muscle produces lactic acids during activity, it has been suggested
that acids are among the “fatigue substances” with
which muscle poisons itself when deprived of circulating blood.
Muscles when active seem to pour into the circulation substances
which, of unknown chemical composition, are physiologically
recognizable by their stimulant action on the respiratory nervous
centre. The effect of the fatigue substances upon the contraction
of the tissue is manifest especially in the relaxation process.
The contracted state, instead of rapidly subsiding after discontinuance
of the stimulus, slowly and only partially wears
off, the muscle remaining in a condition of physiological
“contracture.” The alkaloid veratrin has a similar effect
upon the contraction of muscle; it enormously delays the
return from the contracted state, as also does epinephrine, an
alkaloid extracted from the suprarenal gland.
Nervous System.—The work of Camillo Golgi (Pavia, 1885 and onwards) on the minute structure of the nervous system has Neuron led to great alteration of doctrine in neural physiology. It had been held that the branches of the nerve cells, that is to say, the fine nerve fibres—since all nerve fibres are nerve cell branches, and all nerve cell Neuron Theory. branches are nerve fibres—which form a close felt-work in the nervous centres, there combined into a network actually continuous throughout. This continuum was held to render possible conduction in all directions throughout the grey matter of the whole nervous system. The fact that conduction occurred preponderantly in certain directions was explained by appeal to a hypothetical resistance to conduction which, for reasons unascertained, lay less in some directions than in others. The intricate felt-work has by Golgi been ascertained to be a mere interlacement, not an actual anastomosis network; the branches springing from the various cells remain lifelong unattached and unjoined to any other than their own individual cell. Each neuron or nerve cell is a morphologically distinct and discrete unit connected functionally but not structurally with its neighbours, and leading its own life independently of the destiny of its neighbours. Among the properties of the neuron is conductivity in all directions. But when neurons are linked together it is found that nerve impulses will only pass from neuron A to neuron B, and not from neuron B to neuron A; that is, the transmission of the excited state or nervous impulse, although possible in each neuron both up and down its own cell branches, is possible from one nerve cell to another in one direction only. That direction is the direction in which the nerve impulses flow under the conditions of natural life. The synapse, therefore, as the place of meeting of one neuron with the next is called, is said to valve the nerve circuits. This determinate sense of the spread is called the law of forward direction. The synapse appears to be a weak spot in the chain of conduction, or rather to be a place which breaks down with comparative ease under stress, e.g. under effect of poisons. The axons of the motor neurons are, inasmuch as they are nerve fibres in nerve trunks, easily accessible to artificial stimuli. It can be demonstrated that they are practically indefatigable—repeatedly stimulated by electrical currents, even through many hours, they, unlike muscle, continue to respond with unimpaired reaction. Peripheral Fatigue. Yet when the muscular contraction is taken as index of the response of the nerve, it is found that unmistakable signs of fatigue appear even very soon after commencement of the excitation of the nerve, and the muscle ceases to give any contraction in response to stimuli applied indirectly to it through its nerve. But the muscle will, when excited directly, e.g. by direct application of electric currents, contract vigorously after all response on its part to the stimuli (nerve impulses) applied to it indirectly through its nerve has failed. The inference is that the “fatigue substances” generated in the muscle fibres in the course of their prolonged contraction injure and paralyse the motor end plates, which are places of synapsis between nerve cell and muscle cell, even earlier than they harm the contractility of the muscle fibres themselves. The alkaloid curarin causes motor paralysis by attacking in a selective way this junction of motor nerve cell and striped muscular fibre. Non-myelinate nerve fibres are as resistant to fatigue as are the myelinate.
The neuron is described as having a cell body or perikaryon
from which the cell branches—dendrites and axon—extend,
and it is this perikaryon which, as its name implies,
contains the nucleus. It forms the trophic centre of
the cell, just as the nucleus-containing part of every
cell is the trophic centre of the whole cell. Any part of the cell
Solidarity
of Neuron.
cut off from the nucleus-containing part dies down: this is as
true of nerve cells as of amoeba, and in regard to the neuron
it constitutes what is known as the Wallerian degeneration.
On the other hand, in some neurons, after severance of the axon
from the rest of the cell (spinal motor cell), the whole nerve
cell as well as the severed axon degenerates, and may eventually
die and be removed. In the severed axon the degeneration
is first evident in a breaking down of the naked nerve
filaments of the motor end plate. A little later the breaking
down of the whole axon, both axis cylinder and myelin sheath
alike, seems to occur simultaneously throughout its entire
length distal to the place of severance. The complex fat of
the myelin becomes altered chemically, while the other components
of the sheath break down. This death of the sheath as
well as of the axis cylinder shows that it, like the axis cylinder,
is a part of the nerve cell itself.
In addition to the trophic influence exerted by each part of the neuron on its other parts, notably by the perikaryon on the cell branches, one neuron also in many instances influences the nutrition of other neurons. When, for instance, the axons of the ganglion cells of the retina are severed by section of the optic nerve, and thus their influence upon the nerve cells of the visual cerebral centres is set aside, the nerve cells of those centres undergo secondary atrophy (Gadden’s atrophy). They dwindle in size; they do not, however, die. Similarly, when the axons of the motor spinal cells are by severance of the nerve trunk of a muscle broken through, the muscle cells undergo “degeneration”—dwindle, become fatty, and alter almost beyond recognition. This trophic influence which one neuron exerts upon others, or upon the cells of an extrinsic tissue, such as muscle, is exerted in that direction which is the one normally taken by the natural nerve impulses. It seems, especially in the case of the nexus between certain neurons, Tonic Activity of Neurons. that the influence, loss of which endangers nutrition, is associated with the occurrence of something more than merely the nervous impulses awakened from time to time in the leading nerve cell. The wave of change (nervous impulse) induced in a neuron by advent of a stimulus is after all only a sudden augmentation of an activity continuous within the neuron—a transient accentuation of one (the disintegrative) phase of the metabolism inherent in and inseparable from its life. The nervous impulse is, so to say, the sudden evanescent glow of an ember continuously black-hot. A continuous lesser “change” or stream of changes sets through the neuron, and is distributed by it to other neurons in the same direction and by the same synapses as are its nerve impulses. This gentle continuous activity of the neuron is called its tonus. In tracing the tonus of neurons to a source, one is always led link by link against the current of nerve force—so to say, “up stream”—to the first beginnings of the chain of neurons in the sensifacient surfaces of the body. From these, as in the eye, ear, and other sense organs, tonus is constantly initiated. Hence, when cut off from these sources, the nutrition of the neurons of various central mechanisms suffers. Thus the tonus of the motor neurons of the spinal cord is much lessened by rupture of the great afferent root cells which normally play upon them. A prominent and practically important illustration of neural tonus is given by the skeletal muscles. These muscles exhibit a certain constant condition of slight contraction, which disappears on severance of the nerve that innervates the muscle. It is a muscular tonus of central source consequent on the continual glow of excitement in the spinal motor neuron, whose outgoing end plays upon the muscle cells, whose ingoing
