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Control and coordination (chapter 15):
 The mammalian nervous system is made up of central nervous system (brain and spinal
cord) and peripheral nervous system (cranial and spinal nerves)
 Communication using nerve action potentials (brief changes in the distribution of electrical
change across the cell surface membrane, caused by rapid movement of Na+ and K+ ions) /
impulses which travel along nerve cells (neurones) at very high speeds to their target cells
 Compare the nervous and endocrine systems as communication systems that co-ordinate
responses to changes in the internal and external environment in mammals:
 Differences:

 Similarities:

 There are three different types of neurones:


 Motor neurone:
 Dendrites lead to cell body containing nucleus, many mitochondria and RER
 Has one long axon with synaptic knobs at the end furthest from cell body
 For some of its length, covered in myelin sheath made by specialised cells: Schwann
cells
 Has small uncovered areas of axon between Schwann cells: nodes of Ranvier
 Sensory neurone:
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 Dendrites at the ends of the long axon with synaptic knobs, with the cell body
containing nucleus, many mitochondria and RER near the source of stimuli or
ganglion
 For some of its length, covered in myelin sheath made by specialised cells: Schwann
cells
 Relay neurone found in the central nervous system

 The functions of sensory, relay and motor neurones in a reflex arc:


 Sensory neurone – receives impulses from receptor
 relay neurone – passes impulses on to motor neurone
 motor neurone – sends impulses to the effector
 The transmission of action potential in a myelinated neurone and its initiation from a
resting potential:
 Initially at a resting potential (p.d. between -60 mV to -70mV), as inside is slightly
more negative than the outside, which is produced and maintained by sodium-
potassium pumps in the cell surface membrane (3 Na+ removed for every 2 K+
brought in across the potential gradient by active transport)
 Na+ channels open and Na+ enters the cell down their electrochemical gradient,
where the p.d. becomes positive (+40 mV) due to depolarisation
 Na+ channels close and K+ channels open, hence K+ moves out of cell down their
concentration gradient, hence p.d., becomes negative due to repolarisation
 Local circuits occur
 Myelin sheath acts as an insulator hence prevents movement of ions, hence action
potentials / depolarisation occurs only at nodes of Ranvier, process called saltatory
conduction (action potential jumps from node to node)
 Process is a one-way transmission due to the refractory period
 If the p.d. generated does not reach the threshold potential (between – 60 mV and
–70 mV), action potential does not occur
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 The length of the refractory period determines the maximum frequency at which impulses
are transmitted along neurones, as the transferred region will still be recovering from the
action potential it just had (sodium ion voltage-gated channels are ‘shut tight’ and cannot
be stimulated to open, however great the stimulus)
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 The difference in strength of stimulus causes the different frequency of action potentials,
where a strong stimulus produces a rapid succession of action potentials, each one
following along the axon just behind its predecessor; a weak stimulus results in fewer
action potentials per second; a strong stimulus stimulate more neurones than a weak
stimulus
 The brain can therefore interpret the frequency of action potentials arriving along the axon
of a sensory neurone, and the number of neurones carrying action potentials, to get
information about the strength of the stimulus being detected. The nature of the stimulus,
whether it is light, heat, touch or so on, is deduced from the position of the sensory
neurone bringing the information. If the neurone is from the retina of the eye, then the
brain will interpret the information as meaning ‘light’
 Sensory receptor cell: a cell that responds and converts a stimulus into an electrical
impulse by initiating an action potential (e.g. chemoreceptor)
 The roles of sensory receptor cells in detecting stimuli and stimulating the transmission of
nerve impulses in sensory neurones (e.g. chemoreceptor cell found in human taste buds):
 Chemicals act as a stimulus
 Each chemoreceptors contain a specific receptor protein which detects a particular
chemical
 Sodium ions diffuse into cell via Microvilli, causing the membrane to depolarise,
which increases the positive charge inside the cell known as receptor potential
 Sufficient stimulation (above the threshold potential (below will only cause a local
depolarisation of the receptor cell)) of Na+, stimulates opening of calcium ion
channels, hence calcium ions enter cell, causing movement of vesicles containing
neurotransmitter which is released exocytosis
 Neurotransmitter stimulates action potential in sensory neurone
 Chemoreceptors are transducers as they convert energy in one form into emergy in
an electrical impulse in a neurone
 All or nothing law where neurones either transmit impulses from one end to
another or they do not
 Chemoreceptor cells found in the papilla of the tongue
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 The gap between two neurones is called synaptic cleft; the parts of the two neurones near
the cleft, plus the cleft itself, make up a synapse
 An action potential occurs at the cell surface membrane of the presynaptic neurone
 Action potential causes the release of molecules of transmitter substance into the cleft
 The molecules of neurotransmitter diffuse across the synaptic clef and bind temporarily on
the postsynaptic neurone
 The postsynaptic neurone responds to all the impulses arriving at any one time by
depolarising; sends impulses if the overall depolarisation is above its threshold
 Synapses that uses acetylcholine as its neurotransmitter is known as cholinergic synapses
 How a cholinergic synapse functions:
 Action potential reaches presynaptic membrane causing depolarisation, and Ca2+
channels to open in the presynaptic membrane
 An influx of Ca2+ ions (facilitated diffused down its electrochemical gradient),
stimulates vesicles containing ACh to move towards the presynaptic membrane and
fuse with it
 ACh released into synaptic cleft by exocytosis, and diffuses across the cleft
 ACh binds to receptor proteins on the postsynaptic membrane; proteins change
shape causing Na+ channels to open
 Na+ facilitated diffuse into postsynaptic neurone causing depolarisation of the
postsynaptic membrane creating an action potential, if the potential difference is
above the threshold for that neurone
 Acetylcholinesterase catalyses the hydrolysis of each ACh molecule into acetate and
choline to prevent permanent depolarisation of the postsynaptic neurone; choline
is taken back into the presynaptic neurone to be combined with acetyl CoA to form
ACh once more and transported into the presynaptic vesicles
 Role of calcium ions in synaptic transmission:
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 Enter the presynaptic neurone, and causes vesicles containing acetylcholine (ACh)
to fuse with the presynaptic membrane, hence releasing ACh into the synaptic cleft
(exocytosis)

