The distribution of monoamines (catecholamines and serotonin) in fishes has been previously studied by immunohistochemistry of both the monoamines themselves and their biosynthetic enzymes. But the distribution of neurons containing aromatic L-amino acid decarboxylase, an enzyme involved in the biosynthesis of both catecholamines and serotonin, has up to now not been investigated. In order to improve knowledge about the localization of aromatic L-amino acid decarboxylase, neurons containing this enzyme were mapped immunohistochemically in the goldfish brain. Furthermore, neurons bearing aromatic L-amino acid decarboxylase immunoreactivity have been compared with those containing tyrosine hydroxylase and serotonin immunoreactivities. Our results show that distribution of aromatic L-amino acid decarboxylase immunoreactivity generally coincides with that of tyrosine hydroxylase and serotonin. Nevertheless, the presence of nine D cell groups (containing aromatic L-amino acid decarboxylase but lacking both catecholamines and serotonin) and six groups of neurons which are aromatic L-amino acid decarboxylase-immunonegative but contain tyrosine hydroxylase, and might produce L-DOPA, have been revealed. The occurrence of both D cell groups and presumptive L-DOPA neurons in goldfish brain is discussed in relation to similar findings in fish and mammalian brain.
The administration of 100 i.u. ovine prolactin to male crested newts has been shown to block spermatogenesis by producing a zone of degeneration in spermatogonia which are about to change into primary spermatocytes (Mazzi, Vellano & Toscano, 1967).Since signs of inhibited function of adenohypophysial type II basophils, which may be regarded as producing follicle-stimulating hormone (FSH) (Mazzi, Peyrot, Anzalone & Toscano, 1966), had been observed in prolactin-treated animals, it was assumed that the antigonadal effect of prolactin was secondary to the inhibition of FSH-producing cells. To test this hypothesis, experiments involving the simultaneous injection of prolactin and FSH were carried out.On 13 June 1967, 40 male newts in full spermatogenetic activity were divided into four groups of ten. The first group served as controls; the second group received 100\p=n-\120 i.u. prolactin (ovine, NIH-P-S7) in 0\m=.\6 % NaCl solution, divided into four injections of 0\m=.\1ml. given every other day. The third group received prolactin plus 0\m=.\5 mg. FSH (ovine, NIH-FSH-S3) in the same solution. The fourth group was injected with saline solution only. The animals were killed 48 hr. after the last in¬ jection. The testes were fixed in Sanfelice's fluid, cut at 7 p and stained with light gr een-safranin.In both the non-injected controls and the newts injected with the solvent alone, spermatogenesis was normal, without a trace of degeneration in the late spermatogonia. In seven out of the ten prolactin-treated animals the expected antigonadal effect was observed, with the formation of a zone of degeneration. Two animals had atrophie testes containing proliferating protogonia and spermatogonia.In the ten animals injected with prolactin plus FSH, spermatogenesis seemed quite normal and there was no degeneration among late spermatogonia : the spermatogonia showed a higher mitotic rate than those of the controls.These results make it very likely that in the male-crested newt as in the domestic fowl (Bates, Riddle & Lahr, 1937 ;Nalbandov, 1946 ; Lofts & Marshall, 1958) prolactin exerts its antigonadal effect by inhibiting the adenohypophysial FSH-producing gonadotrophs.
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