Topic 8 - Coordination, Response and Gene Technology
- Syllabus
- 2021
- Topic
- —
- Level
- A2
Every neurone has a cell body with nucleus, processes that receive input and an axon that conducts action potentials to terminals. The relative positions and lengths of these parts distinguish sensory, relay and motor pathways.
| Neurone | Typical structure | Direction and function |
|---|---|---|
| Sensory | Long dendron from receptor to cell body; short axon to CNS | Carries impulses from receptors into CNS |
| Relay | Cell body with many short dendrites and a short axon, entirely within CNS | Connects and integrates sensory and motor pathways |
| Motor | Cell body and dendrites in CNS; long axon to terminals | Carries impulses to a muscle or gland effector |
Schwann cells wrap repeatedly around peripheral axons to form a lipid-rich myelin sheath. Gaps between cells are nodes of Ranvier, where ion channels allow action potentials to be regenerated. Myelin insulates internodes and enables faster saltatory conduction.
A dendron conducts toward the cell body and an axon away from it. A nerve is a bundle of many neuronal axons, while one Schwann cell myelinates only a short axon segment.
The basic pathway is stimulus → receptor → sensory neurone → CNS → motor neurone → effector. The CNS integrates information and the effector produces a response through muscle contraction or gland secretion.
Bright light activates retinal receptors; impulses reach the CNS and motor neurones stimulate circular iris muscles so the pupil constricts. In low light, radial muscles contract and the pupil dilates.
Antagonistic effectors allow opposite outcomes, while a rapid neural pathway limits exposure to harmful conditions.
A receptor detects a change but does not itself perform the response. Keep sensory input, CNS coordination and effector action distinct.
A spinal reflex is an automatic, rapid response organised through the spinal cord. A receptor transduces the stimulus; a sensory neurone carries an action potential into the cord; one or more synapses in grey matter relay it to a motor neurone; the motor neurone activates an effector.
The spinal cord has central butterfly-shaped grey matter containing neurone cell bodies, dendrites and many synapses. Surrounding white matter contains bundles of myelinated axons running up and down the cord. Sensory axons enter through a dorsal route and motor axons leave through a ventral route.
In a withdrawal reflex, a pain receptor activates a sensory neurone, a relay neurone excites the flexor motor neurone and an inhibitory pathway relaxes the antagonist extensor. Information also ascends through white matter so pain can be perceived after the response begins.
A reflex does not mean the brain receives no information. The immediate integration occurs in spinal grey matter; white matter mainly provides longer ascending and descending pathways.
When membrane depolarisation reaches threshold, voltage-gated sodium channels open and sodium ions enter. Potassium ions then leave to repolarise the membrane; the signal propagates as neighbouring sections reach threshold.
The all-or-nothing action potential is regenerated along the axon, so its amplitude does not fade with distance. Refractory periods help maintain one-way transmission.
A stronger stimulus is represented by more frequent action potentials, not a larger action potential, once threshold has been crossed.
Threshold is not a graded “bigger signal”, and ion movement is not the same as the whole impulse physically travelling as one sodium wave.
In a myelinated axon, the sheath insulates the membrane between nodes of Ranvier. Depolarisation is regenerated at the nodes, so the impulse appears to jump along the axon by saltatory conduction.
The insulation reduces ion leakage and increases conduction speed compared with a non-myelinated axon, where the membrane is activated continuously.
Damage to myelin can slow or disrupt signalling even when the axon and its cell body remain present, because the normal node-to-node pattern is lost.
Saltatory conduction does not mean the impulse skips the cytoplasm entirely, and a nerve is a bundle of axons rather than one myelinated cell.
An arriving action potential opens presynaptic voltage-gated Ca2+ channels. Calcium entry triggers acetylcholine-containing vesicles to fuse with the membrane. Acetylcholine diffuses across the cleft, binds complementary postsynaptic receptors and opens ion channels; sufficient depolarisation triggers a new action potential. Acetylcholinesterase hydrolyses acetylcholine so stimulation is brief.
Vesicles and release machinery are presynaptic, while receptors are postsynaptic, making chemical transmission one-way. Synaptic delay, summation and inhibition allow integration rather than simple electrical continuity.
| Light condition | Autonomic output | Iris-muscle response | Pupil |
|---|---|---|---|
| Bright | Parasympathetic pathway favoured | Circular muscles contract; radial muscles relax | Constricts, limiting light entry |
| Dim | Sympathetic pathway favoured | Radial muscles contract; circular muscles relax | Dilates, increasing light entry |
Circular and radial iris muscles are antagonistic; they do not both contract to produce one change. Neurotransmitter crosses chemically, not as an electrical impulse through the cleft.
