15. Control and Coordination Flashcards

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1
Q

What is the purpose of communication systems in living organisms?

A

To pass information between different body parts and coordinate activities, or to regulate substances, or to change activity in response to internal/external stimuli.

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2
Q

Outline the structure and function of the nervous system.

A

Made of the CNS and PNS (cranial + spinal nerves, attached to brain + spinal cord).
Information transmitted as nerve impulses, along neurone CSMs, at high speeds, directly to target cells.
Sensory receptors, decision-making centres in the CNS and effectors are coordinated.

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3
Q

Outline the function of each type of neurone.

A
  • Sensory: transmit impulses from receptors -> CNS.
  • Intermediate/relay/connector: Transmit impulses from sensory -> motor neurones.
  • Motor: Transmit impulses from CNS to effectors.
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4
Q

Outline the structure of a motor neurone.

A
  • Cell body: cytoplasm (with rough ER), nucleus, dendrites. Lies within the spinal cord/brain.
  • Axon (very long, mitochondria and organelles).
  • Terminal branches (synaptic knobs have many mitochondria, transmitter substances and vesicles in cytoplasm).
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5
Q

Describe the structure of dendrites.

A

Branch out from thin cytoplasmic processes extending from the cell body. Dendrites are highly branched to provide a high SA for endings of other neurones.

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6
Q

Outline the structure of a sensory neurone.

A

One long axon with the cell body either near the source of the stimuli OR in a swelling of the spinal nerve (called a ganglion).

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7
Q

How is the myelin sheath synthesised?

A

Schwann cells spiral themselves around the axon (many layers of CSM).
This enclosing sheath = myelin sheath, made of many lipids and some proteins. Gaps in the myelin sheath = nodes of Ranvier.

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8
Q

How are axons arranged within nerves?

A

Groups of axons are enclosed by a perineurium, forming a nerve. Inside the nerve are also connective tissue, veins and arteries.

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9
Q

Define ‘reflex arc’.

A

Pathway along which impulses are transmitted from receptor to effector, without involving ‘conscious’ regions of the brain. Some may have no relay neurone, some may be in the brain.

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10
Q

How does a reflex arc work involuntarily?

A

Within the spinal cord, the impulse is passed to other neurones which take the impulse to the brain, occurs simultaneously with impulses travelling along the motor neurone. Effector responds before voluntary response from conscious regions of the brain. This is known as a reflex action.

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11
Q

Outline how nerve impulses are transmitted.

A

Not by a flow of electrons (current) but by brief changes in distribution of electric charge across CSM, from movement of Na+ in and K+ out of the axon (action potentials).

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12
Q

Describe the resting potential of an axon.

A

The inside of the axon has a slightly negative EP compared to the outside (difference = PD, usually -60 to -70 mV).
Produced and maintained by Na+-K+ pumps using ATP.

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13
Q

How is the resting potential of an axon maintained?

A

Along with the pumps, there are also protein channels which stay open. More of these are for K+ than Na+, so some K+ diffuses out faster, but there are large - molecules inside the cell which attract K+.
There is therefore an overall excess of - ions inside.

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14
Q

How can action potentials occur if the CSM is relatively impermeable to Na+?

A

Steep concentration gradient, inside of membrane negatively charged. Double gradient = electrochemical gradient.

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15
Q

What is an action potential?

A

A rapid, fleeting change in PD across the axon membrane (+30mV). Caused by changes in axon CSM permeability to Na+ and K+.

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16
Q

What do voltage-gated channels do?

A

Allow passage of Na+ and K+, depending on PD across membrane.

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17
Q

Outline the stages in an action potential.

A

1) Stimulus
2) Depolarisationm
3) Action potential
4) Repolarisation
5) Refractory period

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18
Q

1) How does depolarisation work?

A

Electric stimulus opens V channels and Na+ enter (down gradient). The PD across the CSM changes - now less negative on the inside.

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19
Q

2) How is the action potential generated, and by which mechanism?

A

At first only a few channels open, then depolarisation opens more - if the PD reaches -60 to -50mV (threshold potential), many more channels open, and the inside reaches a potential of +30mV compared to outside. Positive feedback mechanism.

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20
Q

Define ‘repolarisation’.

