The Brain

The cerebrum (cerebral hemispheres) is responsible for the higher functions — receiving sensory information, initiating voluntary (conscious) movement, and processes such as learning, reasoning, memory and language.

The cerebellum controls balance, posture and the coordination of muscular movement, making movements smooth and precise.

The medulla oblongata controls non-conscious (autonomic) actions, in particular the rate of the heartbeat and of breathing.

The hypothalamus is the main homeostatic control centre, regulating body temperature and water balance, and it controls the pituitary gland.

A structural scan shows the physical anatomy of the brain — its shape and any abnormalities such as a tumour or area of damaged tissue — but does not show activity. Examples are CT (which uses X-rays) and MRI (which uses magnetic fields).

A functional scan shows which regions of the brain are active, usually while the person is doing a task, by detecting blood flow or metabolism rather than structure. Examples are fMRI (which detects changes in blood oxygenation) and PET (which detects uptake of a radioactive tracer).

A critical (sensitive) period is a particular window of time, usually early in life, during which a part of the brain must receive the appropriate stimulation from the environment in order to develop normally.

If the correct stimulation is received during this window, the relevant connections develop and are strengthened.

If the stimulation is missing during the critical period, the connections fail to develop properly and normal function may never be achieved, even if the stimulation is provided later. This is why early experience is so important for normal brain development.

The hypothalamus is the main homeostatic control centre of the brain. It monitors and regulates conditions such as body temperature, water balance (osmoregulation) and hunger and thirst, keeping the internal environment within narrow limits.

To do this it receives nervous information and responds partly by producing hormones of its own and partly by controlling the pituitary gland, which lies just below it.

The pituitary gland is an endocrine gland — often called the "master gland" — that secretes hormones into the blood. Under the control of the hypothalamus, these hormones regulate processes such as growth and the activity of other endocrine glands.

In this way the hypothalamus links the nervous system (which it monitors using fast electrical signalling) to the endocrine system (slower, hormonal control via the pituitary). It therefore acts as the bridge between nervous and hormonal coordination, allowing the brain to bring about both rapid and longer-term, widespread responses.

Habituation is the decline in response to a stimulus that is repeated and proves to be harmless. It happens because of changes at the synapse.

When the stimulus is received repeatedly, less calcium enters the presynaptic neurone at each impulse, because the calcium ion channels become less responsive. As a result, fewer synaptic vesicles fuse with the presynaptic membrane and less neurotransmitter is released into the synaptic cleft.

With less neurotransmitter binding to receptors on the postsynaptic membrane, the postsynaptic membrane is less likely to reach the threshold needed to trigger an action potential, so fewer or no impulses pass on and the response gradually declines and stops.

This is biologically useful because it allows an animal to stop wasting energy and attention responding to unimportant, repeated stimuli (such as a constant background noise), so it can remain alert and responsive to new or potentially dangerous stimuli instead.

MDMA acts at synapses that use the neurotransmitter serotonin, which is involved in regulating mood.

When MDMA is taken, it causes the presynaptic neurones to release large amounts of serotonin into the synaptic cleft. At the same time, MDMA blocks the reuptake of serotonin back into the presynaptic neurone — normally serotonin is taken back up and recycled, but this is prevented.

Because more serotonin is released and it is not removed from the cleft, serotonin remains in the synaptic cleft for longer and binds to receptors on the postsynaptic membrane for longer. This causes increased and prolonged stimulation of the postsynaptic neurones, which produces the feelings of elation, energy and emotional closeness associated with the drug.

However, this surge uses up the stored serotonin, and with repeated or heavy use the serotonin is depleted faster than it can be replaced; the serotonin-releasing neurones may also be damaged. With less serotonin available afterwards, the synapses cannot transmit normal mood-related signals, leading to low mood (a "comedown") and, with long-term use, possible lasting effects on mood and memory.

This illustrates how a drug that interferes with one step of synaptic transmission (here, neurotransmitter release and reuptake) has both immediate effects and longer-term risks.

The four techniques fall into two groups. CT and MRI are structural — they show the brain's anatomy — whereas fMRI and PET are functional — they show which regions are active.

CT combines X-rays taken from many angles into a structural image. It is quick and relatively cheap, useful in emergencies, but it uses ionising radiation and gives less soft-tissue detail than MRI.

MRI uses strong magnetic fields and radio waves to give very detailed structural images with no ionising radiation. However, the scanner is expensive, the scan is slow and noisy, the patient must keep very still, and it cannot be used on people with certain metal implants.

fMRI detects changes in blood oxygenation in active regions, showing brain activity in near real time with good spatial resolution and no radioactive tracer. Its limitations are that it is expensive and measures activity only indirectly (via blood flow), with a slight time lag.

