Male dogs were injected i.v. with 1 methyl-4-phenyl-1,2,3,6-tetrahydro- pyridine (MPTP) 2.5 mg/kg twice with an interval of 6 days. Twenty minutes after MPTP injection cyclohexyladenosine (CHA) 1 mg/kg i.v. was injected. Ten minutes after CHA injection the MTPT induced tremor, tachycardia and salviation ceased.

1. The response of TSH to TRH and the TRH content of the hypothalamus, following indomethacin, ibuprofen and paracetamol treatment, was measured in male rats. 2. Daily treatment of indomethacin (3 mg/kg)) for 3 days markedly reduced T4 concentration in the serum, the TRH content of the hypothalmus gland and inhibit Pituitary TSH response to the low T4 level in the blood. 3. Ibuprofen (12 mg/kg) and paracetamol (50 mg/kg) did not influence T4 or TSH levels of the serum nor the TRH content of the hypothalmus. 4. TRH-induced TSH secretion was not influenced by indomethacin, ibuprofen or paracetamol treatment.

The effect of intraperitoneally (i.p.) and intragastrically (i.g.) administered ethanol solution, and the influence of voluntary ethanol uptake (20% v/v) on adrenocortical activity of adult male rats was studied. Both i.p. and i.g. ethanol administration resulted in a significant activation of adrenocortical mechanisms, while voluntary ethanol uptake failed to induce elevation of serum corticosterone concentration. No difference was found in blood ethanol concentration among these groups. The responsiveness of adrenocortical mechanisms was also tested in rats which were given the free choice between ethanol solution (5% v/v) and tap-water for three weeks. Unavoidable electric foot-shocks, as stressor, resulted in an elevation of serum corticosterone concentration in control animals, but this response was found to be significantly reduced in chronically ethanol drinking rats.

Avoidance learning and pain sensitivity were studied in rats after chronic ethanol administration (1.1 to 1.7 g per kg b.w. in drinking water) at prenatal, adolescent and adult ages. The behavioural reactions were tested in adulthood by studying passive and active avoidance learning and the threshold of pain sensitivity to electric tail shock. Chronic ethanol consumption led to an impairment of avoidance learning and to hyperalgesia in each experimental series, although the alterations were greater in the prenatally treated groups. The experimental observations are discussed in the light of fetal alcohol syndrome.

Male rat thyroid glands were incubated for two hours in Krebs-Ringer bicarbonate buffer with different amounts of morphine and/or naloxone. Five micrograms/ml morphine produced a significant increase in the T4 concentration of incubation medium, and resulted in an accumulation of cAMP in the tissue. Naloxone did not change the T4 release but its incubation with morphine prevented the morphine-induced changes. Similarly, naloxone inhibited the morphine-induced accumulation of cAMP in the thyroid tissue.

[4,5(3)H]L-Leucine incorporation into proteins in placental slices of alcoholic and normal women was measured in the first and second trimesters of pregnancy, and on the day of birth. In this study, alcoholic women were defined as women who drink daily at least 150 ml, calculated as 100% ethanol. Leucine incorporation into proteins was significantly decreased in alcoholic women compared with normal placentas: 72% in the first, 70% in the second trimester, and 82% in term placenta. The data indicate that not only can chronic maternal alcohol consumption induce defects in protein synthesis, but also that heavy alcohol ingestion, even during the beginning of pregnancy, could be toxic for the human placenta and development of the fetus.

Experiments were designed to demonstrate that morphine may exert a direct short-term effect on the hormone release of the thyroid gland. Groups of male rats were injected with single doses of 1, 5 and 10 mg/kg morphine, or with 2 mg/kg naloxone and in addition with morphine 30 min after naloxone and/or with naloxone 30 min after morphine pre-treatment. The rats were killed by decapitation 15, 30 and 60 min after the injection and serum was collected and stored for subsequent TSH, T4 and T3 radioassays. All doses of morphine resulted in an increase of serum T4 and T3 concentrations 15 and 30 min after the injection, with a tendency to return to control levels by the 60 min samples. Serum TSH concentrations were to suppressed by administration of 5 and 10 mg/kg but not by 1 mg/kg morphine. Naloxone treatment did not increase the T4 and T3 concentrations; however, serum TSH was elevated in the 15 min sample. Naloxone pre-treatment inhibited the morphine induced release of T4 and T3 into the serum, but naloxone administration after morphine pre-treatment failed to prevent the increase of T4 and T3 secretion. These data suggest that morphine may exert a short-term stimulatory effect on the thyroid gland with a concomitant inhibitory action on the hypothalamo-pituitary TSH system.

