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Introduction Recently, we identified a novel hypothalamic dodecapeptide, Ser-Ile-Lys-Pro-Ser-Ala-Tyr-Leu-Pro-Leu-Arg-Phe-NH 2 , in the brain of Japanese quail ( Coturnix japonica ; Tsutsui et al. 2000 ). This avian neuropeptide
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SUMMARY
Bilateral lesions produced by electrocoagulation in the basolateral and medial amygdaloid nuclei, subtotal amygdalectomy as well as implants of actinomycin D and cholesterol were all found to have profound effects on brain ribonucleic acid (RNA) base percentages and ratios. The most consistent effect was that on the pituitary and was produced by all treatments. Generally, the hypothalamus and frontal cortex showed varying effects due to the treatments, but the cerebellum uniformly showed no responses to the various treatments. Lesions placed in the medial amygdaloid complex and subtotal amygdalectomy had the greatest effect in changing the RNA base ratio. The bases adenosine monophosphate (AMP), cytidine monophosphate (CMP), guanosine monophosphate (GMP), and uridine monophosphate (UMP) were found to be the most affected. The newly synthesized RNA was found to be rich in UMP and deficient in AMP and CMP when compared to normal animal brain tissue. The assumption is made that lesions in the amygdala bring about an activation or stimulation of a genomic nature to produce specific RNA for a particular neural function.
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Cytosol prepared from rat brains perfused with saline possesses saturable macromolecular components which form unstable complexes with [3H]progesterone in vitro. The components can be distinguished from the serum protein corticosteroid-binding globulin (CBG) which also binds progesterone. Unlike CBG, the cytosol components did not bind corticosterone and were more unstable in the presence of Sephadex LH-20 than was CBG. Furthermore, the components were precipitated by a concentration of ammonium sulphate in which CBG is soluble. Unlabelled progesterone and testosterone competed equipotently with [3H]progesterone, and 5α-pregnane-3,20-dione and deoxycorticosterone competed to a lesser extent, whereas oestradiol, corticosterone and 11β-hydroxy-pregn-4-en-3,20-dione were not bound. Although present in all brain tissues examined and in uterine and anterior pituitary tissue, the saturable binding was not detectable in cytosols from the spleen or diaphragm.
Complete exchange occurred in the incubation at 0 °C between [3H]progesterone and unlabelled progesterone and the saturable binding sites and the reaction attained apparent equilibrium within 2 h at this temperature. An incubation temperature of 30 °C resulted in an almost complete loss of saturable binding. Scatchard plots obtained from binding isotherms were curvilinear and yielded at least three dissociation constants (K d), two of higher affinity (K d ≃ 10−8 mol/l) and one about sixty times lower.
From these results it is concluded that rat brain cytosol possesses progesterone-selective components which fulfil some of the criteria required for steroid hormone receptors.
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Maternal thyroid hormone (TH) crosses the placenta and is postulated to regulate fetal brain development. However, TH-dependent stages of fetal brain development remain to be characterised. We have therefore compared the levels of several neuronal and glial cytoskeletal proteins in fetal brains from normal (N) and partially thyroidectomised (TX) rat dams by immunoblotting. Pregnancies were studied both before and after the onset of fetal TH secretion, which occurs at 17.5 days gestation (dg) in the rat. Maternal hypothyroidism disrupted fetal growth, so that fetal body and brain weights were reduced near term. Vimentin expression was unaffected, however, indicating normal acquisition of neuronal and glial precursor cells. Fetal brain levels of glial fibrillary acidic protein (GFAP) were reduced at 21 dg, suggesting delayed astrocytic differentiation, although regression analysis demonstrated appropriate GFAP levels for brain weight. Levels of alpha-internexin, the earliest neurofilament protein expressed in fetal brain were reduced at 16 dg in TX dams, but increased at 21 dg. The ontogeny of neurofilament-L was also perturbed in these pregnancies, with deficient levels apparent at both 16 and 21 dg. These effects on neuronal cytoskeletal proteins were unrelated to fetal brain growth retardation. These findings confirm that maternal hypothyroidism disrupts early fetal brain development. Early disturbances in neuronal differentiation are not corrected by the onset of fetal TH secretion. Such disturbances may contribute to the neurological damage observed in children born to hypothyroxinaemic mothers.
