Green Electricity
Almost all life on the planet depends on the ability of plants to capture the energy of the sun and store it as sugar molecules. This process, known as photosynthesis, is the ultimate source of all the food we eat, all the molecules from which our bodies are built, and most of the oxygen in the atmosphere. Photosynthesis involves the conversion of carbon dioxide and water into sugar and oxygen in a reaction powered by sunlight, and it takes place in specialized organelles, known as chloroplasts, that lie within plant cells.
To prevent excessive water loss, the leaves of most plants are covered with a thick waxy cuticle. However, this also restricts the diffusion of oxygen and carbon dioxide into and out of the leaf, so that gas exchange can only take place via dedicated pores on the underside of the leaf, known as stomata, that act like microscopic windows. The problem that plants face is that the stomata not only allow carbon dioxide to enter and oxygen to leave, they also provide a very effective pathway for water vapour to escape. This can put a considerable strain on the plant, for water lost this way must be replaced by absorbing more from the ground. Some desert plants have solved the problem by opening their stomata only at night, greatly restricting water loss during the heat of the day. But this poses another difficulty because photosynthesis normally requires carbon dioxide and sunlight to be present at the same time. It’s a classic catch-22 situation. Consequently, most plants balance photosynthesis and water stress by opening and closing their stomata throughout the day, as the ambient light and humidity conditions dictate.
Stomata are composed of two ‘guard’ cells that both form the aperture of the pore and regulate its opening and closing by adjusting the amount of water they contain. When the guard cells are swollen and turgid the pore between them is forced open, whereas when they lose water and become flaccid the pore collapses shut. The water movements that influence guard cell volume, and thereby stomatal opening, are controlled by a combination of pumps and channels. An increase in light intensity causes positively charged hydrogen ions to be pumped out of the cell, creating a negative potential across the cell membrane. In turn, this change in membrane potential opens potassium channels, allowing potassium ions to enter the guard cells. Water follows the potassium ions, so that the guard cells swell by as much as 40 per cent, forcing open the stomatal pore. As long as the potassium channels remain open, the pore remains ajar. However, when light levels fall or the plant experiences water stress the potassium channels close. Consequently, water leaves the cell, the guard cells shrink and the stomatal pore closes.
In a sense then, by controlling the turgidity of the guard cells, plant potassium channels regulate photosynthesis. Arguably, they are some of the most important ion channels on Earth. I find it strangely pleasing that these potassium channels belong to the same superfamily as the ones I am most passionate about. They must stem from a common ancestor that evolved long ago, before the animal and plant kingdoms divided.
Life in the Slow Lane
Remarkably, a few plants not only have ion channels, they also have the ability to generate action potentials. However, the electrical impulses of plants differ from those of nerves in that they are of longer duration, travel more slowly and are carried by different ions. That of the alga Nitella, for example, is initiated not by an influx of positively charged sodium ions, but instead by the loss of negatively charged chloride ions from the cell. There is a good reason why this is the case. Unlike animal cells, the cells of most terrestrial plants are not bathed in a salty extracellular fluid. Ions are present at very low levels in plant cell walls and thus an influx of sodium ions would not be a viable means of producing an action potential. Instead, plants must rely on chloride efflux.
Carnivorous plants have exploited action potentials to capture their prey. One of the most fascinating is the Venus flytrap, a favourite of Charles Darwin. This plant, he wrote, ‘from the rapidity and force of its movements, is one of the most wonderful in the world’. To cope with the nitrogen-poor soils of the bogs in which it lives, the Venus flytrap supplements its diet by capturing small insects. It attracts them with an enticing ‘trap’ formed from a modified leaf that consists of two brilliant crimson lobes, like the two halves of a cockleshell, fringed by long pinkish-green hairs. At rest, the trap sits invitingly open. No sooner has an unwary fly landed on its sweet, sticky surface, however, than the two halves snap shut, imprisoning the insect inside. The long hairs at the edge of the lobes interlock tightly together like the teeth of a rat-trap, preventing large insects from escaping. Small insects can squeeze out, presumably because it would not be energetically favourable to process a tiny morsel, but larger insects are slowly digested to provide the nitrogen the plant needs to make its own proteins. About seven days later the trap reopens, releasing the indigestible remains.
As you will know if you have ever tried to swat a fly, insects move fast. Thus, to catch one, the Venus flytrap must move even faster and it has evolved a specialized electrical signalling system that enables it to do so. Each lobe of the trap bears several triangular hairs projecting up from its surface that are exquisitely sensitive to touch. If more than two of these are distorted at roughly the same time – for example, by the movement of an insect – the lobes clap shut faster than the blink of an eye.2 The hairs possess mechanosensitive ion channels and touching them elicits an action potential that spreads throughout the lobe cells to the centre of the trap. At rest, the lobes of the trap are bowed upwards, but when the electrical signal arrives at the midline of the trap they flip from a convex to a concave shape, forming a pocket that entraps the prey. Precisely how this happens is still debated, but ion channels that trigger ion and water movements that lead to differential swelling and shrinking of the lobe cells, and thus to dramatic changes in pressure across the leaf, have been invoked.
