal cord.

- Medulla oblongata automatically controls breathing rate and heart rate.

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11
Q

Cerebellum

A
  • Found underneath cerebrum.
  • Has a folded cortex.
  • Important for muscle coordination, posture, coordination of balance.
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12
Q

Pituitary gland

A
  • Found underneath the hypothalamus.
  • Controlled by the hypothalamus.
  • Releases hormones.
  • Stimulates other glands (such as adrenal glands) to release their hormones.
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13
Q

Reflex actions?

A
  • They are extremely fast.
  • They are protective - they help organisms to avoid damage to the body as the response happens so quickly.
  • They are present from birth.
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14
Q

Pathway of a reflex action?

A
  • stimulus
  • receptor
  • sensory neurone
  • relay neurone
  • motor neurone
  • effector
  • response

Not all reflex actions involve a relay neurone, such as the knee-jerk reflex.

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15
Q

Blinking reflex

A

This reflex is to prevent damage to the eye.

  • stimulus: something touches your eye.
  • receptors: touch receptors in the cornea detect the touch stimulus.
  • Nerve impulse is sent along sensory neurone to a relay neurone in the CNS.
  • CNS: nerve impulse is passed from relay neurone to motor neurone.
  • Effectors: nerve impulse is passed from motor neurone to eyelid muscles.
  • Response: eyelid muscles contract and causes eyelids to close quickly to prevent damage to the eye.

This reflex can occur due to other stimuli such as hearing a sudden loud sounds or a flash of bright light.

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16
Q

Knee-jerk reflex

A

This reflex helps to maintain posture and balance.

  • patellar tendon of the quadriceps muscle is stretched.
  • stretch receptors in the quadriceps muscle detect that the tendon is being stretched. Nerve impulse is passed along a sensory neurone.
  • Sensory neurone passes nerve impulse directly to a motor neurone in the spinal cord (CNS) (no relay neurone is involved).
  • motor neurone carries impulse to the quadriceps muscle
  • quadriceps muscle contracts, so the lower leg moves forward quickly.
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17
Q

What is a reflex action?

A

A reflex action is when the body responds to a stimulus without making the conscious decision to respond.

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18
Q

What is the fight or flight response?

A

When an organism is threatened, the fight or flight system is activated. Nerve impulses from sensory neurones arrive at the hypothalamus, activating both the hormonal and sympathetic nervous system.

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19
Q

What happens at the pituitary gland when it is activated in the fight or flight response?

A

Stimulated to release hormone ACTH.

ACTH causes cortex of adrenal gland to release steroidal hormones.

Steroidal hormones from adrenal glands:

  • Includes cortisol and aldosterone.
  • stimulates breakdown of proteins and fats into glucose. This increases the amount of energy available.
  • Increases blood pressure and volume by increasing uptake of water and Na+ by kidneys.
  • suppresses the immune system.
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20
Q

What happens when the sympathetic nervous system is activated in the fight or flight response?

A

Triggers release of adrenaline from adrenal medulla.

Sympathetic nervous system and adrenaline produce a faster response than hormones secreted by adrenal cortex.

Adrenaline:

  • Heart rate increases and heart contracts with more force.
  • airways become wider.
  • intercostal muscles and diaphragm contract faster with more strength, increasing breathing rate and volume.
  • glycogen converted to glucose by glycogenolysis so that more glucose is available for respiration.
  • blood flow is diverted from skin and gut to heart, lungs , skeletal muslces (blood vessels contract at skin and gut, dilate and heart, lungs, skeletal muscles). Blood flow increased to these regions, making them ready for action.
  • erector pili muscles contract causing hairs to stand on end. Makes the animal look bigger.
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21
Q

What part of the brain controls heart rate?

A

The rate at which the SAN generates electrical impulses is unconsciously controlled by the cardiovascular centre in the medulla oblongata.

Controlled by autonomic nervous system.

22
Q

What synoptic topics occur in fight or flight response?

A

e. g
- heart rate
- breathing
- glycogenolysis
- muscle contraction.

23
Q

Why do animals need to alter heart rate?

A

To respond to internal stimuli.

24
Q

What detects blood pressure and where are they located?

A
  • baroreceptors are the pressure receptors.
  • baroreceptors are found in the aorta and carotid arteries.
  • they detect low and high blood pressure.
25
Q

What detects chemical changes in the blood and where are they located?

A
  • chemoreceptors are the chemical receptors.
  • chemoreceptors are found in the carotid arteries and medulla oblongata.
  • they detect changes in O2 levels, CO2 levels and pH of the blood.
26
Q

Overview of the mechanism of heart rate control

A
  • receptors (baroreceptors, chemoreceptors) detect stimuli.
  • nerve impulses sent to cardiovascular system of the medulla oblongata along sensory neurones.
  • cardiovascular system processes the information.
  • nerve impulses are sent from cardiovascular system to the SAN via motor neurones.
27
Q

What 2 motor neurones are involved in heart rate control and when are they used?

