Popular Science Monthly/Volume 57/August 1900/Causes of Degeneration in Blind Fishes
| CAUSES OF DEGENERATION IN BLIND FISHES. |
By Professor CARL H. EIGENMANN,
INDIANA UNIVERSITY.
IT may now be profitable to take up the causes leading to the small degree of degeneration found in Chologaster, the degenerations of the eye in Amblyopsis, Typhlichthys and Troglichthys to a mere vestige, together with the total disappearance of some of the accessory structures of the eye, as the muscles.
In the outset of this consideration we must guard against the almost universal supposition that animals depending on their eyes for food are or have been colonizing caves, or that the blind forms are the results of catastrophes that have happened to eyed forms depending on their eyesight for their existence. This idea, so prevalent, vitiates nearly everything that has been written on the degeneration of the eyes of cave animals.
Another word of warning ought perhaps to be added. The process of degeneration found in the Amblyopsidæ need not necessarily be expected to be identical with the degeneration of the same organs in another group of animals, and, however much the conditions in one group may illuminate the conditions in another, cross-country conclusions must be guarded against.
The degeneration of organs ontogenetically and phylogenetically has received a variety of explanations:
1. The organ diminishes with disuse (ontogenetic degeneration)—Lamarck, Roux, Packard), and the effect of this disuse appears to some extent in the next generation (phylogenetic degeneration—Lamarck, Roux, Packard, Kohl).
2. Through a condition of panmixia the general average maintained by selection is reduced to the birth mean in one generation (ontogenetic—Romanes, Lankester, Lloyd Morgan, Weismann) to the greatest possible degeneration in succeeding generations (phylogenetic—Weismann), or but little below the birth average of the first generation (Weismann's later view, Romanes, Morgan, Lankester).
3. Through natural selection (reversed), the struggle of persons, the organ may be caused to degenerate either (A) by the migration of persons with highly developed eyes from the colony living in the dark (Lankester), or (B) through economy of weight and nutriment or liability to injury (phylogenetic purely—Darwin, Romanes).
4. Through the struggle of parts for room or for food an unused organ in the individual may be crowded (ontogenetic—Roux). This may lead to the development of the used organ as against the disused through a compensation of growth (Goethe, Saint-Hilaire, Roux); this ontogenetic result becomes phylogenetic through transmission of the acquired character (Roux), or is in its very nature phyloblastic (Kohl).
5. Through the struggle between soma and germ to produce the maximum of efficiency of the former with the minimum expenditure to the latter (ontogenetic and phylogenetic—Lendenfeld).
6. Through germinal selection, the struggle of the representatives of organs in the germ (ontogenetic and phylogenetic—Weismann).
The idea of ontogenetic degeneration is intimately bound up with the idea of phylogenetic degeneration. Logically we ought to consider first the causes of individual degeneration, and then the processes or causes that led to the transmission of this. Practically it is impossible to do so, because many of the explanations are general. Only No. 4 of the above may be taken in the ontogenic sense purely, though it was certainly also meant to explain phylogenetic degeneration. In many of the explanations of particular cases of degeneration more than one of the above principles are invoked, though only one was meant to be used. In most cases, however, the discussions of degeneration have been in general terms, without direct bearing on any specific instance of degeneration in all its details. It must be evident that such discussions can only by accident lead to right results.
By the Lamarckian ontogenetic degeneration is considered the result of lack of use and consequent diminished blood supply. The results of the diminution caused by the lack of use during one generation are transmitted in some degree to the next generation, which thus starts at a lower level. A continuation of the same conditions leads finally to the great reduction and ultimate disappearance of an organ.
No one, so far as I am aware, has succeeded in accounting for the degeneration of the eye by means of this view. Packard's[1] explanations are evidently a mixture of Lamarckism and Darwinism.