A

Removal of positive charge from inside the axon, to return the potential difference to -70mV.

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21
Q

3) How does repolarisation work?

A

After about 1ms, Na+ channels close and K+ channels open. K+ diffuse out, down an electrochemical gradient.

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22
Q

What happens during the absolute refractory period?

A

Another AP cannot be generated, as Na+ channels are closed. The axon is unresponsive to depolarisation.

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23
Q

What happens during the relative refractory period?

A

As Na+ channels activate again, a second AP can be generated but it requires a stronger stimulus, as the PD dips below -70mV. K+ are still flowing out of the axon, so they counteract depolarising stimuli.

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24
Q

How do action potentials help to transmit information along a neurone? (1)

A

The temporary depolarisation of the CSM at the site of an AP sets up local circuits between it and the adjacent resting regions. These local circuits depolarise the neighbouring regions and generate APs in them.

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25
Q

How do action potentials help to transmit information along a neurone? (2)

A

In the body, APs start at one end and only generate APs ahead of themselves, because the previous region is still recovering (Na+ channels shut tight, axon unresponsive).

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26
Q

Outline five characteristics of an action potential.

A

1) Discrete
2) Minimum time between APs at a point
3) Length of refractory period determines frequency of impulses.
4) Do not change in size
5) Do not change in speed

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27
Q

If all APs are the same size, how does the brain differentiate between stimuli?

A

Frequency, number of sensory neurones activated, position of sensory neurone (nature of stimulus).
An unusual stimulus will still send the same message (eg. pressure on eyeballs).

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28
Q

Describe two ways in which neurones are adapted for higher speeds of conduction.

A

Myelinated = much faster - insulates CSM so that Na+ and K+ cannot enter. APs and depolarisation can only occur at the nodes of Ranvier (pumps and channels are concentrated here). Local circuits exist from one node to the next - APs ‘jump’ (saltatory conduction).
Thicker axons = faster due to lower resistance.

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29
Q

Define ‘receptor cell’.

A

Cell that responds to a stimulus by generating an AP. Transducers; convert E in one form to E in an electrical impulse in a neurone.

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30
Q

How is the tongue structured to sense taste?

A

Covered in papillae, which are covered in taste buds, which have 50-100 receptor cells with chemoreceptor proteins. These detect chemicals from liquids / from solids (dissolved in saliva).

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31
Q

How do salt chemoreceptors work?

A
  • Na+ diffuses through selective channels in microvilli, depolarising the membrane. Causes an increase in positive charge inside the cell (receptor potential).
  • Ca2+ V channels open, Ca2+ enter cytoplasm and cause exocytosis of NTs from the basal membrane.
  • AP stimulated in sensory neurone, impulses sent to taste centre in the cerebral cortex.
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32
Q

How do sweet chemoreceptors work?

A

Receptor protein shape change stimulates G protein, enzyme activated, cyclic AMP produced, signalling cascade -> K+ channels closed and membrane depolarised.

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33
Q

What happens when a stimulus is not very strong, in terms of receptors?

A

Only local depolarisation of the receptor cell occurs - sensory neurone isn’t activated to send impulses -> CNS.

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34
Q

What is the ‘all-or-nothing’ law?

A

Neurones either transmit impulses from one end to the other, or they do not.

35
Q

Do threshold levels of receptor potentials stay constant?

A

No - they increase with continued stimulation so that higher stimulus is required before an impulse is sent.

36
Q

Outline how impulses are sent across synapses.

A

1) AP arrives at CSM of presynaptic neurone.
2) Neurotransmitters released into cleft.
3) NTs diffuse across and bind temporarily to receptor molecules on the postsynaptic neurone.
4) All arriving impulses at a given time are responded to via depolarisation - if overall depolarisation is above the threshold then the new AP can be generated.

37
Q

How are impulses transmitted across synapses? (1)

A

In cholinergic synapses, AP occurs, local circuits depolarise the next section - Na+ V channels open and AP is propagated.
Ca2+ channels open in the cytoplasm of presynaptic knob (very steep EC gradient, many in TF).
ACh vesicles fuse with CSM, released into cleft. Each vesicle contains roughly 10000.

