1104 



SUBMAMMALIAN VERTEBRATES 



by salt therapy show atrophy of the testes 

 (Herrick and Torstveit, 1938; Herrick and 

 Finerty, 1940) . The atrophy may be caused 

 by the general metabolic disturbances re- 

 sulting from the adrenalectomy. Taber, Sal- 

 ley and Knight (1956) prevented develop- 

 ment of the rudimentary gonad of sinistrally 

 ovariectomized hens (poulards) by pair 

 feeding them with adrenalectomized pou- 

 lards. Both groups showed similar rudimen- 

 tary gonad development. Leroy and Benoit 

 (1954), who maintained their adrenalecto- 

 mized drakes without special measures, 

 found no testicular atrophy. This observa- 

 tion supports the view that testicular 

 atrophy is correlated with the general meta- 

 bolic disturbances resulting from adrenalec- 

 tomy. 



Chester Jones (1957) has reviewed the 

 literature on the interrelation between testes 

 and testicular hormones and size of the ad- 

 renal. The data suggest that long-term cas- 

 tration effects (8 to 11 months after opera- 

 tion) may result in a decrease in adrenal 

 size, whereas short term effects (42 days 

 after operation) result in an increase in 

 adrenal size, which can be jircvented by 

 testosterone injections. 



Administration of adrenal hormones has 

 resulted in contradictory results. Desoxycor- 

 ticosterone acetate (Link and Nalbandov, 

 1955; Boas, 1958) caused atrophy of the 

 germinal epithelium, edema, and decrease in 

 comb size of the fowl. Corticosterone in- 

 creased testicular size and stimulated sper- 

 matogenesis in domestic mallard drakes (Le- 

 roy, 1952) and roosters (Conner, 1959) and 

 an increase in comb size in the latter (Leroy, 

 1952) . Dulin (1955 ) , on the other hand, used 

 three different doses of corticosterone and 

 failed to find stimulation of testes or comb, 

 but he observed decreased testes and comb 

 size at the highest dose used. Cortisone 

 caused a slight but significant increase in 

 comb size of capons. The dose used by Leroy 

 (1952) and the highest dose used by Dulin 

 (1955) are essentially the same, but the 

 length of treatment was shorter in Leroy 's 

 experiment. The most important difference 

 between the two sets of experiments was 

 probably in the age of the birds used. In 

 Leroy's experiment the cockerels were 4 

 months old, whereas Conner (1959) used 



6-week-old cockerels, and Dulin's cockerels 

 were from 20 to 40 days of age. One is re- 

 minded of the similarity between these re- 

 sults and those of the experiments of Kuma- 

 ran and Turner (1949c) in which androgen 

 did not stimulate spermatogenesis at the 

 younger age, but did stimulate it after the 

 formation of spermatocytes had occurred. 

 It seems possible, therefore, that cortisone 

 stimulates the transformation of one type 

 of germ cells (spermatocytes?) to another 

 (spermatids?). This interpretation is not 

 consistent with Leroy's conclusion (1953) 

 that cortisone promotes testicular matura- 

 tion in young cockerels. Unfortunately, 

 Leroy gave no evidence to support his state- 

 ment. Cortisone (Leroy, 1953), like andro- 

 gen (Kumaran and Turner, 1949b), fails to 

 prevent estrogen-induced inhibition of the 

 testes and of comb size in the fowl. 



An observation by Chester Jones (1957) 

 on the relationship between testes and ad- 

 renals should be noted. He observed that 

 the survival of adrenalectomized drakes 

 was inversely related to testicular size at 

 the time of operation. Castrated drakes re- 

 quired lower doses of corticosteroids for sur- 

 vival than did intact drakes. The explana- 

 tion given was that testosterone secretions, 

 by increasing the metabolism of the birds, 

 might increase the requirement for the cor- 

 ticosteroids. 



The effect of epinephrine on the gon- 

 ads has not been studied in great detail. 

 Wheeler, Searcy and Andrews (1942) ob- 

 served that the injection of epinephrine 

 into sexually mature fowl interfered with 

 spermatogenesis and caused damage to the 

 nuclei of the germ cells. In English spar- 

 rows adrenaline caused regression of the 

 testes and disappearance of the black pig- 

 ment from the beak. Adrenaline also pre- 

 vented the gonad stimulation by gonado- 

 trophins (Perry, 1941) but Wolfson (1945) 

 could not confirm this finding for j uncos, 

 Junco oreganus, nor could Lyman (1942) 

 for pigeons. 



4. The Thyroid Gland 



The thyroid gland is required for' normal 

 development of the testes and for the nor- 

 mal response of secondary sex organs and 

 secondary sex characteristics to androgen. 