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The distribution of immunoreactive neurones and fibres was studied in rat brain using an antiserum to rat prolactin. Neurones containing the immunoreactive material were localized in the arcuate, ventromedial, premamillary, supraoptic and paraventricular nuclei of the hypothalamus. Immunoreactive nerve fibres were widely distributed within the brain. No differences were observed in labelling between male and female rats, or as a consequence of hypophysectomy.
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ABSTRACT
Oestrogen-2/4-hydroxylase activity was measured in whole brain, thalamus, amygdala, hypothalamus and pituitary gland of lactating rats and in whole brain of rats on different days of the oestrous cycle. Enzyme activity was increased in whole brain and in each of the brain regions examined (with the exception of the amygdala) in lactating rats. This increase in enzyme activity was associated with an increase in serum prolactin levels. During the oestrous cycle, enzyme activity in whole brain was higher on metoestrus and dioestrus than on pro-oestrus and oestrus. The decrease in enzyme on pro-oestrus was associated with an increase in both serum oestradiol and prolactin levels. These results are consistent with the hypothesis that changes in oestrogen-2/4-hydroxylase activity are associated with changes in prolactin and oestradiol secretion and may play a regulatory role in reproduction.
J. Endocr. (1985) 107, 191–196
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Introduction The hypothalamic–pituitary–thyroid (HPT) axis regulates metabolism and growth, reproduction, and brain development in vertebrates. Similarly, in fish, thyroid hormones (THs) have been demonstrated to regulate growth ( Huang et al
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ABSTRACT
The effects of maternal hypothyroxinaemia during pregnancy on subsequent brain biochemistry in progeny was studied. Normal and partially thyroidectomized rat dams were mated and progeny allowed to grow to adulthood. Brain regions (cerebellum, medulla, midbrain, cerebral cortex and paleocortex) were dissected out and the activities of various cell marker enzymes were determined, along with cholesterol contents.
Maternal hypothyroxinaemia was without effect on body weight, brain weight or thyroid status of adult progeny. Oligodendroglial marker enzyme activities were altered in progeny from thyroidectomized dams. 2′,3′-Cyclic nucleotide 3′-phosphohydrolase was decreased in the medulla (by 37%) and midbrain (by 32%). 5′-Nucleotidase was also diminished in the same brain regions, by 33% in the medulla and by 35% in the midbrain. In contrast, oleate esterase was increased (by 39%) in the paleocortex. Although these enzymes are putatively involved in myelin metabolism, no changes were observed in the concentration of a major myelin lipid (cholesterol). The activity of β-d-glucuronidase (a general neuronal marker) was decreased (by 30%) in the paleocortex, whereas N-acetyl-β-d-galactosaminidase (a general glial marker) was unchanged in all brain regions.
In summary, maternal hypothyroxinaemia has irreversible effects on brain biochemistry in adult progeny. The damage is parameter-selective and brain region-specific, analogous to the pattern of neurological damage seen in offspring born to hypothyroxinaemic women in iodine-deficient endemias.
Journal of Endocrinology (1990) 124, 387–396
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Introduction Brain-derived neurotropic factor (BDNF) signals through the TrkB (or NTRK2) receptor to mediate neuronal survival, differentiation, and plasticity ( Lewin & Barde 1996 , McAllister et al . 1999 ), and its effects in the brain are
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variety of maladaptive syndromes such as anxiety and various forms of depressive disorders ( Sapolsky et al . 2000 ). In addition to regulating its own gene expression, GR also controls expression of other brain genes, such as corticotrophin