PET uses an injected radioactive tracer (such as labelled glucose) to show metabolic activity, which is valuable for studying disease and drug action. However, it gives a radiation dose, is expensive, and has lower spatial resolution than MRI/fMRI.

Overall, the best technique depends on the purpose: to investigate a structural problem such as a tumour or bleed, CT (fast) or MRI (most detailed, no radiation) is best; to study which areas are active during a mental task, fMRI (no tracer) or PET (direct metabolic measure) is required.

A stroke kills neurones in part of the cerebrum, so the original neural pathways controlling certain movements are destroyed. Recovery is possible because of neural plasticity — the ability of the brain to change its structure and connections in response to experience.

Surviving neurones in nearby, undamaged regions can form new synapses and develop new connections, effectively re-routing the control of a movement around the damaged area so that other neurones take over the lost function.

Neural plasticity is activity-dependent: connections that are repeatedly used are strengthened (more synapses form, more receptors are made, more neurotransmitter is released), while connections that are not used are lost. This is the "use it or lose it" principle.

This explains why intensive, repeated practice (rehabilitation) helps. By repeatedly attempting the lost movements, the patient repeatedly activates the relevant pathways, which stimulates the formation and strengthening of new synapses along them. The more a movement is practised, the more strongly the new pathway is reinforced, so the movement gradually becomes possible again.

Without practice, the new connections are not stimulated, so they are not strengthened (and may be lost), and recovery is poorer. Recovery is usually only partial because not all the lost neurones can be replaced and there is a limit to how much re-routing is possible.

Research into brain conditions such as Parkinson's disease, depression and Alzheimer's uses animal models (in which a similar condition is studied or induced in animals to test treatments) and the Human Genome Project, which has identified genes linked to brain conditions and how they interact with environmental factors. Both methods raise ethical issues that can be argued from more than one viewpoint.

Arguments for using animals. Animal research has led to treatments — such as those for Parkinson's disease — that greatly reduce human (and animal) suffering. Animal brains are similar enough to ours to give useful results, and the work is tightly regulated to minimise suffering, following the "3Rs": replacement (use alternatives where possible), reduction (use as few animals as possible) and refinement (reduce the suffering caused). On this view the benefits outweigh the costs.

Arguments against using animals. Animals can suffer pain and distress, and some people argue that humans have no right to harm other species for our benefit. Animal brains also do not perfectly model human brains, so results may be misleading, which questions whether the suffering is justified.

Arguments about the Human Genome Project / genetic data. Identifying genes linked to brain conditions can improve diagnosis, risk prediction and targeted treatment, which is a clear benefit. However, it raises serious concerns about the privacy of personal genetic information, the risk of genetic discrimination (for example by insurance companies or employers who learn that someone carries a risk gene), and the psychological burden of being told you are likely to develop an incurable condition. There is also a risk of over-interpreting genetic risk when conditions also depend strongly on environment.

Conclusion. Both methods can bring real benefits in understanding and treating distressing, currently incurable conditions, so most would argue the research is justified — provided it is strictly regulated: animal use must follow the 3Rs and be limited to where no alternative exists, and genetic data must be kept confidential and protected against discrimination. The benefits should be weighed against the harms in each case, rather than the methods being either wholly accepted or wholly rejected.

Hubel and Wiesel sewed shut one eye of newborn kittens (and young monkeys) for the first weeks of life — monocular deprivation — so that eye received no visual stimulation while the other eye saw normally.

When the deprived eye was reopened, the animal was functionally blind in that eye, even though the eye itself was healthy. Recordings from the visual cortex showed that very few neurones responded to the deprived eye, while many responded to the open eye, and the ocular dominance columns serving the open eye had expanded at the expense of those serving the deprived eye.

This shows the deficit lay in the brain (visual cortex), not the eye: connections serving the deprived eye failed to develop because they were not stimulated, while the used connections of the open eye were strengthened and took over ("use it or lose it").

The genes provide the initial wiring of the visual cortex — this is nature. But the experiments show that this wiring must be refined and maintained by actual visual experience during early life — this is nurture.

Crucially, the effect occurred only in newborn animals: closing an adult cat's eye for the same length of time had no such effect. This demonstrates a critical (sensitive) period — a limited window during which experience is required.

Because the cortex develops normally only when the genetic wiring (nature) receives the correct visual stimulation (nurture) during the critical period, the experiments provide strong evidence that both nature and nurture are necessary — neither alone is sufficient.