EYE FIELD OPERATIONS 50I 



5. The dark and light-adjusted enucleated (and normal) larvae may be transferred 

 to the opposite environment (dark to light and vice versa) to determine the 

 degree of adaptibility (adjustment) in respect to a definite time interval. 

 (Detwller & Copenhaver in 19'+2 state that dark-adapted eyeless larvae are pale 

 "but darken in moderate lighting, while dark-adapted normal larvae tend to be- 

 come lighter colored In moderate lighting. ) 



The conclusions from this set of observations should relate both the growth rate and 

 to the pigmentary responses of eyeless larvae. 



THE EXPERIMENTAL PRODUCTION OF CYCLOPIA 



Adelmann (I936) states: "The hope of one day attaining an adeq^uate understanding of 

 cyclopia is considerably strengthened by two important considerations, first, the fact that 

 the anomaly may be experimentally produced with considerable ease, and secondly, the fact 

 that experimentally produced cyclopean monsters exhibit essentially the same features as 

 those spontaneously arising." Stockard ( I907 to I9IO) produced cyclopean fish with vari- 

 ous concentrations of NaCl, LlCl, NaOH, and anyl alcohol. Others have used acetone, and 

 butyric alcohol and even physical variables. Amphibian cyclopean monsters have been pro- 

 duced by treating the eggs with lithium chloride, ethyl alcohol, chloralhydrate (LePlat, 

 1919, Cotronei, 1922, Guareschi, 195*+, and Adelmann, 193*+) phenol and chloretone ( Lehmann, 

 1935). 



Cyclopia can also be produced by surgical interference with early cleavage stages up 

 to gastrulation, by constriction (Spemann, 190^), and by excision of parts of the archen- 

 teric roof (Mangold, I93I). 



The experimental procedure is in general to expose the early blastula of any Amphibian 

 to from 0.2^ to l.O'jt LlCl for periods up to 2k hours, then returning them to normal medium 

 whereupon many of the surviving embryos will develop cyclopia. The effect is essentially 

 one of vegetalization. Since the procedure is described In detail under "The Chemical 

 Separation of Growth and Development" it will not be further discussed here. 



DISCUSSION : 



The embryonic eye is made up of two major parts, each of which originates from the 

 ectoderm. The optic vesicle is the first to develop, being an evagination from the dien- 

 cephalon. When this brain ectoderm makes contact with the overlying head ectoderm it 

 "induces" the thickening of this ectoderm to form the lens placode. (See exception under 

 the term "double assurance" in the Glossary.) This placode then invaginates to form a 

 lens vesicle which becomes incorporated into the developing optic cup. The head ectoderm 

 (from which the lens was derived) then closes over the lens to form the ectodermal portion 

 of the (transparent) cornea. In the meantime mesenchyme (mesoderm) invades the whole eye 

 structure, to give rise to the blood vessels, connective tissue, and finally the muscles 

 of the eye. 



That the mesentodermal substrate has something to do with the development of the eye 

 field has been demonstrated (Adelmann, 1957) • This eye-field is determined prior to the 

 closure of the neural folds, as proven by excision and transplantation experiments. 



In the heteroplastic and homotopic eye transplantations involving A. punctatum, 

 A. tigrinum, and A. mexicanum (the axolotl) Harrison (I929) has demonstrated that the 

 velocity of growth and, to a certain extent, the ultimate size of the eyes are due to 

 Intrinsic (genetic) factors of the donor tissues. The tigrinum eyes in punctatum hosts 

 often exceeded the donor control eyes, and the punctatum eyes in tigrinum hosts often 

 were smaller than the control eyes, explained by Harrison as due to factors in the circu- 

 lating medium of the host which affected the growth rate of the graft. The form and func- 

 tion of the grafted eyes appeared to be quite normal. Even the intrinsic tendencies of 

 the lens and/or the optic vesicles were maintained when in grafts, when they were from 

 different genetic sources. In all cases where the optic nerve failed to connect, there 

 was marked hypoplasia of the wall of the midbrain on the opposite side. 



