Presence of NMDA Receptor mRNA in the Anterior Pituitary of the Female Rat: Steroid Modulation and Changes during Gonadotropin Surge Induction

N-methyl- -aspartate (NMDA) receptors have been implicated in the regulation of anterior pituitary hormone secretion. A part of the regulatory effect of NMDA on pituitary hormone release could be due to a direct regulatory effect at the pituitary. The present study examined whether mRNA for the NMDA receptor is expressed in the anterior pituitary of female rats. Additionally, the effect of different steroids on pituitary NMDA receptor mRNA levels was also examined. Using Northern analysis, hybridization of the NMDA R1 cDNA probe to female rat anterior pituitary RNA yielded a 4.0-kb band, demonstrating the presence of the mRNA for the NMDA receptor in the pituitary. In the ovariectomized immature rat, estradiol treatment was found to significantly suppress pituitary NMDA receptor mRNA levels. Conversely, pituitary NMDA receptor mRNA levels were elevated by the treatment of estrogen-primed ovariectomized rats with progesterone. The increase of pituitary NMDA receptor mRNA levels by progesterone occurred at a time when progesterone induces an LH surge. Using the pregnant mare serum gonadotropin-primed immature rat, pituitary NMDA receptor mRNA levels were found to increase in a progressive manner throughout the afternoon of proestrus to reach a peak at 2000 h—the time of peak preovulatory LH surge levels. In conclusion, the present study demonstrates that the mRNA for the NMDA receptor is expressed in the anterior pituitary. The NMDA receptor mRNA in the pituitary is regulated by steroids with peak levels paralleling gonadotropin surge expression. As a whole, the present study provides further evidence that the pituitary could be an important site of action for neuroendocrine effects of excitatory amino acids.     

Vitamin A status in children with asthma

Low vitamin A levels have been found in a number of diseases in children. The aim of this study was to examine the vitamin A status in children with asthma and to correlate the changes with severity of disease. Serum levels of vitamin A, retinol‐binding protein (RBP), and albumin were estimated in 35 asthmatic children (24 males) in the age group of 2–12 years (mean 5.89 years) and 29 controls (19 males). Both study and control groups were similar with respect to age, sex, and overall nutritional status. Twenty‐four children in the study group (68.6%) had moderate to severe persistent asthma and eight children had mild persistent asthma. Only three patients suffered from mild intermittent asthma. Vitamin A levels in children with asthma (mean ± SD 22.14 ± 5.38 µg/dl) were found to be significantly lower than their controls (mean ± SD 27.54 ± 4.83 µg/dl) (p = 0.0001). Age, age of onset of asthma, and gender had no correlation with serum vitamin A levels. Low serum vitamin A levels (< 20 µg/dl) were observed four times more commonly in the study group (28.6%) than controls (6.9%). Severity of asthma had a negative correlation with serum vitamin A levels (r = ? 0.61, p = 0.0001). Children with severe persistent asthma had markedly low serum vitamin A levels (mean ± SD 13.42 ± 5.19 µg/dl) as compared with mild intermittent asthma (mean ± SD 24.61 ± 2.32 µg/dl). Therapeutic trials are needed to prove whether low vitamin A levels contribute to asthma severity and the clinical utility of vitamin A supplementation in asthmatic children.     

Lung mitochondria in experimental asbestosis

Alterations in lung mitochondria were followed in guinea pigs at different periods after a single intratracheal injection of chrysotile dust. Cytochrome c oxidase and succinic dehydrogenase activities showed gradual increase after 90 days, whereas monoamine oxidase remained unaffected throughout the study. There was an increase in glutamate dehydrogenase activity in postmitochondrial as well as in mitochondrial fractions, the latter being accompanied by decreased latency of the enzyme. Mitochondria from asbestotic lung appeared to be more swollen than in normal animals at and after 90 days of exposure. There were fluctuations in the contents of different phospholipids as a result of asbestosis. Beyond 90 days, collagen and mucopolysaccharides also increased. The results confirm the contention that pulmonary mitochondria are among the major target sites in asbestosis.