 Some insecticides have a similar structure to acetylcholine, hence affects the functioning of
acethycholinesterase by:
 Acting as a competitive inhibitor – complementary to the active site – hence binds
with the active site, this ACh is not broken down

 A: Na+ cannot enter post-synaptic neurone hence no depolarisation / action potential in


the post-synaptic neurone
 B: Ca2+ cannot enter pre-synaptic neurone hence vesicles cannot move towards the pre-
synaptic membrane
 C: ACh cannot be released into synaptic cleft
 D: ACh is not broken down hence continuous depolarisation / action potential, of post-
synaptic neurone
 Ways in which the toxin (acts at cholinergic synapses) in cobra venom may cause muscle
paralysis:
 Binds to receptors on postsynaptic membrane, hence stops ACh from binding,
inhibiting depolarisation, hence no action potentials / Na+ ion channels stay shut
 Stimulates ACh receptors causing continuous depolarisation / opens Na+ ion
channels
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 Stops the release of ACh from presynaptic neurone
 Inhibits acetyl cholinesterase
 The roles of synapses in the nervous system:
 Ensures one-way transmission as vesicles are only found in the presynaptic
neurone, hence ACh will only be released from presynaptic neurone
 Involved in memory and learning, where an increase in the number of synapses
allows more interconnection of nerve pathways for memory, allowing a wider range
of response
 Allows interconnection of nerve pathways
 Striated muscle tissue makes up the many muscles in the body that are attached to the
skeleton; only contracts when it is stimulated to do so by impulses that arrive via motor
neurones; muscle tissue like this is described as being neurogenic, whereas the cardiac
muscle in the heart is myogenic – it contracts and relaxes automatically, with no need for
impulses arriving from neurones

 Multinucleate muscle fibres are called synctium instead of cell; sacrolemma instead of cell
surface membrane; sarcoplasm instead of cytoplasm; sarcoplasmic reticulum (SR) instead
of endoplasmic reticulum; the deep infolding of the cell surface membrane into the interior
of the muscle fibre is called transverse system tubules or T-tubules, which runs close to
the sarcoplasmic reticulum
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 Membranes of the sarcoplasmic reticulum have huge numbers of protein pumps that
transport calcium ions into the cisternae of the SR
 The sarcoplasm contains a large number of mitochondria, packed tightly between the
myofibrils to carry out aerobic respiration, generating the ATP that is required for muscle
contraction
 Each myofibrils are made up of filaments (made from protein), where parallel groups of
thick filaments (made up of myosin) lie between groups of thin ones (made up of actin),
creating the stripes or striations
 The dark parts of the stripes, the A bands, correspond to the thick (myosin – fibrous
protein with a globular head pointing away from the M line) filaments; the lighter parts,
the I bands, are correspond to the thin filaments (2 chains made of many actins twisted
together, consisting of another twisted fibrous protein – tropomyosin – and protein
attached at regular intervals – troponin)
 The darkest parts of the A band are produced by the overlap of thick and thin filaments,
while the lighter area within the A band, known as the H band, represents the parts where
only the thick filaments are present
 The Z line provides an attachment for the actin filaments, while the M line does the same
for the myosin filaments; the part of a myofibril between two Z lines is called a sarcomere