Packard says: "When a number, few or many, of normal-seeing animals enter a totally dark cave or stream, some may become blind sooner than others," some having the eye slightly modified by disuse, while others may have in addition physical or functional defects, especially in the optic nerves and ganglia. "The result of the union of such individuals and adaptation to their Stygian life would be broods of young, some with vision unimpaired, others with a tendency to blindness, while in others there would be noticed the first steps in degeneration of nervous power and nervous tissue." Packard evidently had invertebrates in mind. He clearly admits the cessation of selection or panmixia in that those born with defects may breed with the others. He supposes that the blind fauna may have arisen in but few or several generations, a supposition that may be applicable to invertebrates, but certainly is not to vertebrates. At first those becoming so modified that they can do without the use of their eyes would greatly preponderate over those 'congenitally blind.' "So all the while the process of adaptation was going on, the antennæ and other tactile organs increasing in length and in the delicacy of structures, while the eyes were meanwhile diminishing in strength of vision and their nervous force giving out, after a few generations—perhaps only two or three—the number of congenitally blind would increase, and eventually they would, in their turn, preponderate in numbers." Packard seems here to admit the principle of degeneration as the result of compensation of growth, the nervous force of the eye giving out with the increase of the tactile and olfactory organs. It is somewhat doubtful in what sense the term 'congenitally blind' is used, but it probably means born blind as the result of transmitted disuse, rather than blind as the result of fortuitous variation. The effects of disuse are thus supposed, through their transmission, to have given rise to generations of blind animals. The continued degeneration is not discussed.
Romanes maintained that the beginning of degeneration was due to cessation of selection, and continued degeneration to the reversal of selection and final failing of the power of heredity. Selection he supposed to be reversed because the organ no longer of use "is absorbing nutriment, causing weight, occupying space and so on, uselessly. Hence, even if it be not also a source of actual danger, economy of growth will determine a reversal of selection against an organ which is now not only useless, but deleterious." This process will continue until the organ becomes rudimentary and finally disappears.
Roux[2] attempted chiefly to explain degeneration in the individual. Degeneration is looked upon as the result of a struggle among the parts for (a) room and (b) food. Without doubting that both these principles are active agents in degeneration, it may be seriously doubted whether they are effective in the degeneration of the eyes in question. Certainly there can be no question of a struggle for room, for the position and room formerly occupied by the eye is now filled with fat, which can not have been operative against the eye. The presence of this large fat mass in the former location of the eye, the large reserve fat mass in the body, the uniformly good condition of the fish and the low vitality, which enables them to live for months without visible food, all argue against the possibility that the struggle for food between parts was an active agent in the degeneration of the eyes.
Kohl[3] considers that "Der Grund und direkter oder indirekter Anlass zum Eintreten der Entivickelungshemmung ist Lichtmangel." The method of operation of the lack of light he conceived to be as follows:
Other organs were developed to compensate for the disuse of the eye; and as the developmental force was used in the formation of these organs, each succeeding generation developed its eye less. The degeneration is thus explained as the result of a struggle of parts, although this term is nowhere used, acting through the principle of compensation. The same objections may be offered to this explanation of Kohl as to all his theoretical discussions—they are based on the assumption of conditions and processes that have no existence. The high development of 'compensating' organs is not primarily the result of the loss of the eye, but the high development of the former organs permitted the disuse and later degeneration of the latter. His whole process is a phylogenetic one, without a preceding ontogenetic one, though on this point he does not seem to be very clear himself, for on one page we are told that degeneration leads to retardation, and on another that degeneration is a consequence of retardation.
Ledenfeldt[4] endeavors to apply Roux's Kampf der Theile, with reversed selection, to explain the conclusions reached by Kohl on the processes and causes of degeneration. The struggle is represented as taking place between the germ and soma, the former endeavoring to keep the latter at the lowest efficient point as weapon for the germ. If a series of individuals get into the dark the organs of vision are of no advantage and reversed selection will bring about their degeneration. The saving in ontogeny appears first as a retardation and then as a cessation of development.
Weismann[5] more recently accepts the view of Romanes, Morgan and Lankester on the inadequacy of panmixia to explain the whole phenomena of degeneration, and in his 'Germinal Selection' rejects the idea of reversed selection, and suggests a new explanation for what Romanes attributed to the failure of heredity and the Lamarckians to transmission of the effects of disuse. The struggle of the parts of Roux has been crowded by him back to the representatives of these parts in the germ.
