SNAB Topic 8 works out from a single action potential to the whole brain. You will cover the resting and action potential, synapses, vision, plant responses, brain imaging, habituation, the effects of drugs, and the genetics and ethics of the Human Genome Project.
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Schwann cells wrap repeatedly around the axon, forming the myelin sheath. Myelin is a lipid, so it is an electrical insulator: the membrane can only depolarise at the gaps, the nodes of Ranvier. The impulse therefore jumps from node to node — saltatory conduction — which is far faster than the continuous conduction of an unmyelinated axon. Conduction is also faster in a wider axon and at a higher temperature.
Reflex arc: receptor → sensory neurone → relay neurone (in the spinal cord) → motor neurone → effector. It is fast (few synapses) and involuntary — the brain is informed afterwards, which is why you have already pulled your hand back before you feel the pain.
The pupil reflex (8.2): in bright light the circular muscles of the iris contract and the radial muscles relax, constricting the pupil (an antagonistic pair, controlled by the autonomic nervous system). In dim light the radial muscles contract and the pupil dilates.
Resting potential (about −70 mV): the sodium–potassium pump actively transports 3 Na⁺ out for every 2 K⁺ in, using ATP. The membrane is far more permeable to K⁺ than to Na⁺ (potassium leak channels are open), so K⁺ diffuses back out. The result is a net excess of positive charge outside — the inside is negative. The axon is polarised.
Action potential:
All-or-nothing: either the threshold is reached and a full-sized action potential fires, or nothing happens. A stronger stimulus does not make a bigger impulse — it makes them more frequent (and recruits more neurones). During the refractory period the Na⁺ channels cannot reopen, which ensures the impulse travels in one direction only and sets the maximum firing frequency.
Tap an event, then tap where it belongs.
Transmission across a cholinergic synapse:
Synapses ensure unidirectional transmission (only the pre-synaptic neurone has vesicles), and they allow summation (many weak stimuli combining), divergence and convergence.
Drugs (8.15): an agonist mimics the neurotransmitter (nicotine at acetylcholine receptors); an antagonist blocks the receptor; some drugs inhibit reuptake (cocaine blocks the reuptake of dopamine; SSRIs block the reuptake of serotonin, so it stays in the cleft for longer); others inhibit the breakdown enzyme (organophosphates inhibit acetylcholinesterase).
A receptor is a transducer: it converts one form of energy (here, light) into a nerve impulse. Light bleaches the pigment in a photoreceptor, and the resulting change in membrane permeability generates a generator potential. If it reaches the threshold, the bipolar neurone fires.
Phototropism: IAA (indoleacetic acid, an auxin) is made at the shoot tip and transported down. It is redistributed away from the light to the shaded side, where it causes cell elongation (by loosening the cell wall). The shaded side grows faster, so the shoot bends towards the light — a positive phototropic response. In the root, the same auxin inhibits elongation, so roots show positive gravitropism.
Phytochrome: a light-sensitive pigment that exists in two interconvertible forms.
Pfr is the active form. In daylight, Pfr accumulates. It promotes germination of light-sensitive seeds and controls flowering: in long-day plants Pfr promotes flowering; in short-day plants Pfr inhibits it — which is why what actually matters is the length of the uninterrupted dark period, during which Pfr slowly reverts to Pr.
Nervous vs hormonal coordination (8.7): nervous — electrical impulses along neurones, very fast, very localised (a specific effector), short-lived effect. Hormonal — chemical messengers in the blood, slower, widespread (any cell with the right receptor), longer-lasting.
Tap what it shows on the left, then the technique.
The critical period (8.10): a window early in development during which the nervous system must receive the right stimulation to develop normally. Hubel and Wiesel showed that if one eye of a kitten is deprived of light during this period, the neural connections serving that eye are lost and it remains functionally blind — even after the eye is reopened. In humans, an untreated squint or cataract in infancy can cause permanent amblyopia. The visual cortex shows plasticity: the connections that are used are strengthened, and those that are not are pruned.
