Eye, Brain, and Vision
Home
Book
Illusions
Biography
Publications
David Hubel's
Home
Book
Illusions
Biography
Publications
HMS
                                                                                    
       
   
 
Each eye has its position controlled by six separate muscles, two of which are shown here. These, the external and internal recti, control the horizontal rotation of the eyes, in looking from left to right or from close to far. The other eight muscles, four for each eye, control elevation and depression, and rotation about an axis that in the diagram is vertical, in the plane of the paper.


The initial stages of the mammalian visual system have the platelike organization often found in the central nervous system. The first three stages are housed in the retina;
the remainder are in the brain: in the lateral geniculate bodies and the stages beyond in the cortex.

To speak, as I do here, of separate stages immediately raises our problem with genealogy. In the retina, as we will see in Chapter 3, the minimum number of stages between receptors and the output is certainly three, but because of two other kinds of cells, some information takes a more diverted course, with four or five stages from input to output. For the sake of convenience, the diagram ignores these detours despite their importance, and makes the wiring look simpler than it really is. When I speak of the retinal ganglion cells as "stage 3 or 4", it's not that I have forgotten how many there are.
To appreciate the kind of transfer of information that takes place in a network of this kind, we may begin by considering the behavior of a single retinal ganglion cell. We know from its anatomy that such a cell gets input from many bipolar cells—perhaps 12,100, or 1000—and that each of these cells is in turn fed by a similar number of receptors. As a general rule, all the cells feeding into a single cell at a given stage, such as the bipolar cells that feed into a single retinal ganglion cell, are grouped closely together. In the case of the retina, the cells connected to any one cell at the next stage occupy an area i to 2 millimeters in diameter; they are certainly not peppered all over the retina.
Another way of putting this is that none of the connections within the retina are longer than about i to 2 millimeters.
If we had a detailed description of all the connections in such a structure and knew enough about the cellular physiology—for example, which connections were excitatory and which inhibitory—we should in principle be able to deduce the nature of the operation on the information. In the case of the retina and the cortex, the knowledge available is nowhere near what we require. So far, the most efficient way to tackle the problem has been to record from the cells with microelectrodes and compare their inputs and outputs. In the visual system, this amounts to asking what happens in a cell such as a retinal ganglion cell or a cortical cell when the eye is exposed to a visual image.
In attempting to activate a stage-3 (retinal ganglion) cell by light, our first instinct probably would be to illuminate all the rods and cones feeding in, by shining a bright light into the eye. This is certainly what most people would have guessed in the late 1940s, when physiologists were just beginning to be aware of synaptic inhibition, and no one realized that inhibitory synapses are about as plentiful as excitatory ones. Because of inhibition, the outcome of any stimulation depends critically on exactly where the light falls and on which connections are inhibitory and which excitatory. If we want to activate the ganglion cell powerfully, stimulating all the rods and cones that are connected to it is just about the worst thing we can do. The usual consequence of stimulating with a large spot of light or, in the extreme, of bathing the retina with diffuse light, is that the cell's firing is neither speeded up nor slowed down—in short, nothing results: the cell just keeps firing at its own resting rate of about five to ten impulses per second. To increase the firing rate, we have to illuminate some particular subpopulation of the receptors, namely the ones connected to the cell (through bipolar cells) in such a way that their effects are excitatory. Illuminating only one such receptor may have hardly any detectable effect, but if we could illuminate all the receptors with excitatory effects, we could reasonably expect their summated influences to activate the cell—
and in fact they do. As we will see, for most retinal ganglion cells the best stimulus turns out to be a small spot of light of just the right size, shining in just the right place. Among other things, this tells you how important a role inhibition plays in retinal function.


                                         VOLUNTARY MOVEMENT
Although this book will concentrate on the initial, sensory stages in the nervous system, I want to mention two examples of movement, just to convey an idea of what the final stages in the diagram on page 24 may be doing.
Consider first how our eyes move. Each eye is roughly a sphere, free to move like a ball in a socket. (If the eye did not have to move it might well have evolved as a box, like an old-fashioned box camera.) Each eye has six extraocular muscles attached to it and moves because the appropriate ones shorten.
How these muscles all attach to the eye is not important to us here, but we can easily see from the illustration that for one eye, say the right, to turn inward toward the nose, a person must relax the external rectus and contract the internal rectus muscles. If each muscle did not have some steady pull, or tone, the eye would be loose in its socket; consequently any eye movement is made by contracting one muscle and relaxing its opponent by just the same amount.
The same is true for almost all the body's muscle movements. Furthermore, any movement of one eye is almost always part of a bigger complex of movements. If we look at an object a short distance away, the two eyes turn in; if we look to the left, the right eye turns in and the left eye turns out; if we look up or down, both eyes turn up or down together.
    All this movement is directed by the brain. Each eye muscle is made to contract by the firing of motor neurons in a part of the brain called the brainstem. To each of the twelve muscles there corresponds a small cluster of a few hundred motor neurons in the brainstem. These clusters are called oculomotor nuclei. Each motor neuron in an oculomotor nucleus supplies a few muscle fibers in an eye muscle. These motor neurons in turn receive inputs from other excitatory fibers. To obtain a movement such as convergence of the eyes, we would like to have these antecedent nerves send their axon branches to the appropriate motor neurons, those supplying the two internal recti. A single such antecedent cell could have its axon split, with one branch going to one oculomotor nucleus and the other to its counterpart on the other side. At the same time we need to have another antecedent nerve cell or cells, whose axons have inhibitory endings, supply the motor neurons to the external recti to produce just the right amount of relaxation. We would like both antecedent sets of cells to fire together, to produce the contraction and relaxation simultaneously, and for that we could have one master cell or group of cells, at still another stage back in the nervous system, excite both groups. This is one way in which we can get coordinated movements involving many muscles Practically every movement we make is the result of many muscles contracting together and many others relaxing. If you make a fist, the muscles in the front of your forearm (on the palm side of the hand) contract, as you can feel if you put your other hand on your forearm. (Most people probably think that the muscles that flex the fingers are in the hand. The hand does contain some muscles, but they happen not to be finger flexors.) As the diagram on this page shows, the forearm muscles that flex the fingers attach to the three bones of each finger by long tendons that can be seen threading their way along the front of the wrist. What may come as a surprise is that in making a fist, you also contract muscles on the back of your forearm. That might seem quite unnecessary until you realize that in making a fist you want to keep your wrist stiff and in midposition: if you flexed only the finger flexor muscles, their tendons, passing in front of the wrist, would flex it too. You have to offset this tendency to unwanted wrist flexion by contracting the muscles that cock back the wrist, and these are in the back of the forearm. The point is that you do it but are unaware of it. Moreover, you don't learn to do it by attending 9 A.M. lectures or paying a coach. A newborn baby will grasp your finger and hold on tight, making a perfect fist, with no coaching or lecturing. We presumably have some executive-type cells in our spinal cords that send excitatory branches both to finger flexors and to wrist extensors and whose function is to subserve fist making. Presumably these cells are wired up completely before birth, as are the cells that allow us to turn our eyes in to look at close objects, without thinking about it or having to learn.

   
 
 
Contents
Next Page
When we flex our fingers by making a fist, the muscles responsible have to pass in front of the wrist and so tend to contract that joint too. The extensors of the wrist have to contract to offset this tendency and keep the wrist stiff.
 
 
 
 
 
Any one stage in the diagrams on the previous page and on this page consists of a two-dimen-sional plate of cells. In any one stage the cells may be so densely packed that they come to lie several cells deep; they nevertheless still belong to the same stage.


Next Page
Contents