"The phenomena observed in the stunting, or degeneration, of parts rendered useless. . . show distinctly that ordinary selection, which operates by the removal of entire persons—personal selection, as I prefer to call it—can not be the only cause of degeneration, for in most cases of degeneration it can not be assumed that slight individual vacillations in the size of the organ in question have possessed selective value. On the contrary, we see such retrogressions effected apparently in the shape of a continuous evolutionary process determined by internal causes, in the ease of which there can be no question whatever of selection of persons or of a survival of the fittest—that is, of individuals with the smallest rudiments. The gradual diminution continuing for thousands and thousands of years and culminating in its final and absolute effacement" can only be accomplished by germinal selection. Germinal selection as applied to degeneration is the formal explanation of Romanes' failure of heredity through the struggle of parts for food. "Powerful determinants will absorb nutriment more rapidly than weaker determinants. The latter, accordingly, will grow more slowly and will produce weaker determinants than the former." If an organ is rendered useless, the size of this organ is no longer an element in personal selection. This alone would result in a slight degeneration. Minus variations are, however, supposed to rest "on the weaker determinants of the germ, such as absorb nutriment less powerfully than the rest. This will enable the stronger determinants to deprive them even of the full quantum of food corresponding to their weakened capacity of assimilation, and their descendants will be weakened still more. Inasmuch, now, as no weeding out of the weaker determinants of the hind leg [or eye] by personal selection takes place on our hypothesis, inevitably the average strength of this determinant must slowly but constantly diminish—that is, the hind leg [or eye] must grow smaller and smaller until it finally disappears altogether. . . . Panmixia is the indispensable precondition of the whole process; for, owing to the fact that persons with weak determinants are just as capable of life as those with strong. . . . solely by this means is a further weakening effected in the following generations."
This theory presupposes the complex structure of the germ plasm formulated by Weismann and rejected by various persons for various reasons. But granting Weismann the necessary structure of the germ plasm, can germinal selection accomplish what is claimed for it? I think not. Granting that variations occur about a mean, would not all the effects claimed for minus variations be counteracted I)y positive variations? Eye determinants, which, on account of their strength, secure more than their fair share of food, and thereby produce eyes that are as far above the mean as the others are below, and leave descendent determinants that are still stronger than their ancestry would balance the effect produced by weak-eye determinants. It is evident that a large, really extravagant development of the eye in such a fish as Chologaster would not effect the removal of the individual by personal selection; still less so in Amblyopsis, which not only lives in comparative abundance, but has lived for twenty months in confinement without visible food, and in which the eye is minute. It seems that all the admitted objections to degeneration by panmixia apply with equal force to germinal selection. This, however, would be changed were the effect of disuse admitted to affect the determinants, and this it seems Weismann has unconsciously admitted. So far we have considered germinal selection in the abstract only. All its suppositions are found to be but a house of cards when the actual conditions of degeneration are considered. We find that degeneration is not a horizontal process affecting all the parts of an organ alike, as Weismann presupposes, not even a process in the reverse order of phyletic development, but the more vital, most worked parts degenerate first with disuse and panmixia; the passive structures remain longest. The rate of degeneration is proportional to the past activity of the parts, and the statement that "passively functioning parts—-that is, parts which are not alterable during the individual life by function—by the same laws also degenerate when they become useless'* finds no basis in fact, and is an example of the inexact utterances abundant in the discussion of degeneration on which it is entirely unsafe to build lofty theoretical structures. As one example of the unequal degeneration we need only call attention to the scleral cartilages and the rest of the eye of Troglichthys rosæ.
All are agreed that natural selection alone is insufficient to explain all, if any, of the processes of degeneration. All either consciously or not admit the principle of panmixia, and all are now agreed that this process alone can not produce extensive degeneration. All are agreed that the important point is degeneration beyond the point reached by panmixia, the establishment of the degenerating process, whatever it may be, in the germ, or, in other words, the breaking of the power of heredity. It. is in the explanation of the latter that important differences of opinion exist.
Weismann attempts to explain the degeneration beyond the point which panmixia can reach by a process which not only is insufficient, even if all his premises are granted, to produce the desired result without the help of use transmission, but has as its result a horizontal degeneration which has no existence in fact.
Romanes supposed degeneration, beyond the point which may be reached by panmixia, to be the result of personal selection and the failure of the hereditary force. The former is not applicable to the species in question, and is denied by such an ardent Darwinist as Weismann to be applicable at all in accounting for degeneration. Moreover, the process as explained by Romanes would result in a horizontal degeneration which has no existence in fact. The second assumption, the failure of hereditary force, is not distinguishable, as Morgan has pointed out, from the effect of use transmission.