A
  • Vagus nerve (decreases heart rate). Parasympathetic motor neurone.
  • Accelerator nerve (increases heart rate). Sympathetic motor neurone.
28
Q

Heart rate control mechanism - High blood pressure

A
  • Baroreceptors (in aorta and carotid arteries) detect high blood pressure and send nerve impulses along sensory neurones to the cardiovascular system (in medulla oblongata).
  • Information is processed in the cardiovascular centre and nerve impulses are sent along parasympathetic neurones (vagus nerve) to SAN.
  • Parasympathetic neurones secrete acetylcholine, which binds to the receptors on the SAN.
  • Causes the heart rate to slow down and decrease blood pressure to normal levels.
29
Q

Heart rate control mechanism - low blood pressure

A
  • Baroreceptors detect low blood pressure and send nerve impulses along sensory neurones to the cardiovascular centre.
  • Information is processed in the cardiovascular centre and nerve impulses are sent along sympathetic neurones (accelerator nerve) to SAN.
  • sympathetic neurones releases noradrenaline, which binds to receptors on the SAN.
  • Cause heart rate to increase and increase blood pressure to normal levels.
30
Q

Heart rate control mechanism - High blood O2, low CO2, high pH

A
  • Chemoreceptors (in carotid arteries and medulla oblongata) detect chemical changes in the blood and send nerve impulses along sensory neurones to the cardiovascular centre.
  • Information is processed in the cardiovascular centre, and nerve impulses are sent along parasympathetic neurones (vagus nerve) to SAN.
  • parasympathetic neurones secretes acetylcholine, which binds to receptors on the SAN.
  • Causes heart rate to decrease in order to return O2, CO2 and pH levels back to normal.
31
Q

Heart rate control mechanism - Low blood O2, High CO2, low pH

A
  • Chemoreceptors detect chemical changes in the blood and send nerve impulses along sensory neurones to the cardiovascular centre.
  • Information is processed in the cardiovascular centre and nerve impulses are sent along sympathetic neurones (accelerator nerve) to the SAN.
  • sympathetic neurones releases acetylcholine, which binds to receptors on the SAN.
  • Causes heart rate to increase in order to return O2, CO2 and pH levels back to normal.
32
Q

Heart rate control mechanism - HORMONAL

A
  • When an organism is threatened (or at other times of stress), adrenal medulla secretes adrenaline and noradrenaline.
  • Adrenaline and noradrenaline binds to specific receptors in the SAN.
  • They cause an increase in frequency of impulses produced by the SAN.
  • Results in increased heart rate at heart pumps more blood around the body.
33
Q

Advantages of using an electronic heart rate monitor over manually taking pulse?

A
  • a monitor can take a continual record of how heart rate changes, whereas manual measurements must be done at intervals.
34
Q

What is the student’s t-test used for?

A

It is used to figure out whether there is a significant difference in the means of two data sets.
- Value obtained is compared to a critical value.

For a t-test, you need 2 sets of data and involves calculating standard deviation first, before plugging these values into the equation for t-test.

35
Q

How to carry out t-test

A
  • Identify null hypothesis. Always the same. There is no significant difference between the means of the 2 data sets. E.g There is no significant difference between the mean resting heart rate of people who received endurance training and those who did not.
  • calculate mean of each data set.
  • calculate standard deviation of each data set.
  • calculate t-value.
  • calculate degrees of freedom (n1+n2-2).
  • look at a table of critical values.
  • if the t-value is greater than the critical value at the p=0.05, state reject null hypothesis, there is a significant difference in the mean heart rate of people who received endurance training and those who did not, and the difference is not due to chance.
  • If t-value is smaller than critical value at the p=0.05, state do not reject null hypothesis, there is no significant difference in the mean heart rate of people who received endurance training and those who did not, and the difference is due to chance.
36
Q

Structure of skeletal muscle

A
  • Skeletal muscles are made up of muscle fibres.
  • Cell membrane of the muscle fibres is called sarcolemma.
  • Sarcolemma has bits which fold inwards across the muscle fibre and stick into the sarcoplasm called transverse (t) tubules.
  • t tubules help to spread depolarisation throughout the sarcoplasm, so they reach all parts of the muscle fibre.
  • throughout the sarcoplasm, there is a network of internal membranes called sarcoplasmic reticulum. It stores and releases Ca2+ ions that are needed for muscle contraction.
  • muscle fibres contain lots of mitochondria to provide ATP for muscle contraction.
  • muscle fibres are multinucleated.
  • muscle fibres are composed of myofibrils, which are made up of different proteins, and are highly specialised for contraction.
37
Q

