Strike a funny bone and your arm jerks before you decide anything. Drink a coffee at four in the afternoon and you lie awake at midnight. A blow to the head changes a person's memory or temper. Someone stops taking a medicine and their mood shifts. In each case something happened in tissue, and something happened in experience, and the two cannot be pulled apart.
Biological psychology is the course where psychologists meet that fact. Its job is not to explain the mind by pointing at the brain. It is to learn what the tissue does, in what units, at what speed, and, just as important, which popular stories about "the chemical for love" or "the part of the brain for fear" are too neat to be true.
The human brain holds about 86 billion neurons, according to a careful 2009 count that replaced the round "100 billion", along with a roughly equal number of supporting cells. A neuron is a cell that collects inputs and, when enough arrive, sends a brief electrical pulse down its fibre. At rest its inside sits about 70 millivolts below the outside. If inputs push it up to about −55 mV, the threshold, channels open, sodium rushes in, and the voltage swings to roughly +30 mV for about a millisecond before resetting. That pulse is the action potential. Alan Hodgkin and Andrew Huxley worked out its mechanism in 1952 on the giant axon of a squid, and shared a Nobel Prize for it in 1963.
Two facts matter more than the details. First, it is all or none: a neuron cannot fire a weak spike. A stronger input does not make a bigger pulse, it makes pulses come more often. The rate is the message. Second, the spike travels along the fibre, and fatty myelin wrapped around it makes the signal jump, so speeds reach roughly 100 metres per second in the fastest fibres, against about a metre per second in thin unwrapped ones.
A textbook model, not a real cell: time constant 20 ms, rest −70 mV, threshold −55 mV, 2 ms refractory period. Input is the voltage above rest that the cell would reach if it never fired.
Below 15 mV of drive, nothing happens, however long you wait. At 20 mV the cell fires about 34 times a second; at 40, nearly 90. The size of every spike is identical. This is the brain's coding trick: not louder, but faster.
Neurons do not touch. They are separated by a gap about 20 nanometres wide, the synapse, and the signal crosses it as chemistry. Otto Loewi showed in 1921, with two frog hearts, that a nerve releases a substance rather than just a current. When a spike arrives, the cell releases a neurotransmitter, which binds receptors on the next cell and nudges it toward firing (excitation) or away from it (inhibition). Then the leftover is cleared: pumped back (reuptake) or broken down. In the brain, glutamate is the main excitatory transmitter and GABA the main inhibitory one.
Pop psychology turns each transmitter into a mood: dopamine is pleasure, serotonin is happiness, oxytocin is love. The truth is messier. Dopamine neurons fire strongly for unexpected rewards and cues, a "better than expected" signal, which is why they matter for learning and wanting, and not simply for enjoying. Most of the body's serotonin sits in the gut, not the brain. Oxytocin does affect social behaviour, but results from squirting it up the nose have been inconsistent, and many early findings shrank as samples grew. One transmitter plays many roles in different circuits; one behaviour uses many transmitters.
A toy model in arbitrary units: each spike adds one unit; the gap clears at a rate of 10 + 50 × reuptake per second.
With full reuptake, a 10 Hz neuron keeps the gap at about 0.16 units; block 80% of reuptake and the level triples to 0.5. That is, roughly, what drugs like SSRIs do within hours. Yet their effect on mood takes weeks, and the slogan "depression is a chemical imbalance" is a simplification that psychiatrists themselves avoid. A 2022 review argued there is no consistent evidence that low serotonin causes depression; others replied that this was never the standard claim and that the drugs still beat placebo on average (a large 2018 comparison of 21 antidepressants found all outperformed placebo, with modest average effects). What can be said: transmitters matter, the story is not one chemical, and no one should change a medicine because of a diagram. Talk to a prescriber.
Hormones are the slow cousin. Glands release them into the blood and they act over minutes to days: cortisol, from a chain called the HPA axis, prepares the body for demands; adrenaline acts in seconds. A nerve impulse reaches your foot in a few hundredths of a second; a hormone takes minutes. Two systems, two timescales.
Where things happen in the brain is one of the oldest questions. In 1848 railway foreman Phineas Gage survived an iron bar through the front of his skull, and accounts say his behaviour changed (the details were exaggerated in retelling). In 1861 Paul Broca examined a man who could understand speech but say almost only one syllable; the damage was in the left frontal lobe. In 1953 surgeons removed parts of Henry Molaison's temporal lobes to treat epilepsy; he could no longer form new lasting memories of events, yet he could still learn a new motor skill. Cases like these show that some functions depend on particular tissue.
Do not conclude that each part has one job. Functions are networks: damage to one place can break a skill that many places share. Three myths to drop. We do not use 10% of the brain; imaging shows activity throughout, and the brain, about 2% of body weight, uses around a fifth of the body's resting energy. "Left-brained" and "right-brained" people do not exist; a 2013 analysis of over 1,000 scans found no person-wide dominance, although the two halves do specialise a little (language is usually left). And the neuron count is lopsided: the cerebellum, tucked under the back of the brain and often thought of as just for coordination, holds roughly 80% of the neurons.
A cartoon, not an atlas. Pick a region or tap its circle. Deficits are textbook summaries of famous cases and vary by person.
A scan of the brain is not a photograph of thinking. MRI shows structure. fMRI measures the blood-oxygen signal (BOLD): active neurons use oxygen, blood flow rises a few seconds later, and the scanner sees the change. So it is indirect, slow (seconds) and blurry (millimetres), whereas EEG catches the brain's electrical rhythms in milliseconds but cannot say precisely where they come from. Neither shows a thought, and neither shows cause. For that you need a lesion, a drug, or brain stimulation.