 The sliding filament model of muscular contraction (shortening of I-band):


 When sarcoplasmic reticulum (SR) depolarised
 Calcium ion channels open
 Tropomyosin covers / uncovers the myosin binding sites on actin; when calcium
ions diffuse down a potential gradient through open channels from the SR to bind
to troponin hence changes shape (so tropomyosin and troponin move away),
allowing myosin to bind to actin, forming cross-bridges
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 ATP hydrolysis (ATP → ADP + Pi) causes myosin head (acts as ATPase) to tilt
 ADP and Pi detach and myosin head swings back / returns to previous position
 Actin is moved and power stroke occurs
 New ATP binds
 Myosin head detaches from actin and the cross-bridges break
 No ATP in striated muscle results to:
 No pumping of calcium ions into SR
 No detachment of myosin heads:
 Hence no hydrolysis of ATP
 Hence no cross bridge formation
 Hence no power stroke / pulling of actin
 Hence no recovery stroke / myosin head does not return to original position ;
 Stimulating contraction in striated muscle:
 Action potential arrives resulting to the opening of Ca2+ channels in the presynaptic
membrane, hence Ca2+ enters into the presynaptic neurone
 Releasing vesicles containing acetylcholine to move towards and fuse to the
presynaptic membrane
 Acetylcholine released by exocytosis and diffuses across the cleft; binds to
receptors on the sacrolemma
 Na+ channels open, hence Na + ions enter to depolarise the sacrolemma and
generate action potential
 Impulses then pass along the T-tubules towards the centre of the muscle fibre
 Causing Ca2+ ions to bind with the troponin molecules
 When there is no longer stimulation from the motor neurone, no impulses
conducted along the T-tubules, hence the Ca2+ channels close and calcium pumps
move Ca2+ back into stores in the SR; as Ca2+ leaves the binding sites on troponin,
tropomyosin moves back to cover the myosin-binding sites, hence no more cross-
bridges
 Muscles also have another source of ATO produced from creatine phosphate, keeping
their stores in their sarcoplasm as their immediate source of energy

 Once energy demand has slowed down, ATP molecules produced by respiration can
be used to ‘recharge’ the creatine

 Whereas if energy is still being demanded and there is no ATP spare to regenerate
creatine phosphate, the creatine is converted to creatinine and excreted in urine
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 The menstrual cycle – approximately 28 days:
 Middle of this cycle, the female gamete is released in the oviduct, and if fertilisation
occurs, the embryo develops in the uterus lining

 Coordinated by glycoprotein hormones released by the anterior pituitary gland –


follicle stimulating hormone (FSH) and luteinising hormone (LH) which controls
the activity of the ovaries – and ovaries (developing follicles secrete oestrogen,
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whereas when the female gamete is released from the ovary at ovulation, the
remains of the follicle (corpus luteum) secretes progesterone