Myofibrils

A
  • composed of bundles of thick and thin myofilaments.
  • the thick myofilaments are made of protein myosin.
  • the thin myofilaments are made of protein actin.
  • dark bands consist of the thick myosin filaments and some overlapping thin actin filaments (A bands). A bands are basically the length of the myosin filaments.
  • light bands consists of thin actin filament only (I bands).
  • myofibrils are made up of short units called sarcomeres.
  • Ends of each sarcomere are marked with Z line.
  • Middle of sarcomere is M line, which is the middle of the thick myosin filaments.
  • H zone only contains the thick myosin filaments.
  • so the only section that contains both actin and myosin filaments is the A band (dark bands).
38
Q

Explain the sliding filament model

A
  • myosin and actin filaments slide over one another to make the sarcomeres contract.
  • the myofilaments do not contract themselves.
  • simultaneous contraction of many sarcomeres means that myofibrils and muscle fibres contract.
  • sarcomeres return to their original length as the muscle relaxes.

When muscles contract, what happens to the different components of sarcomeres?

  • A bands stay same length.
  • I bands get shorter.
  • H zones get shorter.
  • Z lines get closer together.
  • sarcomeres get shorter

^^Notice how the only thing that remains the same length is the A band (myosin filaments and some overlapping actin filaments. Is is basically the length of the myosin filament, and we know that in muscle contraction, the myofilaments do not contract themselves, so A band does not alter in length).

39
Q

myosin filaments structure

A
  • they have hinged globular heads

- each myosin head has a binding site for actin and a binding site for ATP.

40
Q

actin filaments structure

A
  • they have binding sites for myosin heads called actin-myosin binding sites.
  • 2 proteins tropomyosin and troponin are found here.
  • troponin holds tropomyosin in place.
41
Q

Binding sites in the myofilaments in a resting muscle

A
  • actin-myosin binding site is blocked by tropomyosin.
  • this means that the globular myosin heads cannot bind to the actin actin filaments.
  • the myofilaments cannot slide past each other.
42
Q

Muscle contraction steps in the myofilaments

A
  • Action potential from motor neurone stimulates muscle cell.
  • Sarcolemma is depolarised.
  • Depolarisation spreads down T-tubules to the sarcoplasmic reticulum.
  • This causes the sarcoplasmic reticulum to release Ca2+ ions into the sarcoplasm.
  • The influx of Ca2+ ions triggers muscle contraction.
  • Ca2+ binds to troponin, causing it to change shape.
  • This pulls the attached tropomyosin out of the actin-myosin binding site.
  • The actin-myosin binding site on the actin filament is now exposed, allowing the globular myosin head to bind to it, forming an actin-myosin cross bridge.
  • Ca2+ ions also activate enzyme ATPase, which breaks down ATP to ADP and Pi, to provide energy for the myosin head to move to the side. This pulls the actin filament along in a rowing action.
  • Hydrolysis of ATP provides energy to break the actin-myosin cross bridge, so the myosin head detaches from actin filament after it is moved.
  • the myosin head returns to its original position (again energy provided by hydrolysis of ATP), and reattaches to a different actin-myosin binding site, forming a new actin-myosin cross bridge.
  • cycle is repeated (attach, move, detach, reattach to new binding site), as long as Ca2+ ions are present and bound to the troponin protein.

Return to resting state:

  • Muscle cell has stopped being stimulated.
  • Ca2+ leave binding site on troponin molecules and return to sarcoplasmic reticulum by active transport (requires ATP).
  • Troponin molecules return to original shape, pulling attached tropomyosin molecules with them.
  • Tropomyosin molecules block the actin-myosin binding sites again.
  • Globular myosin heads can no longer bind to actin filaments to form actin-myosin cross bridges, so muscles aren’t contracted.
  • actin filaments slide back to relaxed positions, sarcomeres lengthen.
43
Q

What are the functions of Ca2+ in muscle contraction?

A
  • Binds to troponin and causes it to change shape. The attached tropomyosin is pulled out of the actin-myosin binding site, exposing it.
  • Ca2+ ions activate the enzyme ATPase (Hydrolyses ATP to ADP to release energy).
44
Q

How is energy/ATP provided for muscle contraction?

A
  • Aerobic respiration
  • Anaerobic respiration
  • ATP-creatine phosphate system

Aerobic respiration:

  • Most ATP generated by oxidative phosphorylation in mitochondria.
  • occurs when oxygen is available.
  • good for long periods of low-intensity exercise (e.g walks).

