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Spontaneous alar plate hyperplasia in the chick Embryo.

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Spontaneous Alar Plate Hyperplasia in the
Chick Embryo
WESLEY J. BIRGE
Department of Zoology, University of Illinois, Urbana
A great many "deficiency" experiments ponents of the neuroepithelium may be(extirpations, etc.) have been carried out come hyperplastic depends largely on the
on the developing neural tube in various developmental stage of the embryo at the
vertebrate groups (Birge and Hillemann, time of surgery. Due to a differential and
'53; Detwiler, '47; Harrison, '47; Holtzer, progressive loss of mitotic potential on the
'51; Kallh, '55; Wenger, '50, and many part of these cell types, structural defiothers). In many such cases, patterns of ciencies in the reconstituted lateral half of
regenerative growth have been described. the cord become increasingly more exSuch regulative development invariably tensive as successively older larvae are
stems from a hyperplasia of some neigh- used for the operation. When such deboring tissue components. Accordingly, in ficiencies are instituted prior to the early
order to learn more of the mechanisms of neurula period, complete regulation usually
regulative development, and to approach results. By the early neurula period, howan analysis of the factors governing cellu- ever, the cells of the motor outer mantle
lar proliferation, it is essential that we primordium begin to lose their regulatory
broaden our understanding of hyperplastic ability, and corresponding deficiencies retissue growth. With special reference to sult in the basal plate of the regulating side
the developing neural tube, it is desirable of the cord. The alar plate cells that give
that we have as much detail information rise to the sensory outer mantle begin to
as possible regarding (1) an identification lose their regenerative potentiality by midof those areas or divisions which possess dle neurula stages, and by stages 33-40,
regulatory potentialities, ( 2 ) the develop- the primordial cells of the internuncial
mental periods during which such po- masses become restricted similarly.
tentialities can be exhibited, and ( 3 ) the
Unfortunately, much less is known
factors (physiological and mechanical) re- about the regulatory potentialities of the
sponsible for the initiation and mainte- incipient spinal cord of the chick embryo.
nance of a hyperplastic condition.
Wenger ('50) has described this region of
As a result of the studies of Detwiler the early chick neural tube as a rigid
('44, '46, '47), Harrison ('47), Holtzer mosaic system which lacks any significant
('51), and many others, the regulatory regenerative ability. To the contrary, Watcapacity of the amphibian neural tube is terson and Fowler ('53) have indicated
well understood. In Ambystoma, when that the cord region of the chick neural
hemilateral segments are surgically re- tube possesses a distinct capacity for removed from the neural plate or early gulative development, at least under cerneural tube, they are generally recon- tain conditions.
The study presented herein concerns an
stituted, at least in large measure. This
results from a hyperplasia which develops analysis of a neural tube anomaly found
in the intact half of the neural tube seg- to occur in a series of chick embryos. Inment involved, and a cross-migration of volved in this anomaly is a spontaneous
cells from the intact side into the deficient alar plate hyperplasia which is very simiarea. According to Holtzer ('51), who per- lar in nature to the hyperplastic growth
formed hemilateral extirpations on the that often follows induced neural tube
brachial cord region of Ambystoma, the deficiencies. An interpretation of this dedegree to which the various cellular com- velopmental condition will contribute to a
135,
136
WESLEY J. BIRGE
better understanding of (1) the regulatory capacity of the chick neural tube, and
( 2 ) the circumstances which lead to the
onset of alar plate hyperplasia.
MATERIALS AND METHODS
Five chick embryos were utilized in this
study, each one bearing the previously
mentioned anomaly in some portion of the
cord region of the neural tube. All 5 embryos had been previously sacrificed at the
third day of development, serially sectioned, and stained in Harris' hematoxylin.
Except for the spinal cord anomaly, these
embryos were normal in other respects.
Four of the subjects were of the White
Leghorn variety and the remaining embryo
was of the New Hampshire Red strain.