Similar trapping mechanisms are found in other bog and heathland plants, such as sundews, as well as in the wonderfully named waterwheel plant, which sets its snares underwater. Shutting of the waterwheel trap is one of the fastest of plant movements known, taking only 10 to 20 milliseconds, five times faster than the Venus flytrap.
Although plants do not have nerves, a few have specialized conducting pathways that enable electrical impulses to transmit information for some distance. Tap the leaflets of Mimosa pudica, the sensitive plant, and the whole leaf folds up, collapsing from its junction at the stem. Specialized cells transmit the signal from the leaf to its base, where ion movements then cause changes in cell volume that result in the collapse of the whole leaf. By contrast, in the Venus flytrap, the action potentials spread in random fashion throughout the leaf, via electrical synapses between adjacent cells, before finally reaching the swelling cells that close the trap. Nevertheless, impressive as it is that plants have action potentials, they propagate far more slowly than those of animals (around 10 metres per second compared to 250 metres per second). Plants, it seems, simply live their lives at a much slower pace.
9
The Doors of Perception
If the doors of perception were cleansed every thing would appear to man as it is, infinite. For man has closed himself up, till he sees all things thro’ narrow chinks of his cavern.1
William Blake, The Marriage of Heaven and Hell
Imagine you are sitting here with me in my garden on a perfect late summer evening, listening to the blackbird’s joyous song, and enjoying a glass of wine and the faint heat of the sun on your skin. You raise your glass and admire the pale-golden colour of the liquid and the glint of the crystal in the sunlight, then bend your head, swirl the wine gently around the glass, and appreciate the light aroma of gooseberries, of sunshine locked in alcohol. You sip and savour the cool taste of the wine. As this simple pantomime illustrates, even something as simple as drinking a glass of wine involves all of our senses.
Pleasure, pain, indeed the evolutionary success of any organism, ourselves included, depends on our ability to perceive the world around us: to see, hear, smell
, taste and touch it. Our sense organs convert the myriad signals that constantly bombard us in multiple modalities into a single form that the brain can interpret – the electrical energy encoded in our nerve impulses. And in all cases ion channels are needed to transduce sensory information into that electrical signal. Ion channels are truly the doors of perception as everything we sense is detected, transmitted or processed by them. Consequently, defects in ion channel genes produce a variety of human sensory disorders, from hearing loss to colour blindness. This chapter tells some of the remarkable stories of how ion channels determine our ability to perceive what lies around us. It is concerned with Blake’s ‘narrow chinks’ through which we view the world – our sense organs.
Eye Spy
Our eyes are our windows on the world. Open them, and there lies the world in all its richness of form, movement, brightness and colour. As I sit writing these lines, I gaze out on a painted landscape of countless colours: the clear blue sky of an Indian summer, the faded gold of ripe wheat, a vast palette of different greens laced with splashes of brightly coloured flowers. Nothing is still, for the poplar is shaking its leaves in the breeze and the late roses are being tossed around by the wind.
At one level, our eyes operate like a simple camera. They have a clear cornea and a crystalline lens that work together to focus light rays onto a layer of photosensitive cells known as the retina at the back of the eye. They possess an iris that continuously adjusts the amount of light entering the eye. And they have a protective lens cap – the eyelid – that can shut the light out completely when necessary. Unlike most cameras, however, our eyes have a brain attached that processes and interprets the images projected on the retina. Some processing also takes place in the retina itself.
Every second, our eyes handle thousands of images, transforming light signals into upside-down images on the retina, and converting these into nerve impulses that are sent on to the brain for processing. The transparent outer layer of your eye, the cornea, is responsible for about two-thirds of the focusing power of the eye: the remainder is the province of the lens, which is suspended behind the pupil by thousands of fine ligaments. The cornea has a fixed focus, but that of the lens can change, for muscles attached to its edge pull it thicker or thinner as you focus on near and far objects, respectively. As we grow older the elasticity of the lens decreases, making it harder to change its focus, which why most people over fifty need reading glasses.
The pupil is the aperture through which light passes. It appears black because no light returns through it. The iris – the coloured bit of your eye – contains muscles that adjust the size of the pupil to the intensity of the ambient illumination, dilating it in dim light and shrinking it to a pinpoint in very bright light. The size of the pupil even signals feeling, for it expands in response to fear, pain or if you see something of interest – someone you love, perhaps.
Left. A cross-sectional view of the eye, showing the positions of the cornea, lens and retina. Right. A single rod photoreceptor. The outer segment is crammed with stacks of membrane discs that are densely packed with the visual pigment rhodopsin. The other end of the cell is packed with vesicles containing a neurotransmitter. Chemical and electrical signals transmit the light stimulus captured by the photopigment from the discs to the rod terminal and from there on to the next cell in the chain.