Anaerobic respiration:

  • ATP is rapidly made by glycolysis.
  • End product of glycolysis is pyruvate, which is converted to lactate by lactate fermentation.
  • Lactate can quickly build up in muscles and cause muscle fatigue. It is broken down in the liver.
  • Good for short periods of hard exercise.

ATP-creatine phosphate system:
- creatine phosphate acts as a inorganic phosphate reserve.
- ATP is made by phosphorylating ADP with an inorganic phosphate group from CP.
- CP is stored inside cells.
- This system generates ATP very quickly.
- This system is anaerobic and does not form any lactate.
- CP runs out quickly after a few seconds.
- Good for short bursts of vigorous exercise.
ADP + CP -> ATP + C (creatine).

45
Q

The different types of muscle?

A
  • Skeletal muscle
  • Involuntary (smooth) muscle
  • Cardiac muscle

Skeletal muscle:

  • contraction is controlled consciously.
  • composed of many muscle fibres that are multinucleate.
  • some contract quickly - used for speed and strength, but fatigue quickly.
  • some contract slowly - used for endurance and posture and fatigue slowly.
  • striated appearance (cross-striations are visible).

Involuntary muscle:

  • contraction is controlled unconsciously.
  • does not have a striated appearance.
  • Found in walls of hollow internal organs.
  • muscle fibres are uninucleate.
  • fibres are spindle-shaped with pointy ends.
  • They contract slowly and don’t fatigue.

Cardiac muscle:

  • Myogenic (contracts on its own).
  • contraction is controlled unconsciously.
  • found in walls of the heart and function is to pump blood around the body.
  • made of muscle fibres connected by intercalated discs, which have low electrical resistance so nerve impulses can easily pass between cells.
  • muscle fibres are branched to allow impulses to spread quickly throughout whole muscle.
  • rate of contraction is controlled involuntarily by the autonomic nervous system, and can change in response to different stimuli.
  • each muscle fibre is uninucleate.
  • fibres are shaped like cylinders.
  • weakly striated appearance (weaker compared to skeletal muscle (striations are not as strong)). (weak cross-striations are visible).
  • muscle fibres contract rhythmically and do not fatigue.
46
Q

What is a neuromuscular junction?

A

A synapse between a motor neurone and a muscle cell. They work in the same way as synapses between neurones; they release neurotransmitters which triggers depolarisation in the postsynaptic cell.

Neuromuscular junctions use the neurotransmitter acetylcholine, which binds to cholinergic receptors on the postsynaptic membrane.

Acetylcholinesterase (stored in clefts on postsynaptic membrane) is released to break down acetylcholine after use.

47
Q

What is a cholinergic synapse?

A

A cholinergic synapse uses the neurotransmitter acetylcholine (released by presynaptic neurone), which binds to cholinergic receptors (on postsynaptic membrane).

48
Q

What happens at a cholinergic synapse?

A
  • Action potential arrives at the synaptic knob of the presynaptic neurone.
  • This stimulates voltage-gated calcium ion channels to open.
  • Ca2+ ions diffuse into the synaptic knob.
  • Influx of Ca2+ ions causes synaptic vesicles containing ACh to move to the presynaptic membrane.
  • The synaptic vesicles fuse with the presynaptic membrane.
  • ACh (stored in the vesicles) is released into the synaptic cleft by exocytosis.
  • ACh diffuses across the synaptic cleft and binds to specific cholinergic receptors on the postsynaptic membrane.
  • The binding causes sodium ion channels in the postsynaptic neurone to open.
  • Influx of Na+ ions into the postsynaptic neurone causes depolarisation, and an action potential on postsynaptic membrane is generated if the threshold is reached.
  • ACh unbinds from the cholinergic receptors and is removed from the synaptic cleft to prevent the response from keep happening.
  • ACh is broken down by enzyme acetylcholinesterase and the products are reabsorbed by the presynaptic neurone, and are used to make more ACh. Basically, ACh is recycled.
49
Q

The effects of chemicals on neuromuscular junctions

A

Some chemicals, like a drug, may block the release of the neurotransmitter or affect the way it bind to the receptors on the postsynaptic membrane. This could prevent an action potential from being passed onto the muscle, so it doesn’t contract.

Chemicals that affect the action of neuromuscular junctions can be fatal if the affect muscles involved in breathing such as diaphragm and intercostal muscles. If they cannot contract, ventilation cannot happen, and the organism will not be able to respire aerobically.

50
Q

What would happen at a neuromuscular junction if the enzyme acetylcholinesterase is inhibited?

A

The drug would stop AChE from breaking down ACh so there would be more ACh in the synaptic cleft and would be there for longer.
This increases the chance of ACh binding to cholinergic receptors on the postsynaptic membrane and increases the chance of depolarisation occuring at the postsynaptic cell.