These specimens have been collected by
the author over the period of the last 4
years from both personal and teaching
slide collections of early chick embryonic
materials. The methods used in determining the extent of alar plate hyperplasia
were essentially the same as those previously described by Birge and Hillemann
( ' 5 3 ) . For the sake of convenience, the
5 embryos considered in this study have
been designated as cases A1 through A5.
OBSERVATIONS
laterally so as to meet and fuse with the
medial surface of the adjacent neural tube
wall at a level near or just dorsal to the
lower border of the alar plate area (fig. 1).
Also, these two abnormal inward folds
fused together where they adjoined each
other in the midline of the tube. It also
seems that a medially directed longitudinal
fold or ingrowth has occurred along each
side of the neural tube just below the
twinned portion of the cord. This pattern
of foldings, which is illustrated in figure
1, has resulted in the formation of a tripartite neurocoel.
As indicated above, this abnormal folding process was fed by a hyperplasia which
developed in the dorsal half of the cord,
and this condition resulted in the partial
twinning of the dorso-lateral plates. In
embryo A' (fig. 1) the anomaly extends
between the 19th and 26th pairs of
somites. Throughout this region, the tissue
volume of the dorsal half of the cord averages 87% above normal and the frequency
of mitotic figures is 81% above normal.
Concerning embryos Aa (fig. 2), A3 (fig. 3),
A4 (fig. 4 ) and A5, the anomalous regions
are located between somite pairs 23 to 28,
17 to 24, 18 to 22 and 16 to 20 respectively. In the same order, the tissue volume
of the dorsal half of the anomalous cord
segments averages above normal by 51%,
3 8 % , 30% and 78% and the frequency of
division figures exceeds the normal frequency by 6 0 % , 25%, 37%, and 81%.
As indicated above, this study involves
a description and an analysis of a developmental anomaly found to occur in the
cord region of the chick neural tube. The
conditions found to exist in these 5 emDISCUSSION AND CONCLUSIONS
bryos are very similar except for the locaAs
a
result of this study and the previous
tion and the extent of the hyperplastic tissue growth. This anomaly is perhaps best work of Watterson and Fowler ( ' 5 3 ) , it is
described as a partial twinning of approxi- evident that significant degrees of hypermately the dorsal half of certain neural plastic alar plate development can occur,
tube segments. It has involved primarily at least under certain developmental condithe alar-roof plate system, as the presump- tions, in the cord region of the early chick
tive basal and floor plates are relatively nor- neural tube. Furthermore, such developmal. Apparently this condition arose, at ment does not necessarily have to follow
least in part, through the abnormal closing or be initiated by actual mechanical imof the neural folds. Instead of fusing in pairment of the neural tube, but it may
the usual manner, the dorsal margins of arise spontaneously as in the 5 cases cited
the folds appear to have flexed medially here. Most likely, this alar plate twinning
and ventrally during the late neural fold was a result of the incomplete closure of
stage and, as a consequence, they grew the neural folds. It is becoming increasdown into the cavity of the developing ingly evident that if the folds are prevented
neural tube. With further hyperplastic from properly fusing together by anomaldevelopment, each of these two abnormal ous growth or if the lateral halves of the
folds apparently flexed around ventro- early neural tube are separated by experi-
ALAR PLATE HYPERPLASIA IN T H E CHICK
mental means, the alar plate areas tend to
undergo an “overgrowth” which, in many
cases, leads to a partial or complete twinning of these areas.
Support for this hypothesis is found in
the work of Watterson and Fowler (’53).
They separated the lateral halves of sections of the early chick cord by surgical
means and blocked the halves apart with
transplanted somites. They noted, in most
cases, the occurrence of excessive proliferation (hyperplasia) in the alar plates
of such regions. This regulative growth
resulted in the partial or nearly complete
twinning of the alar plate derivatives on
each side of the cord, a condition very
similar to the anomalous twinning reported here. Watterson (’54) and Fowler
(’53) have also demonstrated that merely a
longitudinal slit made in the roof plate of
the early chick neural tube regularly produces a hyperplastic condition in the adjacent alar plates. Regardless of whether
such alar plate twinning is experimentally
produced or effected by anomalous malclosure of the neural folds, the mechanisms initiating the hyperplastic growth are
probably the same. Evidently, the alar
plate regions possess a greater growth potential under such conditions than they do
during normal neural tube development.