The retina is packed with light-sensitive cells, which come in two different varieties: the rods and the cones. Together, they enable us to detect the two fundamental properties of light: intensity and wavelength (colour). Rods cannot discriminate colour, but they are exquisitely sensitive to low light intensities and can even detect a single photon of light (a single quantum or light particle). In dim light we see entirely with our rods, which is why the world appears in shades of silver and grey in starlight and moonlight. Across most of the retina, rods markedly outnumber the cones: there are around 120 million of them against 6.5 million cones. The exception is at the fovea, the region of the retina where light rays are most accurately focused and cones are far more dense. Cones are therefore responsible for our visual acuity, as well as our colour vision. They work best in bright light, which explains why in the dark it is often easier to see things out of the corners of your eyes, where more rods are found. As you will have found, a faint star is far brighter if you do not focus on it directly. The only part of your retina where there are neither rods nor cones is where the optic nerve leaves the eye: this is known as the blind spot, as in the absence of light-sensitive cells nothing can be detected.
Photodetection
The essential feature of any eye, the ability to detect light, is due to dedicated molecules that convert light into chemical energy. We have several such photopigments in our eyes, each of which is specialized to capture different wavelengths (colours) of light. All contain a derivative of vitamin A, retinal, attached to a protein called opsin. The retinal part of the molecule is responsible for absorbing light, which explains why lack of vitamin A decreases the sensitivity of the eye to light and can lead to night blindness.2 During World War II, the British government spread a rumour that their fighter pilots had been fed extra rations of carrots, which contain a lot of vitamin A, to explain their increased success rate at shooting down enemy bombers. There was no substance in the story, however; it was merely a disguise to cover the introduction of radar, which was in fact responsible for the enhanced ‘hit’ rate.
The opsin component of the visual pigment tunes the spectral sensitivity of retinal. Thus, by using different opsins, different wavelengths of light can be detected. The photopigment in your rods, known as rhodopsin, is most sensitive to blue–green light, which has a wavelength of 498 nanometres. We have three different types of cones in our eyes, each of which contains a unique photopigment that absorbs maximally at a different wavelength of light. The conventional, but inaccurate, shorthand has been to call these red, green and blue cones, but in fact they detect yellow–green (long, 564 nanometres), green (medium, 535 nanometres) and blue–violet (short, 433 nanometres) light. All of the myriad different hues we can distinguish are created by combining the electrical signals from these three types of cone, in the same way that a colour television uses just three colour signals to produce the many different colours we see on the screen.
Whenever one of the photopigments captures a photon its shape changes. This sets in motion a complex cascade of events that eventually results in a change in the electrical properties of the light-sensitive cells. Our ability to see begins with this transduction of light into an electrical signal, in which ion channels play an intimate role. Both rods and cones contain millions of pigment molecules, crammed together within the membranes of a series of intracellular discs that are stacked up in the outer segment of the cell. The enormous number of molecules greatly increases the chance that a photon travelling through the eye will be captured, and trigger a visual response. But the location of the photopigment presents a problem, for it lies far away from the vesicles containing the transmitter that the photosensitive cell uses to signal to its neighbour. Thus photoreceptors employ an intracellular messenger service to link the light-induced conformational change in the photopigment to transmitter release. This consists of a chemical known as cyclic GMP, which relays information from the intracellular discs to the surface membrane of the cell. Here, the chemical signal is converted into a much faster electrical one that is rapidly conducted to the transmitter release sites. At the heart of this complex signalling cascade is a special kind of ion channel that opens when it binds cyclic GMP.
In the dark, cyclic GMP levels in the rods and cones are high, so that the cyclic GMP-gated channel is held open. Sodium ions flooding in through the channel pore produce a positive swing in the membrane potential that spreads over the surface membrane to the other end of the rod or cone cell. There, it stimulates calcium channels to open, enabling calcium ions to enter the cell and trigger the release of a transmitter that stimulates the next cell in the chain and the
reby tells the brain that it is dark.
Light-induced changes in the visual pigments activate a signalling cascade that leads to the destruction of cyclic GMP. As a consequence, the cyclic GMP-gated channel closes, switching off transmitter release and signalling ‘Light!’ The exquisite sensitivity of our vision derives from this complicated chain reaction, which constitutes a powerful amplification system. Many cyclic GMP molecules are destroyed for every photon captured, ensuring that enough channels close to switch off all transmitter release. As you will already have appreciated, the other remarkable thing about our rods is that they signal continuously when they are not being stimulated, being active in the dark and switched off by light. This feature is also thought to enhance our sensitivity to light.
Viagra (sildenafil) is widely used to counter impotence and enhance sexual performance, as the many junk emails I receive testify. But it also has a lesser-known effect. At high concentrations, it can literally turn your world blue. Men taking high doses of the drug sometimes find that it produces a transient mild blue tinge to their vision and an increased sensitivity to light. This is because Viagra has a weak inhibitory effect on the activity of the enzyme that destroys cyclic GMP in rod cells and so enhances their sensitivity to light. Because of the possibility that Viagra can interfere with colour vision, and impair the ability to distinguish blue and green lights on airport taxiways, the Federal Aviation Administration prohibits pilots from flying within six hours of using the drug.
The Spark of Life: Electricity in the Human Body Page 20
