The Spark of Life: Electricity in the Human Body

by Ashcroft, Frances

  Dancing Hair Cells

  The outer hair cells are far more numerous than the inner ones. Although they play little, if any, role in signalling sounds to the brain, they are essential for normal hearing as they mechanically amplify sound vibrations by ‘dancing’ in time to the beat. This amplification is critical for detecting low-intensity, high-frequency noises because the vibrations of the sound waves are damped down as they pass through the fluid-filled canals of the inner ear.6 Without magnification of the signal, the inner hair cells are not stimulated sufficiently to activate the auditory nerves. The cochlear amplifier, as it is known, also sharpens the ability of the ear to discriminate different frequencies. It may have evolved to enable the first mammals to hear the faint high-pitched cries of their young; now it helps us hear the squeak of a bat.

  The existence of a natural amplifier in the ear was first proposed in 1948, but the idea was rejected and it was not until the late 1970s that its validity was established. The fact that hair cells could be seen to ‘dance’ provided the clue to how it worked. An outer hair cell will twitch in time to music piped directly into the cell via an electrode connected to an amplifier. I’ve not forgotten the time I visited Jonathan Ashmore’s laboratory at University College London and looking down the microscope was amazed to see a tiny hair cell bopping away to ‘Rock around the Clock’. It kept perfect time. The contractions of the hair cell are powered by prestin, a molecular motor that is sensitive to the voltage difference across the cell membrane, and changes in this voltage difference produced by the exogenous electrical stimulus caused the cell to dance. In life, such voltage changes are produced by opening of mechanosensitive ion channels in response to the movement of the hair bundle within, as Huxley so evocatively put it, the storm in the cochlear fluid. The twitching of the outer hair cells amplifies the movement of the basilar membrane, leading to greater stimulation of the sensory inner hair cells. This intrinsic biological amplifier is the basis of our ability to hear very quiet sounds. High doses of aspirin inhibit the motor protein and induce a reversible hearing loss.

  The Song of the Ear

  It may come as a surprise, but your ears can also generate sounds. Technically known as otoacoustic emissions, these are produced by the outer hair cells. They arise because the vibrations the hair cells produce as they bounce up and down set up waves in the cochlear fluid, which in turn are passed on to the air in the middle ear and ultimately back to the eardrum. The sounds made by healthy ears are quieter than a whisper and those of individuals with cochlear damage are even weaker. However, they can be picked up by a special microphone placed within the ear canal, and such ‘ear songs’ provide doctors with a valuable non-invasive measure of the health of the ear and a simple way to check if a young baby has impaired hearing. This enables a child to be fitted with a hearing aid or cochlear implant before the time window for learning speech has passed.

  Living Under a Deaf Sentence

  Helen Keller, who was both blind and deaf, once said that whereas blindness separates people from things, deafness separates people from people. The isolation, confusion, frustration and depression often experienced by those who lose their hearing is poignantly stated by Ludwig van Beethoven in his ‘Heiligenstadt Testament’, written at the age of thirty-two, six years after he had started to go deaf. ‘Oh you men who think or say that I am malevolent, stubborn or misanthropic, how greatly do you wrong me. You do not know the secret cause which makes me seem that way to you [. . .] it was impossible for me to say to people, “Speak louder, shout, for I am deaf.” [. . .] for me there can be no relaxation with my fellow men, no refined conversations, no mutual exchange of ideas. I must live almost alone, like someone who has been banished.’ By the time he was forty-five, Beethoven was almost totally deaf. Yet although performance became impossible, he continued to compose and conduct. At the première of his Ninth Symphony (when he was fifty-four), he had to be gently turned around to witness the rapturous applause of the audience, for he could hear nothing. He wept at the sight.

  Unlike a musician, a deaf painter is still able to practise his art. Indeed, in Goya’s case it seems to have led to his greatest works. After a serious illness left him stone deaf, the devastating isolation he experienced precipitated a remarkable change in his art: increasingly, he focused on nightmarish fantasies, black visions and satirical portrayals of human behaviour. Liberated from the cacophonous distractions of daily life, it is said, he saw the world for what it was – although whether Goya, like the art critics, perceived his deafness as a blessing is questionable.