Predict a drug effect by locating its target—axon channel, transmitter synthesis/release, receptor, breakdown or reuptake—and then tracing whether postsynaptic depolarisation and action-potential frequency rise or fall.
| Drug/toxin | Neural target and action | Main consequence |
|---|---|---|
| Nicotine | Agonist at nicotinic acetylcholine receptors; opens their cation channels | Stimulates postsynaptic neurones and reward pathways; repeated exposure can alter receptor responses |
| Lidocaine | Blocks voltage-gated Na+ channels in sensory axons | Prevents action-potential propagation, producing local anaesthesia |
| Cobra venom alpha toxin | Binds nicotinic acetylcholine receptors at neuromuscular junctions without activating them | Blocks muscle stimulation and can cause paralysis |
| L-DOPA | Crosses blood-brain barrier and is converted to dopamine | Partly restores dopaminergic signalling in Parkinson's disease |
| MDMA | Promotes serotonin release and reduces its reuptake | Prolongs serotonergic stimulation; later transmitter disturbance contributes to adverse effects |
Agonists activate a receptor; antagonists block it. A treatment that improves signalling does not replace lost neurones or prove that one transmitter alone explains a disorder.
In darkness, rhodopsin is intact and cGMP-gated cation channels remain open. Sodium and other cations enter the rod outer segment, keeping the cell relatively depolarised and causing continuous neurotransmitter release onto bipolar cells.
A photon absorbed by rhodopsin changes retinal and separates/activates the opsin component. The signalling cascade lowers cGMP, so cation channels close. Sodium entry falls while potassium loss continues, hyperpolarising the rod and reducing neurotransmitter release.
The change in transmitter alters bipolar-cell activity and then ganglion-cell firing. Ganglion-cell axons form the optic nerve, where information is carried as action potentials; the rod itself signals mainly by graded membrane-potential change.
Many rods converge onto shared pathways, giving high sensitivity in dim light but lower spatial resolution and no colour discrimination compared with cones.
Light does not depolarise a rod: it closes cation channels and hyperpolarises it. Rhodopsin contains opsin plus retinal; action potentials are formed in downstream optic neurones, not normally in the rod cell.
Habituation occurs when repeated harmless stimulation produces a smaller response. The animal saves energy because fewer calcium ions enter the presynaptic neurone, less neurotransmitter is released and the postsynaptic cell is less likely to reach threshold.
A snail may take less time to re-emerge after repeated gentle touches. If the sound or touch becomes stronger, the response can return because the stimulus is no longer identical.
The change is in synaptic transmission, not a loss of all sensory ability. The animal can still respond when the stimulus becomes relevant.
Habituation is not fatigue, permanent damage or forgetting every similar stimulus. Control stimulus intensity and use a consistent endpoint when measuring it.
The central nervous system (CNS) is the brain and spinal cord; the peripheral nervous system (PNS) carries information between the CNS and receptors or effectors. Sensory and motor pathways connect the two.
This division separates integration from transmission. A receptor detects a stimulus, the CNS coordinates a response, and motor neurones carry the output to muscles or glands.
A skin receptor sends an impulse through a sensory neurone in the PNS to the spinal cord; a motor pathway then activates an effector.
The PNS is not only voluntary movement, and the CNS is not simply a cable. Identify the direction and function of each pathway.
Plants coordinate responses with receptors and chemical signals that alter gene transcription and cell behaviour. Phytochrome detects red/far-red light history, while auxin (IAA) and gibberellins act as growth regulators in responsive tissues.
| Signal | Perception and transcriptional effect | Resulting response |
|---|---|---|
| Phytochrome | Red light converts Pr to active Pfr; far-red reverses it. Pfr influences transcription of light-responsive genes | Germination and flowering respond to wavelength and night length |
| Auxin (IAA) | Auxin-receptor signalling removes transcriptional repressors, allowing auxin-response genes to be expressed | Cell elongation; unequal auxin in shoots produces phototropic curvature |
| Gibberellin | Receptor signalling removes repressors of gibberellin-responsive transcription | Stem growth, flowering in some plants, and amylase synthesis during cereal germination |
In a shoot lit from one side, more auxin action on the shaded side promotes greater elongation, bending the shoot toward light. In a germinating cereal, embryo gibberellin reaches aleurone cells and induces transcription of amylase genes, mobilising endosperm starch.