The struggle of parts in the organism has not affected the eye through the lack of room, since the space formerly occupied by the eye is now filled by fat and not by an actively functioning organ. It is not
| Figs. 1-6.—Photographs of the upper halves of the heads of specimens of nearly the same length under the same magnification, to show the gradual decrease of the eye. The dotted line leads to the eye in all cases. | |
| Fig. 1.—Zygonectes notatus. | Fig. 4.—Ambliopsis spelitus. |
| Fig. 2.—Chologaster papilliferus. | Fig. 5.—Troglichthys rosæ. |
| Fig. 3.— Chologasiter Agassizii. | Fig. 6.—Typhlichthys subterraneus. |
affected by the struggle for food, for stored food occupies the former eye space. It could only be affected by the more active selection of specific parts of food by some actively functioning organ. It is possible that this has in fact affected the degeneration of the eye. The theory explains degeneration in the individual, and implies that the effect in the individual should be transmitted to the next generation. This second part seems but the explanation of the workings of the Lamarckian factor.
The Lamarckian view—that through disuse the organ is diminished during the life of the individual, in part, at least, on account of the diminution of the amount of blood going to a resting organ, and that this effect is transmitted to succeeding generations—not only would theoretically account for unlimited progressive degeneration, but is the only view so far examined that does not on the face of it present serious objections. Is this theory applicable in detail to the conditions found in the Amblyopsidæ? Before going further, objections may again be raised against the universal assumption that the cessation of use and the consequent panmixia was a sudden process. This assumes that the caves were peopled by a catastrophe. But it is absolutely certain that the caves were not so peopled, that the cessation of use was gradual, and the cessation of selection must also have been a gradual process. There must have been ever-widening bounds within which the variation of the eye would not subject the possessor to elimination.
Chologaster is in a stage of panmixia as far as the eye is concerned. It is true the eye is still functional, but that the fish can do without its use is evident by its general habit and by the fact that it sometimes lives in caves. The present conditions have apparently existed for countless generations—as long as the present habits have existed—and yet the eye still maintains a higher degree of structure than reverse selection, if operative, would lead us to expect, and a lower than the birth mean of fishes depending on their eyes, the condition that the state of panmixia alone would lead us to expect. There is a staying quality about the eye with the degeneration, and this can only be explained by the degree of use to which the eye is subjected.
The results in Chologaster are due to panmixia and the limited degree of use to which the eye is put. Chologaster Agassizii shows the rapid diminution with total disuse.
The difference in the conditions between Chologaster and Amblyopsis, Typhlichthys and Troglichthys, is that in the former the eyes are still in use, except when living in caves; in the latter they have not been in a position to be used for hundreds of generations. The transition between conditions of possible use and absolute disuse may have been rapid with each individual after permanently entering a cave. Panmixia, as regards the minute eye, continued. Reversed selection, for economy, can not have affected the eye for reasons already stated. The mere loss of the force of heredity, unless this was caused by disuse, or the process of germinal selection, can not have brought about the conditions, because some parts have been affected more than others.
Considering the parts most affected and the parts least affected, the degree of use is the only cause capable of explaining the conditions. Those parts most active during use are the ones reduced most—viz., the muscles, the retina, optic nerve and dioptric appliances, the lens and vitreous parts. Those organs occupying a more passive position, e. g., the scleral cartilages, have been much less affected. The lens is one of the latest organs affected, not at all during use, possibly because during use it would continuously be in use. It disappears most rapidly
after the beginning of absolute disuse both ontogenetically and phylogenetically. All indications point to use and disuse as the effective agents in molding the eye. The process, however, does not give results with mathematical precision. In Typhlichthys subterraneus the pigmented layer is affected differently from that of Amblyopsis. The variable development of the eye muscles in different species would offer another objection if we did not know of the variable condition of these structures in different individuals. Chilton has objected to the application of the Lamarckian factor to explain degeneration, on account of the variable effects of degeneration in various invertebrates. But such differences in the reaction are still less explainable by any of the other theories.