  Hear Today, Gone Tomorrow

  It is estimated that about nine million people in the UK – as many as one in seven of the population – suffer from some degree of hearing loss. Almost inevitably, it seems, as we grow older our ability to hear high frequencies declines. Alan Bennett wrote, ‘I did not think my hearing had deteriorated at all but [. . .] R. asks me if I can hear the crickets and I cannot believe that, the night tingling with the sound, I am dead to it.’ Such high frequency hearing loss often creeps up on you gradually, almost unnoticed, until suddenly hearing is gone. The poet Philip Larkin only discovered it when a friend remarked on the beauty of a skylark’s song and he was unable to hear it. For him, as for many others, partial deafness darkened his melancholy. Age-related high frequency hearing loss has even been exploited by the manufacturers of a controversial device termed the Mosquito that emits an ear-splitting high-pitched whine, audible to teenagers but not to adults. Its painful buzz has been used to disperse loiterers and prevent antisocial behaviour on UK streets. In an ironic twist to the story, ingenious teenagers subsequently stole the frequency and used it as a mobile phone ringtone that they – but not their teachers – could hear.

  The deterioration in hearing we all experience with age is caused because our hair cells naturally die off with time and once gone they are lost forever. Loud noises destroy our hearing even faster. The rock musician Pete Townshend7 instantly lost the hearing in one ear in a famous incident in which a staged explosion was far louder than expected. Thousands of troops fighting in Iraq and Afghanistan returned home with permanent hearing loss, mostly caused by roadside bombs. The thunder of warfare, the deafening sound of a pop concert, the roar of jets and loud machinery – all exact a heavy toll. This is because our outer hair cells are very vulnerable and can be irretrievably damaged by loud noises.

  Left. Normal hair cells, showing the three layers of outer hair cells and, below, the single layer of inner hair cells. Right. Loud noises damage the outer hair cells before the inner ones.

  Chronic exposure to moderately loud sounds can also cause permanent hearing loss because there is no time for partially damaged hair cells to recover. Many people, often unwittingly, routinely subject their ears to noise levels that can ruin their hearing. Exposure to sounds louder than 85 decibels for an extended period of time can cause hearing loss: this noise level is similar to that associated with using a power drill, riding a motorcycle, going to the cinema and many other everyday pursuits. It is also lower than the maximum volume levels on many portable MP3 players. Turn up the volume too loud for too long and you may be unable hear your grandchildren in later life. Sadly, it seems inevitable that within the next few decades many people will become far more interested in how their ears work than they might wish.

  One of the first signs of damage is a chronic ringing in the ears known as tinnitus. The Times’ music critic Richard Morrisson, who tested a device that simulates tinnitus, described it as a horrible, high-pitched whistling that made listening to music a nightmare. ‘It was like listening to the drifting signal of some Algerian radio station through the crackling static of an old wireless. Only much more distressing.’ Morrisson found immediate relief by ripping the simulator off his ears but for those unfortunates whose hair cells are ruined tinnitus can be a lifelong ordeal. For them, silence is never silent. Beethoven, who suffered from severe tinnitus from his late twenties, complained that his ears whistl
ed and buzzed continually, day and night, and described his condition as truly frightful. It is extraordinary that despite this handicap he was able to compose some of the world’s greatest music.

  Although tinnitus is often associated with hearing loss, this is not always the case and many tinnitus sufferers hear perfectly well. What causes these internally generated sounds to be perceived is still far from clear, but we do know that they originate from changes that take place within the brain.

  A Matter of Taste

  I first tasted the miracle fruit one hot summer’s afternoon in Puerto Rico. This smooth oval-shaped red fruit, about the size of a coffee bean, comes from the shrub Synsepalum dulcificum, a native of West Africa, and has the extraordinary property of making sour things taste sweet. It felt cold and hard as I rolled it over my tongue and I bit into it with a mixture of anticipation and trepidation. It had a thin, bitter skin surrounding yellow, slightly astringent flesh and a quite unremarkable taste. Ten minutes later I was able to eat a lemon without wincing and, somewhat tentatively, sip vinegar. With my eyes closed, many foods were barely recognizable; beer, in particular, tasted most peculiar. Happily, the effect wore off within a couple of hours.

