性腺刺激ホルモンの分泌調節における脳内アミンの役割に関する研究

II.ラツト中脳部における神経切断の性腺刺激ホルモン分泌に及ぼす影響

抄録

Although it is well known that the limbic-preoptic-hypothalamic system regulates gonadotropin secretion from the pituitary gland, there have been few studies on the involvement of the midbrain in the control of ovulation. Therefore, in the present study, an investigation was made to determine which portion of the midbrain is involved in the control of ovulation and the proestrous surge of gonadotropins and prolactin (PRL) by placing various transections in the rat brain, and their effects were evaluated by comparison with those under other hormonal conditions.
Wistar male rats and females showing two consecutive regular 4 day estrous cycles were used for the experiments. Blood samples were taken through an indwelling atrial cannula without anesthesia, and serum LH, FSH and PRL were measured by radioimmunoassay. Bilateral lesions in the ventral tegmental area (VTA) were made by applying 2.5 mA of DC current for 20 sec through a platinum electrode. In order to cut the neural element in the three different portions of the midbrain, a small knife of bayonet shape was used.
The following results were obtained :
(I) Bilateral lesions in the VTA made in the morning of proestrus, which destroyed more than 50% of the bilateral sides of the VTA, blocked ovulation in 5 out of 10 animals (P<0.05), delayed the peak of the proestrous surge of FSH and PRL by 2 hrs, and significantly lowered serum LH, FSH and PRL levels at 1800 hr of proestrus. Similarly, incomplete lesions in the VTA partially inhibited the gonadotropin surge whereas they failed to block ovulation.
(II) Midline transections placed in the morning of proestrus, which cut the neural tissue in the ventromedial portion of the midbrain (VMT), were effective in blocking ovulation in 9 out of 10 animals, and in the ovulation-blocked rats, the proestrous surge of LH, FSH and PRL was completely eliminated. Midline transections, which cut the neural tissue in the dorsal portion of the midbrain, neither blocked ovulation nor affected serum gonadotropins and PRL levels at any time. Bilateral transections (LT), which interrupted the neural tissue located laterally to that transected by VMT, failed to block ovulation. Following this type of transection, rather significantly higher serum LH levels were observed at 1400, 1600 and 2000 hr of proestrus as compared to those of the sham transected control group.
(III) VMT made in the evening of proestrus had no effect on the secondary rise in serum FSH which occurred at midnight between proestrus and estrus. Furthermore, VMT did not affect the postcastration rise in serum LH and FSH in males which was observed at 24 hr after orchidectomy. Although some ovariectomized or orchidectomized animals with VMT showed pulsatile. LH release with decreased frequency and high amplitude, complete disappearance of pulsatile release could be observed in only 1 out of 5 animals.
The findings described above showed that the ventromedial portion of the midbrain contains the neural structure indispensable for the occurrence of the proestrous surge of gonadotropins and PRL. The specificity of the effects of VMT was demonstrated by the failure of VMT to have any effects on the other conditions of gonadotropin secretion. In view of the fact that LT, which is considered to interrupt a greater portion of the ventral noradrenergic pathway projecting to the preoptic area and the hypothalamus than does VMT, was without effect in blocking ovulation, it is possible that the essential neural element is not noradrenergic. Furthermore, the neural mechanism for the secondary rise in serum FSH was shown to be different from that for the proestrous surge of FSH which is associated with LH release, and it was also suggested that the lateral area to the essential neural structure for ovulation contains an inhibitory mechanism for LH release.