Pr and Pfr are two forms of a photoreceptor, not hormones. A response requires a competent target tissue: hormone presence alone does not make every cell elongate or transcribe the same genes.
Amylase secreted by germinating cereal tissue hydrolyses starch in agar, leaving a clear region after iodine is added. A controlled gibberellin comparison can locate which grain tissue responds and show enzyme production indirectly.
Independent variables may be tissue type and gibberellin treatment. Control grain variety/age, portion size, solution volume/concentration, agar depth, incubation time and temperature. A known amylase positive control can confirm that the starch-iodine detection works.
Iodine detects remaining starch, not amylase directly. A clear zone supports starch hydrolysis only after sterile water, tissue-size and incubation controls exclude alternative explanations.
Nervous control uses rapid electrical impulses and targeted neurotransmitter release; hormonal control uses chemicals carried in blood, usually with slower onset and longer-lasting, broader effects. Both use receptors, coordination centres and effectors.
A reflex can move a hand away quickly, while adrenaline or thyroxine changes metabolism across several tissues. The best system depends on speed, duration and distribution.
The systems can interact: neural signals can trigger hormone release, and hormones can alter the sensitivity or activity of nervous tissues.
Hormones do not always act slowly and nerves do not always produce a brief response. Compare route, target, timing and persistence rather than memorising a single slogan.
The named brain regions are anatomically connected, but each has characteristic locations and major functions that can be recognised in a side view or section.
| Region | Location | Main functions |
|---|---|---|
| Cerebral hemispheres | Largest upper/outer forebrain, with folded cortex | Conscious sensation, voluntary movement, language, learning, memory and higher cognition |
| Hypothalamus | Small forebrain region below thalamic area and above pituitary | Homeostasis, including temperature and osmoregulation; autonomic and endocrine coordination |
| Pituitary gland | Small gland hanging below hypothalamus by a stalk | Releases hormones controlling other endocrine glands and body functions |
| Cerebellum | Folded region at rear, beneath posterior cerebrum | Coordinates timing and precision of movement, posture and balance |
| Medulla oblongata | Lowest brainstem, continuous with spinal cord | Autonomic control including ventilation, heart rate and blood-vessel responses |
A specialised region contributes to a function but rarely acts alone; distributed pathways connect sensory, motor, cognitive and endocrine responses. Do not confuse the posterior cerebellum with the medulla at the base of the brainstem.
Select imaging by whether the clinical question concerns soft-tissue anatomy, rapid structural assessment or a map of activity. Resolution, time, radiation exposure and what the signal represents all limit interpretation.
| Method | Signal and output | Main brain use | Key limitation |
|---|---|---|---|
| MRI | Strong magnetic field and radio waves generate detailed hydrogen-based soft-tissue images | Tumours, lesions and fine anatomy | Slow; unsuitable with some metal implants; no direct activity measure |
| fMRI | MRI detects blood-oxygen-level-dependent changes during tasks | Maps activity-associated changes in brain function | Indirect, delayed blood-flow proxy; motion sensitive |
| PET | Injected positron-emitting tracer, often linked to a metabolic substrate, reveals regional uptake | Metabolism, transmitter systems and functional pathology | Ionising radiation and relatively limited temporal/spatial resolution |
| CT | Multiple X-ray projections reconstructed as slices | Rapid detection of bleeding, fracture and gross structural change | Ionising radiation; less soft-tissue detail than MRI |
Compare a patient with reference data or the same person across conditions. Increased fMRI or PET signal supports involvement or altered metabolism, not that one region alone causes the behaviour. Diagnosis combines imaging with clinical evidence.
MRI and CT are primarily structural, while fMRI and PET provide functional proxies. A coloured activity map is processed measurement data, not a direct picture of thoughts or neurone firing.
Some disorders are associated with altered neurotransmitter levels or signalling. Parkinson’s involves reduced dopamine from lost neurones; antidepressant drugs can increase serotonin or noradrenaline signalling.
A drug may mimic a transmitter, supply a precursor, block breakdown or inhibit reuptake. These mechanisms change synaptic transmission, but symptoms usually involve networks and multiple contributing factors.