  The miracle fruit contains a protein called miraculin that interacts with sweet taste receptors and enables them to be activated by sour chemicals. Other natural modifiers of taste are also known. If you have ever eaten a fresh globe artichoke you will be aware that everything, including water, tastes sweet afterwards.8 This is because artichokes contain cynarin, which appears to work by suppressing the activity of bitter taste receptors while enhancing that of sweet ones. Whatever the mechanism, it makes it notoriously difficult to choose a wine to drink with globe artichokes. In contrast, gymnemic acid, from the south Asian herb Gymnema sylvestre, suppresses the intensity of sweet perception, but not that of bitter, so that many foods taste unusually bitter and sugar tastes of ashes.

  Taste cells are not nerve cells but a specialized kind of epithelial cell (the cells that line the gut, mouth and nasal passages). They are very short-lived, being continually replaced every couple of weeks, and they are packed together in barrel-shaped taste buds. Humans have about 10,000 taste buds distributed over the surface of the tongue, each containing 50 to 100 taste cells.9 Each taste cell sends a long finger-like process, tipped with fine hairs that bear the taste receptors, up to the opening of the taste bud on the surface of the tongue where stimuli are received. The other end of the taste cell contacts the sensory nerve.

  We can discriminate five basic tastes – sweet, salt, sour, bitter and savoury (umami). All the many different flavours we taste, however, are really smelt, for these two senses work in combination. This explains why your sense of taste seems impaired when you have a head cold and your nose is blocked. Anthelme Brillat-Savarin, the seventeenth-century gastronome, tells of meeting a man whose tongue had been cut out, yet who retained a full appreciation of tastes and flavours. He therefore concluded that, ‘smell and taste are in fact but a single composite sense, whose laboratory is the mouth and its chimney the nose’.

  When you eat something, chemicals contained in the food dissolve in your saliva. This enables them to bind to the receptors at the tip of the taste cells, and so trigger a cascade of events that ultimately releases a chemical transmitter from the base of the taste cell. In turn, this excites the sensory nerve, and nerve impulses are then transmitted to the brain where the information is decoded, processed and tastes are identified.

  Different tastes arise because different types of receptor are stimulated. Two tastes – salt and sour – are directly detected by ion channels sensitive to the ions involved, which are respectively sodium ions and hydrogen ions (protons). Salty tastes are mediated by the epithelial sodium channel (ENaC) we met in the previous chapter. Several kinds of ion channel that are sensitive to protons detect sour tastes. The carbon dioxide in fizzy drinks and champagne is also detected by sour taste receptors because it yields protons when dissolved in water. Interestingly, some soda-water manufacturers recognized this long before science showed it to be true – sauerwasser10 and similar seltzers are named for their sour, slightly acidic taste. Umami, from the Japanese word umai, meaning ‘delicious’, describes the savoury taste of food containing monosodium glutamate. Some of the receptors that detect glutamate are also ion channels. Somewhat surprisingly, the giant panda lacks functional umami receptors, but whether this is the cause or the consequence of the fact that, unlike other bears, it prefers a strict vegetarian diet is unclear.

  Sweet and bitter substances do not activate ion channels directly. Instead they bind to specific receptors, so setting in train a cascade of biochemical events that eventually leads to the opening of a specialized ion channel (known as TRPM5) that is common to both pathways. The ability to discriminate between sweet and bitter substances arises because the two types of receptors are found in different populations of taste cells, which signal separately to the brain. Thus whether something tastes sweet or bitter is decided by the brain. We have over twenty different receptors for bitter taste, but only one for sweet taste, reflecting the evolutionary drive to identify bitter-tasting substances, which are often poisonous. The sweet taste receptor is composed of two different proteins and variants in either of the genes that encode these proteins give rise to different sensitivities to sweet substances; it seems that some people really do have more of a ‘sweet tooth’ than others. Reduced sensitivity to sugar is most common in sub-Saharan African populations, suggesting that that the ability to sense sugar is more important in cold climates, where sugar sources are rare. But in today’s society the beguiling pleasure of sweet taste brings in its wake terrible public health problems – obesity and tooth decay are the handmaidens of Sachertorte, raspberry ice cream and sugary drinks.

