§ 4.323 CONTROL OF THE SECRETION OF KINETIC HORMONES 161 



is fading out and being replaced by a return to secretion of 

 oestrone. Many theories have been put forward to explain these 

 effects of prolactin. The effects may perhaps be determined in 

 part by the state of the glands upon which the hormone acts, the 

 corpus luteum, for instance, only secreting when it has reached a 

 certain level of growth, under the action of the luteinizing hormone 

 LH. If this fails, as gestation ends, the corpus luteum may lose its 

 power to secrete, despite the continuing presence of LSH. 

 Equally the mammary glands do not grow enough to be able to 

 secrete until they have been stimulated by oestrone as well as 

 progesterone, and this does not begin until the end of pregnancy 

 is near. In this way, the action of prolactin might appear to be 

 switched from one type of gland to the other at the time of 

 parturition, but proof is lacking (Cowie and Folley, 1955). Such 

 a situation would not necessitate a control of LSH different from 

 that exerted by the brain over the other endocrinokinetic hormones ; 

 but what this is remains uncertain. 



One view is that these hypophysial gonadotrophins and also 

 ACTH and TSH (acting upon the adrenal cortex and the thyroid) 

 depend for their stimulation upon one or more chemical substances 

 that diffuse or circulate from the brain, rather than on nerve 

 impulses; but the evidence relates chiefly to the morphogenetic 

 effects of these hormones rather than to their endocrinokinetic 

 actions. Recent experiments on rats have shown that if the 

 adenohypophysis is removed from the brain and implanted in, say, 

 the kidney, it undergoes partial degeneration in about 4 weeks, 

 and ceases to secrete any of its hormones except LSH. By re- 

 implanting it in contact with the median eminence of the brain, 

 whence it originally came, the various cell types are induced to 

 differentiate and regain much of their secretory capacity. The 

 effect is first apparent on the growth-promoting fractions of 

 ACTH and TSH (§ 4.221), and later upon the morphogenetic 

 gonadotrophins, FSH and LH ; there is also some slight evidence 

 for the re-activation of the secretion-inducing action of TSH 

 (§ 4.221). Re-implanting the adenohypophysial tissue in contact 

 with other parts of the brain does not have this re-activating effect. 

 Since there is no question of renewed nervous connection, it is 

 claimed that the effect is due to a chemical cortical-releasing 