The TRH, pyroglutamyl-histidyl-proline amide was the first of the hypothalamic releasing factors to be purified and identified (

FEBS LettersVolume 110, Issue 1 p. 62-64 Full-length articleFree Access Study of proton pumps by phospholipid-impregnated millipore filters A. Moran, A. Moran Faculty of Medicine and Department of Biology, Technion - Israel Institute of Technology, Haifa, IsraelSearch for more papers by this authorE. Tal, E. Tal Faculty of Medicine and Department of Biology, Technion - Israel Institute of Technology, Haifa, IsraelSearch for more papers by this authorE. Eytan, E. Eytan Faculty of Medicine and Department of Biology, Technion - Israel Institute of Technology, Haifa, IsraelSearch for more papers by this authorN. Nelson, N. Nelson Faculty of Medicine and Department of Biology, Technion - Israel Institute of Technology, Haifa, IsraelSearch for more papers by this author A. Moran, A. Moran Faculty of Medicine and Department of Biology, Technion - Israel Institute of Technology, Haifa, IsraelSearch for more papers by this authorE. Tal, E. Tal Faculty of Medicine and Department of Biology, Technion - Israel Institute of Technology, Haifa, IsraelSearch for more papers by this authorE. Eytan, E. Eytan Faculty of Medicine and Department of Biology, Technion - Israel Institute of Technology, Haifa, IsraelSearch for more papers by this authorN. Nelson, N. Nelson Faculty of Medicine and Department of Biology, Technion - Israel Institute of Technology, Haifa, IsraelSearch for more papers by this author First published: January 28, 1980 https://doi.org/10.1016/0014-5793(80)80023-8Citations: 11AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume110, Issue1January 28, 1980Pages 62-64 ReferencesRelatedInformation

From the Department of Orthopaedics and Traumatology, Sick Fund Hospital Meir, Kfar-Saba, Israel, and the Sackler Medical School, University of Tel-Aviv, Israel

Use of a cerebral electro-therapy (CET) device, called PENTA, for weather-sensitive patients is described here. It applies 6–45 V D.C. monopolar triangular shaped pulses of 0.75 ms duration, allowing an input of 0–600 mA mean current via 2 frontal and 1 indifferent occipital electrode. To avoid adaptation it is programmed to two alternating frequencies of 20 and 65 Hz. Its successful application to 15 cases of disturbed neuro-endocrine regulation in weather sensitivity is reported. It resulted in cures for 3–12 months, depending on the type of weather sensitivity treated. The mechanism of CET treatment may be due to a bio-feedback on the limbicsystem, involving hypothalamic and pituitarian hormones. The normalising effects described here were followed up by neurohormone urinalysis of 17-KS, 17-OH, adrenaline, noradrenaline, serotonin, 5-HIAA, histamine and thyroxine.—This method proved itself as a valuable and objective tool for psychosomatic complaints due to weather sensitivity.

The correlation between 3′,5′, c-AMP levels, TSH content and secretion of separated thyrotropic cells was studied. Incubation of the separated cells with 1, 10 and 100 ng of TRH does not change the 3′,5′, c-AMP levels, despite the significant rises of the TSH level. Dibutyryl c-AMP causes rise in TSH content, with no indication of its secretion. PGE2 10−5 increased 3′, 5′, c-AMP levels with no change in the content or secretion of TSH in separated thyrotropic cells.

A method for the enrichment of live thyrotrophic pituitary cells is described. Pituitary glands of young male rats were removed into Earle's solution and dispersed in a 0.1% trypsin solution containing 0.5% bovine serum albumin, pH 7.2. Nylon fibres (25 microgram) were used for the separation of the thyrotrophic cells, by stringing them across a plastic frame which fitted a plastic Petri dish containing the cell suspension. The fibres were washed with light petroleum (b.p. 60--80 degree C) and carbon tetrachloride, hydrolysed with 3 M-HCL for 30 min at room temperature and washed with distilled water and phosphate-buffered saline (pH 7.2). The fibres were treated with thyrotrophin releasing hormone (TRH) alone or in the presence of soluble carbodiimide solution. After incubation for 1 h at room temperature, the fibres were transferred to a new Earle's medium and cells were released from the fibres by plucking them with a needle. The separated thyrotrophic cells were identified by radioimmunoassay and by electron microscopy. Using the above-mentioned methods, enrichment of thyrotrophic cells was obtained. Thus, the amounts of TSH, prolactin, LH and GH released, during 2 h of incubation, by 1.5 x 10(6) unseparated cells were 6.8 +/- 0.65, 4.1 +/- 0.47, 4.8 +/- 0.52 and 5.2 +/- 0.68 microgram respectively, while the same number of purified thyrotrophic cells released 76.1 +/- 0.42, 1.2 +/- 0.3, 0.6 +/- 0.35 and 1.6 +/- 0.22 microgram of the same hormones (means +/- S.E.M.).