It is undoubtedly this extra growth potential which is drawn upon in regulative
neural tube development such as that described in the chick hindbrain (Birge and
Hillemann, ’53; Kallh, ’55) and midbrain
(Birge. in press). Following the hemilateral ablation or removal of one alar
plate in these brain regions during early
tube stages, a substantial regulatory hyperplasia develops in the intact alar plate.
This regulatory hyperplasia is, more than
likely, identical in many respects to that
which occurs during alar plate twinning.
With regard to the various studies considered above, it is evident that the early
alar plates hold a greater or less restricted
growth potential when they are partially
or completely separated from one another
than they do under normal developmental
circumstances. Not only does this indicate
some very interesting aspects of neural
tube growth control, it also reveals a remarkable capacity for defect regulation on
behalf of the early chick neural tube.
137
SUMMARY
This study concerns an analysis of
several cases of spontaneous alar plate
twinning found to exist in cord segments
of early chick neural tubes. In such instances, the alar plate on each side of the
cord has been partially duplicated as the
result of hyperplastic growth. It seems
evident that this alar plate hyperplasia was
initiated by the anomalous mal-closure of
the neural folds. These data indicate that
if the neural folds are prevented from properly fusing during neurulation, the alar
plate areas tend to undergo an “overgrowth” which usually leads to the partial
twinning of these areas. Evidently, the
alar plates possess an increased (or less
restricted) growth potential under such
conditions. It is also apparent from this
study that such neural tube hyperplasia
may result without being preceded by
surgery or other forms of induced mechanical injury. Also, pertinent discussion is
rendered on the relationship of the spontaneous alar plate hyperplasia described
herein to various cases of post-operative
hyperplasia.
LITERATURE CITED
Birge, W. J., and H. H. Hillemann 1953
Metencephalic development and differentiation
following experimental lesions in the early
chick embryo. J. Exp. Zool., 124: 545-569.
Detwiler, S. R. 1944 Restitution of the medulla
following unilateral excision in the embryo.
Ibid., 96: 129-142.
1946 Midbrain regeneration i n Amblystoma. Anat. Rec., 94: 229-237.
1947 Restitution of the branchial region
of the cord following unilateral excision in the
embryo. J. Exp. Zool., 104: 53-68.
Fowler, I. 1953 Responses of the chick neural
tube i n mechanically produced spina bifida.
Ibid., 123: 115-151.
Harrison, R. G. 1947 Wound healing and reconstitution of the central nervous system of
the amphibian embryo after removal of parts
of the neural plate. Ibid., 106: 27-83.
Holtzer, H. 1951 Reconstitution of the urodele
spinal cord following unilateral ablation. Part
I. Chronology of neuron regulation. Ibid., 117:
523-557.
KalICn, B. 1955 Regeneration i n the hindbrain
of neural tube stages of chick embryos. Anat.
Rec., 123: 169-182.
Watterson, R. 1954 Development of the glycogen body of the chick spinal cord. IV. Effects
of mechanical manipulation of the roof plate
at the lumbosacral level. J. Exp. Zool., 125:
285-330.
138
WESLEY J. BIRGE
Watterson, R. L., and I. Fowler
1953 Regula-
tive development in lateral halves
of
neural tubes. Anat. Rec., 117: 773-804.
chick
Wenger, E. 1950 An experimental analvsis of
relations between parts of the branchial-spinal
cord of the embryonic chick. J. Exp. Zool..
114: 51-85.
PLATE 1
EXPLANATION OF FIGURES
1 Cross section through the cord region displaying alar plate twinning i n embryo A1
Arrows indicate the folding pattern of the neuroepithelium. x 250.
2
Section through the cord region of embryo A2 showing alar plate duplication.
3
Section showing partial alar plate twinning in embryo A3.
4
Section showing partial alar plate duplication in embryo A4. x 250.
x 250.
x 250.
ALAR PLATE HYPERPLASIA IN THE CHICK
Wesley J. Birge
PLATE 1
139
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