Animal models (8.11–8.12): they made the discovery possible, but they raise real ethical problems. Arguments for: without them we would not understand visual development or have effective treatments; the animals’ welfare is regulated by law; the potential benefit is enormous. Arguments against: the animals cannot consent and suffer real harm; results in one species may not transfer to humans; and alternatives (cell culture, computer modelling, human imaging) increasingly exist.
Habituation (8.13): the simplest form of learning — a decreasing response to a repeated, harmless stimulus. Repeated stimulation means less Ca²⁺ enters the pre-synaptic neurone, so less neurotransmitter is released, the post-synaptic threshold is not reached, and the response fades. It is adaptive: it stops an animal wasting energy responding to a stimulus that carries no threat.
Parkinson’s disease — the dopamine-secreting neurones of the substantia nigra die, so dopamine levels fall. Because dopamine is needed for the control of movement, the result is tremor, muscle rigidity and slow movement (bradykinesia). Treatments raise dopamine activity: L-dopa (a precursor that, unlike dopamine, can cross the blood–brain barrier and is then converted to dopamine), dopamine agonists, and MAO-B inhibitors which slow the breakdown of dopamine.
Depression is associated with low levels of serotonin. SSRIs (selective serotonin reuptake inhibitors) block the reuptake transporter, so serotonin stays in the synaptic cleft for longer and is more likely to bind post-synaptic receptors.
Note the careful language: associated with. A low serotonin level and depression correlate — establishing which causes which is much harder, and it is exactly the kind of point SNAB expects you to make.
Genome sequencing (8.16): the outcomes are used to identify genes associated with disease, to develop new drugs, and to move towards personalised medicine — matching a drug to a patient’s genotype. Ethical questions: who owns the data, could insurers or employers use it, and how do you counsel someone about a risk rather than a certainty?
Drugs from GM organisms (8.17–8.18): a human gene (e.g. for insulin or a clotting factor) is cut out with a restriction enzyme, joined into a plasmid vector using DNA ligase, and taken up by a bacterium, which then makes the human protein. GM plants and animals (“pharming”) can make more complex proteins in milk or leaves. Benefits: pure, unlimited, no risk of disease transmission from donated human tissue, and no ethical objection from those who reject animal-derived insulin. Risks and objections: escape of the transgene into wild populations, unknown long-term effects, the welfare of GM animals, and the concentration of patents in a few companies.
Nature and nurture (8.19): the classic methods are twin studies — comparing concordance in monozygotic (genetically identical) and dizygotic twins, and especially MZ twins reared apart — and adoption studies, comparing a child with their biological and adoptive parents. A higher MZ than DZ concordance implies a genetic contribution; that concordance is never 100 % implies an environmental contribution. Almost every trait is both.
Neurones: sensory (receptor → CNS), relay (within CNS), motor (CNS → effector). Schwann cells form the myelin sheath; the gaps are the nodes of Ranvier, which allow saltatory conduction.
Resting potential (−70 mV): the Na⁺/K⁺ pump moves 3 Na⁺ out for every 2 K⁺ in (active transport), and the membrane is far more permeable to K⁺ than Na⁺.
Action potential: stimulus → threshold → voltage-gated Na⁺ channels open → depolarisation to about +40 mV → Na⁺ channels close and K⁺ channels open → repolarisation → hyperpolarisation → resting potential restored. All-or-nothing; intensity is coded by frequency.
Synapse: Ca²⁺ enters → vesicles fuse → neurotransmitter diffuses across → binds receptors on the post-synaptic membrane → Na⁺ channels open. Synapses ensure one-way transmission.
Eye: rods (rhodopsin, high sensitivity, many rods to one bipolar neurone → high sensitivity but low acuity, monochrome); cones (iodopsin, one-to-one → high acuity, colour, need bright light).
Plants: IAA (auxin) causes cell elongation on the shaded side (phototropism); phytochrome Pr ⇌ Pfr controls flowering and germination.
Brain: cerebral hemispheres, hypothalamus, cerebellum, medulla oblongata. Imaged with CT/MRI (structure), fMRI and PET (function/activity).
Nature and nurture: studied using twin (MZ vs DZ concordance) and adoption studies; almost every trait is both.
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