38
Q

How are impulses transmitted across synapses? (2)

A

Part of ACh and receptor molecule are complementary - they can temporarily bind and the receptor changes shape.
Na+ channels open, Na+ diffuse into cytoplasm and depolarise CSM. Chemically gated ion channels.

39
Q

How is permanent binding of ACh prevented?

A

Acetylcholinesterase catalyses hydrolysis to acetate and choline.
Choline combined with acetyl CoA -> ACh, moved to presynaptic vesicles.

40
Q

Describe the structure of the ACh receptor.

A

5 protein subunits in a cylinder (transmembrane), two contain ACh receptor sites.
Binding causes shape change, channel opens.
Parts contain negatively charged amino acids which attract Na+.

41
Q

Outline the structure of a neuromuscular junction.

A

Motor neurone forms motor end plate with each muscle fibre - synapse = NM junction.
AP produced in the fibre, causing contraction.

42
Q

Name four roles of synapses. (1)

A

Ensuring one-way transmission (NT released on one side, received on the other.

43
Q

Name four roles of synapses. (2)

A

Integration of impulses - sensory neurones branch to relay neurones, which connect to the soma of motor neurones.
Motors only transmit impulses if the relay neurones’ effect is above the threshold, so those with low frequency don’t reach the brain.

44
Q

Name four roles of synapses. (3)

A

Interconnection of nerve pathways - sensory and relays have axons which branch out to form synapses with many other neurones.
Motors + relays are connected to multiple neurone endings - one neurone can integrate information from different parts.

45
Q

Name four roles of synapses. (4)

A

Memory + learning - frequent, simultaneous info about two stimuli forms new synapses, linking the involved neurones. Info from one source will flow along the other pathway too.

46
Q

Describe the three types of muscle tissue.

A

Striated - muscles attached to skeleton, neurogenic (contracts due to impulses from motors).
Cardiac - striations, uninucleate, short, branched cells, parallel myofibril bundles, myogenic.
Smooth - uninucleate, long, unbranched cells, tubular structures, organs, neurogenic (arteries also BP).

47
Q

Describe the structure of striated muscle.

A

Many muscle fibres, each with contractile proteins arranged into myofibrils.
Multinucleate (syncytium). Sarcolemma, sarcoplasm, SR.
Sarcolemma has deep infoldings (transverse system tubules) close to the SR.
Membranes of SR have many protein pumps (Ca2+ to cisternae).
Many mitochondria, packed tightly between myofibrils.

48
Q

Describe the components of myofibrils.

A

Parallel groups of thick filaments (myosin) between those of thin filaments (actin).
Darker parts of striations = A bands (A+M), lighter = I bands (A).
Lighter parts of A band = H band (M).
A attached to Z line, M attached to M line. Between two Z lines = sarcomere.
Myofibrils are cylindrical, so Z line is a disc (Z disc).

49
Q

Describe the structure of a thick filament.

A

Many myosin molecules (fibrous with globular head). Fibrous part anchors myosin into the filament.
Myosin molecules lie in a bundle with heads facing away from the M line.

50
Q

Describe the structure of a thin filament.

A

Two chains of many globular actin molecules, twisted together.
Fibrous tropomyosin twists around the chains, troponin attached to actin chain at regular intervals.

51
Q

What is the mechanism by which muscles contract?

A

Sliding filament model of muscle contraction - sarcomeres in each myofibril shorten as the Z discs are pulled together.

52
Q

How do muscles contract? (1)

A

REQ: ATP supply and free binding sites.

  • Ca2+ released from SR stores and bind to troponin.
  • Troponin changes shape, this and tropomyosin move to a different position.
  • Myosin binding sites are exposed, thick and thin linked.
53
Q

How do muscles contract? (2)

A
  • Myosin heads tilt, pulling actin towards the centre of the sarcomere.
  • ATP hydrolysed by myosin heads (ATPase). Energy allows release from actin.
  • Heads return to previous positions and bind again - thin filaments have moved due to power stroke, so the binding is now closer to the Z disc.
54
Q

How are muscles stimulated to contract? (1)

A

AP in sarcolemma (same way as synapse). Impulse passes across the sarcolema and T-tubules, towards the centre of the fibre.
Ca2+ channels in SR open, Ca2+ diffuse into sarcoplasm surrounding myofibrils (steep gradient).