L-dopa is converted into dopamine in the brain, while an SSRI reduces serotonin reuptake so more remains in the synaptic cleft.
“Low neurotransmitter causes the disorder” is stronger than the evidence usually supports. Distinguish an association, a treatment mechanism and a complete explanation.
Drug production requires a coding sequence, suitable regulatory DNA, a vector and a host able to make and process the product. Recombinant cells are selected, grown under controlled conditions, and the therapeutic molecule is extracted, purified and tested.
| GM host | Production route | Strength and constraint |
|---|---|---|
| Microorganism | Recombinant bacteria or yeast cultured in fermenters; product recovered from cells or medium | Rapid, scalable growth; bacteria may not perform human protein modifications |
| Plant | Transformed plants or plant cells express product in tissue or culture | Scalable biomass and low animal-pathogen risk; variable expression and containment of pollen/seed matter |
| Animal | Transgene directs a therapeutic protein into milk, eggs or another recoverable secretion | Mammalian protein processing; slower, costly and raises welfare issues |
Recombinant bacteria can produce human insulin; a suitable promoter drives expression, fermenter conditions are controlled, and insulin is purified rather than administering the organism itself.
Insertion does not guarantee correct expression, folding or safe dosage. The final drug requires identity, purity, activity and contamination testing regardless of host.
Recombinant DNA is formed when DNA from different sources is joined. A restriction enzyme cuts the desired gene and vector, complementary ends pair, and DNA ligase seals the sugar-phosphate backbone.
PCR can amplify the target before insertion, while a plasmid provides replication or expression signals in the host. The construct must be introduced into cells and selected or screened.
A gene coding for insulin can be joined to a bacterial plasmid; the plasmid is then transferred into bacteria where the gene may be expressed.
Cutting DNA is not the same as expressing it. A recombinant construct needs a compatible host, promoter and verification before useful protein is produced.
After recombinant DNA is assembled in a plasmid or other vector, it must cross a host-cell membrane or be delivered into a nucleus. The method depends on the cell type; selection confirms uptake, while separate tests confirm integration and expression.
| Host/cell | Example insertion method | Principle |
|---|---|---|
| Bacterium | Heat shock or electroporation | Makes the membrane temporarily permeable to plasmids |
| Plant cell | Gene gun or disarmed bacterial vector | DNA-coated particles enter cells, or a vector transfers DNA; transformed cells can be selected and regenerated |
| Animal cell/embryo | Microinjection, liposome, electroporation or engineered viral vector | DNA is physically delivered or carried across the membrane |
Use a selectable or screenable marker to identify candidate cells, then PCR or another DNA test to verify the construct. Measure RNA or protein to show expression, because vector entry and marker survival alone do not prove a functional therapeutic product.
Transformation means DNA uptake, not guaranteed stable integration or expression. Antibiotic-marker growth identifies candidates but does not show the target protein is correctly made.
A microarray uses labelled nucleic acids from samples to measure which genes are expressed relative to a reference. Complementary binding at spots produces a pattern that can be compared between tissues or conditions.
The result is a relative expression profile, not a direct measurement of every protein or a guaranteed cause. Controls, normalisation and probe specificity determine how confidently differences can be interpreted.
A gene spot with stronger signal in diseased tissue suggests higher transcript abundance, but follow-up experiments are needed to test whether the gene drives the phenotype.
A microarray signal is not automatically protein activity, and a difference in expression is not proof of causation.
Bioinformatics uses databases and computational tools to compare DNA, RNA or protein sequences, predict relationships and identify patterns. The output depends on the input sequence, reference database and comparison method.
Check alignment quality, sequence length, conserved regions and the scoring or statistical assumptions before interpreting a match.
A high sequence similarity can support common ancestry or a shared function, while a low-quality or partial sequence may produce a misleading result.
A database hit is not proof of function or causation. Distinguish similarity, homology, prediction and experimental confirmation.
Genetic modification can add a useful characteristic, such as producing a medicine or resisting a pest. Its value depends on effectiveness, containment, ecological effects, ownership, welfare and who receives the benefit.
Benefits may include reliable therapeutic protein production or reduced losses; risks include unintended gene flow, resistance, ecological disruption and ethical objections to animal or food applications.
A GM microorganism making insulin is contained and purified, whereas a GM crop releasing a trait into wild relatives raises a different monitoring problem.
“GM” is not automatically safe or harmful. Judge the specific organism, gene, environment and evidence rather than using a blanket claim.