 FSH/LH, released by anterior pituitary during menstruation resulting to the


development of Graafian follicle
 In the ovary, due to the presence of LH and FSH, follicle cells secrete oestrogen
 Oestrogen concentration rises for the first 12 days stimulating the endometrium to
grow, thicken and develop numerous blood capillaries
 The presence of oestrogen in the blood has a negative feedback effect on the
production of LH and FSH, hence their concentrations decrease
 Once the oestrogen levels have reached a high level (around day 14), it stimulates a
surge in the secretion of LH and, to a lesser extent, of FSH; causes follicle to burst
and shed its gamete into the oviduct (ovulation)
 The follicle then collapses and form the corpus luteum, which secretes
progesterone (maintains the lining of the uterus (endometrium) and inhibits the
anterior pituitary from secreting FSH so no more follicle develop)
 If no fertilisation, secretion of FSH/LH inhibited – as high levels of oestrogen and
progesterone in the second half inhibit the secretion of FSH and LH – corpus luteum
degenerates and progesterone concentration falls, resulting to the breakdown of
the endometrium (menstruation)
 Decrease also causes FSH to be secreted as anterior pituitary gland is no longer
inhibited
 LH receptors located in the follicle cells, while FSH receptors located in the corpus luteal
cells
 Female mice without FSH receptors were sterile; they were found to have normal primary
and secondary follicles in their ovaries, but no Graafian (ovarian) follicles or corpora lutea.
Explain these observations:
 Early follicle development is not dependent on FSH
 With no FSH / no FSH receptors, follicle development stops
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 With no FSH / no FSH receptors, Graafian / ovarian, follicle does not develop
 With no FSH / no FSH receptors, there is no ovulation
 No corpus luteum because these form from Graafian follicle / after ovulation
 Outline how the oestrogen/progesterone/combined contraceptive pill works to prevent
pregnancy:
 Synthetic hormones used as they do not get broken down quickly hence act for
longer
 Oestrogen / progesterone concentrations remain high, hence inhibits secretion of
FSH and LH from anterior pituitary gland, where the presence of oestrogen in the
blood has a negative feedback effect on the production of LH and FSH, hence their
concentrations decrease, so Graafian follicle does not develop, thus inhibits
ovulation
 Thickens cervical mucus to prevent sperm from fertilising the egg
 Thin endometrium prevent embryo implantation on endometrium
 It is taken daily for 21 days; stops for 7 days to allow menstruation
 Discuss the biological, ethical and social implications of using this contraceptive pill:
 Biological – negative
 Rise in blood pressure
 Nausea and headaches
 Increased risk of breast cancer
 Increase in STDs
 Biological – positive
 Regular menstruation
 Reduced risk of developing, ovarian cancer
 Reduced risk of uterine infections
 Social / ethical – negative
 Sexual freedom has led to more marriage breakdowns, hence more single
parent families
 Religious/cultural, objection
 Social / ethical – positive
 Reduction in unwanted pregnancies and abortions
 Women have control over their fertility
 Acts as a population control
 Venus fly trap:
 Each trap consists of a pair of modified leaves joined by a midrib of hinge cells
 The modified leaves have touch-sensitive hairs; if two hairs are touched within 20
seconds, or the same hair is touched twice in rapid succession, the trap closes
 The surface of the lobes has many glands that secrete enzymes for the digestion of
trapped insects
 The touch of insects on the sensory hairs activates calcium ion channels in cells at
the base of the hair to open, causing an influx in Ca2+ to generate action potential
 Auxin increase triggered in hinge cells
 H+ ions pumped into the cell walls and calcium pectate ‘glue’ in cell wall dissolved
 Ca2+ ions enter hinge cell
 Water follows by osmosis down its water potential gradient
 Hinge cells expand
 Trap lobes, flip from convex to concave (change in elastic tension)
 Two types of plant growth regulators (hormones):
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 Auxins: influence many aspects of growth including elongation growth which
determines the overall length of roots and shoots; synthesised in the growing tips
(meristems) of shoots and roots, where cells are dividing; actively transported from
cell to cell
 Gibberellins: involved in seed germination and controlling stem elongation
 Role of auxin in cell elongation in plants:
 Acid-growth hypothesis
 Auxin stimulates proton pumps in the cell surface membrane
 H+ pumped into the cell wall by active transport, hence the pH of cell wall
decreases, so pH-dependent enzymes activated (expansins) and loosen the bonds
between cellulose microfibrils
 Cell wall ‘loosens’ / becomes more elastic / able to stretch, hence more water
enters the cell and turgor pressure increases, resulting to the expansion of the cell
wall

 The role of gibberellin in the germination of wheat or barley:


 Seed is initially dormant
 When the seed absorbs water, embryo produces gibberellin
 Gibberellin diffuses onto the aleurone layer and stimulate the cells to synthesise
amylase, by the affecting the gene transcription of mRNA for amylase (breakdown
of DELLA proteins which inhibit germination)
 Amylase hydrolyses starch in the endosperm to soluble maltose molecules, which
are converted to glucose and transported to the embryo for respiration (ATP for
growth)
 Amylase hydrolyses starch in the endosperm to soluble maltose molecules, which
are converted to glucose and transported to the embryo for respiration (ATP for
growth)
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 The height of some plants is partly controlled by their genes, e.g. tallness in pea plants is
affected by a gene with two alleles; if the dominant allele, Le, is present, the plants can
grow tall, but plants homozygous for the recessive allele, le, always remain short
 The dominant allele of this gene regulates the synthesis of the last enzyme in a
pathway that produces an active form of gibberellin, GA1
 Active gibberellin stimulates cell division and cell elongation in the stem, so causing
the plant to grow tall
 A substitution mutation in this gene gives rise to a change from alanine to
threonine in the primary structure of the enzyme near its active site, producing a
non-functional enzyme; this mutation has given rise to the recessive allele, le;
hence homozygous plants, lele, are genetically dwarf as they do not have the active
form of gibberellin

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