  Many patients taking anti-cancer drugs complain that food tastes terrible – less sweet and more bitter. This is because, like all epithelial cells, taste cells have a very rapid turnover and thus are especially sensitive to chemotherapeutic drugs, which destroy rapidly dividing cells. Taste is also influenced by context (although this is largely the province of the brain). I love the smell of coffee but gave up drinking it over twenty years ago and now take only tea. On the odd occasion when I am accidentally handed the wrong drink and take a sip of coffee it tastes very strange. The ability to identify the correct flavour is also reduced if the food is the wrong colour; raspberry juice does not taste quite right if it is coloured orange or green. Try it, and see if you agree.

  Making Sense of Scents

  Scents, as Marcel Proust famously observed, can evoke remembrance of things past. The spicy, peppery smell of lupins reminds me of my great-aunt’s garden, crammed with colourful flowers and butterflies, and humming with bees. That of mown hay evokes other childhood memories – of lying in the grass watching the village cricket match, hearing the distant cuckoo and the strangely comforting thwack of leather on willow.

  The cells that detect smells lie high up in the nose, almost seven centimetres away from the nostril. These are the olfactory neurones, which send processes to the olfactory epithelium in the nose. Each nerve process terminates in a small bunch of olfactory cilia, fine hair-like processes that project up into the viscous mucous layer that covers the moist surface of the inner nose and greatly increase the membrane surface area available for odorant detection. Odorant receptors lie embedded in the surface of the cilia, ready to capture smells borne on the air you breathe.

  Humans have around 350 distinct types of olfactory receptor proteins,11 although each olfactory neurone carries only a single kind. But we can detect far more than 350 aromas: most people can distinguish many thousands of substances, often in tiny amounts. A good ‘nose’, such as an expert perfumier or sommelier, has even finer discrimination. Thus it is clear that there is not a specific receptor dedicated to a given odour. Rather, it is believed that each receptor recognizes a class of odour molecule (or a specific molecular feature), that a single odorant
may bind to more than one receptor, and that it is the specific combination of receptors that are stimulated that enables us to discriminate smells. In the same way that the letters of the alphabet can be used to construct a vast vocabulary, so the different combinations of odorant receptors produce a cornucopia of pure odours. Scents are even more complex and varied as they are composed of many different odours.

  It is widely believed that humans have a poor sense of smell. But tests show that we can detect some odours almost as well as dogs and much better than rats, and that we easily outperform highly sensitive measuring instruments. One reason for our supposed poor sense of smell is that we walk around with our noses high in the air, while scents are at their strongest close to the ground and quickly dissipated by air currents at higher levels, as can easily be seen by watching how a tracker dog follows a trail. Moreover, despite being able to recognize many different aromas, most of us are not very good at describing this difference in words. Yet the ability to identify a wine as distinct from all others is a highly complex and demanding task, and even those of us who are untrained find no difficulty in distinguishing the scents of oranges and lemons, which are simply mirror images of the same molecule, limonene.

  When you smell a rose, the scent is wafted up to your olfactory epithelium, where the many different chemicals that make up the smell bind to their receptors on different sets of olfactory neurones. Precisely how odorants stimulate their receptors is still unclear, but it appears to be due to the different sizes and shapes of the odorant molecules. One idea is that they bind to the receptor in a lock-and-key fashion. Just as your right glove will only fit your right hand, so right-handed molecules will only bind to right-handed receptors; this explains why orange and lemon (which are left- and right-handed versions of limonene) smell different. Binding of an odorant to its receptor triggers a cascade of events in the neurone that leads to opening of a specific kind of ion channel – related to, but different from, those in the rods and cones – so giving rise to a current that in turn sets up a stream of action potentials in the olfactory neurone itself. These impulses pass along the olfactory nerve to a region of the brain known as the olfactory bulb, where they hand their signals on to other nerve cells in deeper regions of the brain. One of these is the limbic system, which is involved in emotion, which explains why smells can trigger such powerful emotions and memories.