55
Q

How are muscles stimulated to contract? (2)

A

No stimulation = no impulses along T-tubules - Ca2+ channels close, pumps move Ca2+ back into SR stores.
Ca2+ leaves troponin, tropomyosin moves to cover it.
No cross-bridges between thick and thin - pulling force lengthens sarcomeres so they are ready to contract.

56
Q

Define ‘muscle antagonist’.

A

A muscle that restores sarcomeres of the other muscle back to their original lengths when it contracts.

57
Q

How is ATP provided for muscle contraction?

A

Some lies in the fibre itself, but is used up quickly.
More is made by aerobic respiration (mitochondria) and lactic fermentation (sarcoplasm).
Creatine phosphate stores in sarcoplasm (Pi removed, combined with ADP).
When demand decreases, ATP from respiration reverses the reaction (‘recharging’). If there is still demand but no ATP to recharge creatine, it is converted to creatinine.

58
Q

Why does nervous communication require a large amount of energy?

A

Maintaining resting potentials (Na+-K+ pumps), protein synthesis (channels + pumps) and maintaining cells involved.

59
Q

What is a hormone?

A

Chemical messenger made in an endocrine gland. Cell signalling molecule.

60
Q

Define ‘gland’.

A

Group of cells that produces and releases one or more substances, via secretion. Endocrine glands have secretory cells that pass products to the blood (ductless).

61
Q

What is the difference between water-soluble hormones and steroid hormones?

A

Steroid hormones are lipid-soluble, so they can diffuse through the CSM and bind to receptors in the cytoplasm/nucleus.

62
Q

Which hormones are involved in coordinating the menstrual cycle?

A

Glycoproteins released by the APG and ovaries.

  • APG releases FSH and LH (ovary activity).
  • During the ovarian cycle, follicles develop and secrete oestrogen. After ovulation, the remains secrete progesterone.
63
Q

Describe the stages of the menstrual cycle (follicular phase).

A
  • Menstruation - APG secretes FSH and LH (conc. increases).
  • Ovaries: one follicle becomes dominant, surrounding cells secrete oestrogen (LH and FSH).
  • Oestrogen has a negative feedback effect - FSH and LH decrease, endometrium grows + thickens, many blood capillaries.
  • Primary follicle develops into a secondary follicle, which develops into an ovarian/Graafian follicle.
64
Q

Describe the stages of the menstrual cycle (ovulation).

A

Oestrogen level at 2-4x its original causes a surge of LH (primarily) and FSH.
- LH causes the dominant follicle to burst and shed its gamete into the oviduct, 14-36h after the surge.

65
Q

Describe the stages of the menstrual cycle (luteal phase).

A
  • Follicle collapses and turns into the corpus luteum, which secretes progesterone and some oestrogen (maintaining endometrium).
  • P inhibits APG from secreting FSH - no more follicles.
  • O and P inhibit release of LH and FSH - less stimulation of corpus luteum.
  • Less O and P therefore secreted, endometrium breaks down and menstruation can occur again.
  • APG released from inhibition, FSH can be secreted again.
66
Q

What are the two methods of birth control?

A
  • Contraception (preventing fertilisation during intercourse).
  • Anti-implantation (IUD, morning-after etc.).
67
Q

Describe the birth control method of ‘combined oral contraceptives’.

A

O and P (usually synthetic), taken for roughly 21 days and stopped during menstruation.

  • LH and FSH secretion inhibited via negative feedback (usually highest when O is low and P just starts).
  • LH and FSH prevented from reaching ovulation-stimulating levels (mimics luteal phase).
68
Q

How else can O and P be administered for birth control?

A
  • Skin patch, injection or inserting an implant under the skin (no menstruation).
  • Pills with only P may allow ovulation - they reduce the ability of the sperm to fertilise the egg, and thicken the cervical mucus.
69
Q

Describe the birth control method of the ‘morning-after pill’.

A

Up to 72h after intercourse, contains a synthetic P-like hormone.
Reduces chance of sperm from reaching + fertilising the egg / by stopping implantation.

70
Q

How do most plant responses work?

A
  • Changing an aspect of growth to respond to gravity, light, water availability, CO2 changes, grazing, infection.
  • Quick changes in turgidity (eg. stomatal closing and opening.
71
Q

How do action potentials work in plants?