The classic warning is a dead Atlantic salmon. In 2009 Craig Bennett and colleagues put one in a scanner, "showed" it photographs of people, and found voxels (3D pixels) that lit up, because with tens of thousands of voxels, each tested at p < .05, some pass by chance. They used it to argue for corrections for multiple comparisons, and it won an Ig Nobel Prize in 2012. Two related traps: "reverse inference" (the amygdala was active, therefore the person felt fear: it is active in many states) and tiny samples. A 2022 study by Scott Marek and colleagues found that linking brain scans to behaviour in the general population needs thousands of people, not the dozens typical of older studies.
Every voxel is pure noise. The grid shows 2,000 of the voxels; the readout counts them all. Bonferroni correction divides the threshold by the number of tests.
With 50,000 voxels at p < .05 you expect 2,500 false "activations". Uncorrected, a scan of nothing finds a brain at work. Correcting the threshold for 50,000 tests keeps the chance of any false alarm near 5%. Modern studies correct, share data and replicate; but an old headline of the "this region lights up when…" kind deserves the same suspicion as any small study (see Research Methods in Psychology, 35/19).
Sleep is not the brain switching off. Over a night it cycles about every 90 minutes through lighter and deeper stages and REM sleep, discovered in 1953 by Eugene Aserinsky and Nathaniel Kleitman, when the brain is highly active and most vivid dreams occur. A 2015 expert consensus recommended that adults regularly sleep at least seven hours; needs vary between people and across life, and no single "right" number fits everyone.
The standard picture, proposed by Alexander Borbély in 1982, is the two-process model. Process S is a sleep pressure that rises the longer you are awake and drops during sleep (adenosine is a leading candidate for part of it, which is why caffeine, an adenosine blocker, delays sleepiness without removing the debt). Process C is the circadian clock, set mainly by a tiny region called the suprachiasmatic nucleus and by light, which makes you more alert at some hours than others. You feel sleepy when S is high and C is low. Jet lag and shift work are C and S out of step.
Schematic model after Borbély, with rise time 18.2 h and fall time 4.2 h as in early human fits, scale 0 to 1. The circadian curve is a simple wave peaking at 18:00. Illustrative, not a prediction for any person.
With 8 hours' sleep and bed at 23:00, pressure at waking falls to about 0.09 of the scale and ends the day near 0.62. Cut sleep to 5 hours and the morning level only gets down to about 0.22: you begin each day with leftover debt, and it does not clear itself overnight.
In 1949 Donald Hebb proposed that when one cell repeatedly helps to fire another, the connection between them strengthens. The slogan "cells that fire together wire together" is a later paraphrase. The effect, called long-term potentiation, was shown in rabbit hippocampus by Tim Bliss and Terje Lømo in 1973. It is the leading model of learning: experience changes connection strengths, not the number of cells.
Input A already drives the cell. Input B is too weak alone. Present them together and watch B's connection grow.
Rule: when the cell fires, each active input's weight w grows by 0.2 × (1 − w). The cell fires when the summed active weights reach 0.5. Cartoon of the Hebb rule, not a cell model.
After three pairings B alone crosses the threshold. The adult brain stays plastic in far larger ways: in a 2000 study, London taxi drivers who had passed the demanding street test had a larger posterior hippocampus than controls, in proportion to years of driving. But claims that new neurons keep forming in adult humans are disputed. Two 2018 papers, one finding almost no new cells in adult hippocampus and one finding plenty, are still argued over. What is solid is that the brain changes with use throughout life, more in youth, and less than the popular word "rewiring" suggests.
The mind runs on cells that signal by firing rate, chemicals that cross a gap, hormones that travel slowly, and connections that change with use. That is a powerful picture and a limited one: slogans about single chemicals or single brain regions, and strong claims from small brain scans, need the same scepticism as any psychological finding.
Try this: this week, notice a mood shift (after poor sleep, a late coffee or a skipped meal) and think of the two layers: what the tissue is doing, and what you are feeling. Neither explains the other alone.
Sources. Action potential and leaky integrate-and-fire model: standard textbook (Kalat; Bear et al.); Hodgkin & Huxley (1952), Nobel 1963. Neuron count: Azevedo et al., Journal of Comparative Neurology (2009): about 86 billion neurons, about 80% in the cerebellum. Loewi (1921). Reward prediction error: Schultz, Dayan & Montague, Science (1997). Antidepressants: Cipriani et al., The Lancet (2018); Moncrieff et al., Molecular Psychiatry (2022), with published replies. Gage (1848), Broca (1861), Molaison (1953, Scoville and Milner). Left/right brain: Nielsen et al., PLoS ONE (2013). Dead salmon: Bennett et al. (2009); Ig Nobel 2012. Marek et al., Nature (2022). REM: Aserinsky & Kleitman (1953). Sleep duration: Watson et al., consensus statement, Sleep (2015). Two-process model: Borbély (1982); Daan, Beersma & Borbély (1984). Hebb (1949); Bliss & Lømo (1973). Maguire et al., PNAS (2000). Adult neurogenesis: Sorrells et al. and Boldrini et al., both 2018. Simulated numbers are toy models computed live. This is descriptive, not medical advice. If you are struggling, a doctor or local helpline (findahelpline.com) can help.