A

Depolarisation caused by outflow of Cl-, repolarisation by outflow of K+. No neurones, but their cells can transmit waves of e- activity.
APs travel along CSMs and through plasmodesmata lined by cell membrane (slower but longer-lasting).

72
Q

Give three examples of APs in plants.

A
  • Mimosa (touch = folding leaves).
  • Soya bean leaves (acid similar to acid rain pH = AP).
  • Potato plant leaves (Colorado beetle larvae feeding).
73
Q

How is a Venus flytrap structured to feed itself?

A
  • Leaves divided into two lobes and a midrib.
  • Inside each lobe red, with nectar-secreting glands around the edge.
  • Each lobe has 3 stiff sensory hairs.
  • Outer edges have stiff hairs that interlock.
  • Surface has glands to secrete digestive enzymes.
74
Q

How does the Venus flytrap respond to touch?

A
  • Deflection of sensory hair activates Ca2+ channels at the base.
  • Ca2+ flow in, generate receptor potential.
  • Two touches generates action potential, travels across trap (two touches = E saved).
75
Q

How does the Venus flytrap close?

A

Lobes bulge upward when open (convex), then quickly change (concave) and bend down to close.

  • Not due to water movement but to a release of elastic tension in the cell walls.
  • Ongoing stimulation completely seals trap (more APs force the edges together).
76
Q

How does the Venus flytrap digest its ‘food’?

A

Further deflections stimulate Ca2+ entry into gland cells - exocytosis of digestive enzymes (1 week).
After digestion, cells on upper surface of midrib grow slowly, repoening the leaf and building elastic tension in the cell walls of the midrib cells.

77
Q

Where, and how, do plant hormones function?

A

Move from cell-cell (diffusion/AT) or via xylem/phloem.
Some stay near the site of synthesis (tissues, not glands) and affect nearby cells.
Interact with CSM/cytoplasm/nuclear receptors, initiating a series of chemical/ionic signals that amplify and transmit the initial signal.

78
Q

Outline the roles of two plant growth regulators.

A
  • Auxins (growth, elongation of roots and shoots)

- Gibberellins (seed germination + stem elongation)

79
Q

Outline the role of auxins in elongation growth.

A

Synthesised in meristems of roots and shoots (where mitosis occurs). Transported down the shoot / up the root via AT or phloem.
Three growth stages: division by mitosis, cell elongation by water absorption (auxin), cell differentiation.
Principal auxin = IAA (indole 3-acetic acid).

80
Q

How do auxins stimulate growth?

A
  • Auxin binds with receptor on CSM, stimulating ATPase proton pumps.
  • H+ pumped into cell wall, acidifying it and activating expansins.
  • Non-covalent interactions between cellulose microfibrils and surrounding matrix (eg. hemicelluloses) are disrupted.
  • Microfibrils can slide past each other.
  • Cells absorb water by osmosis, Ψp stretches the wall.
  • K+ channels also open, increasing conc. in cytoplasm so water enters through aquaporins, via osmosis.
81
Q

How do gibberellins stimulate stem elongation?

A

Eg. pea plants - Le (synthesis of last enzyme in pathway producing active gibberellin - GA1) and le (inactive - GA2).

  • GA1 stimulates cell division and stem elongation (increase in internode length).
  • Sub mutation in the gene gives rise to le (alanine -> threonine in primary enzyme structure near active site).
82
Q

Describe the structure of a seed.

A
  • Dormant (little water, metabolically inactive) - allows survival in adverse conditions. Covered by hard, waterproof testa.
  • Seed contains embryo, surrounded by endosperm (contains starch).
  • Outer layer of endosperm has aleurone layer (protein-rich).
83
Q

How is germination caused?

A
  • Absorption of water through the microphyle stimulates embryo to synthesise gibberellins.
  • GA diffuses to the aleurone layer, stimulates cells to synthesise amylase.
  • Amylase hydrolyses starch -> maltose -> glucose - the embryo uses this in respiration to release energy for growth.
84
Q

How do gibberellins stimulate amylase synthesis?

A

Regulating genes involved in the synthesis.
- Barley seeds - increase in mRNA transcription coding for amylase. Achieved by promoting destruction of DELLA proteins which inhibit factors that promote transcription.