The economic potential in Europe of five novel oilseed crops for applications within the chemical industry, particularly in paints and lubricants, was investigated within a multidisciplinary integrated research and development project. The entire production chain was subjected to a study. The following five oilseed crops were evaluated: Lunaria annua, Calendula officinalis, Dimorphotheca pluvialis, Lesquerella grandiflora and Euphorbia lagascae. It was concluded that Calendula was nearest to commercialization, and that Calendula oil showed excellent behaviour in several paint formulations. Lunaria and Euphorbia oils showed good lubricating performance, but feasible commercial production of these oils does not seem realistic in the near future.

Previous results have indicated that the median eminence (ME) plays a key role in the regulation of estrogen and dopamine receptors in the anterior pituitary (AP). Since 3H-labeled gamma-aminobutyric acid ([3H]GABA) receptors have been described in the pituitary as well as in the brain, the aim of the present work was to investigate whether those receptors are also under hypothalamic control. Ovariectomized adults rats were divided into two groups. In the first one, the ME was lesioned by an anodic current (MEL); the second group consisted of sham-operated controls. Animals were used 7-14 days thereafter to study [3H]GABA binding in a crude mitochondrial membrane fraction prepared from the anterior pituitary, the hypothalamic-preoptic suprachiasmatic area, or the frontoparietal cortex. Binding of [3H]GABA was a saturable process, with high affinity in all studied structures. In AP Scatchard analysis of the saturation curves indicated similar Kd values in sham and MEL rats; the maximal number of binding sites increased from 0.65 +/- 0.005 pmol/mg protein in controls to 1.05 +/- 0.006 pmol/mg protein in MEL rats (P less than 0.001). In the hypothalamus, Kd values were similar in both groups, but the maximum number of binding sites (Bmax) increased about 50% in MEL animals. In the frontoparietal cortex, Kd values were similar in control and lesioned animals; but the Bmax decreased by 40% after the lesion. Animals with lesions showed hyperprolactinemia and a reduction in serum levels of LH, FHS, and TSH. Thus, Kd values were of similar magnitude in all studied regions and were not altered by ME destruction. Bmax values in controls were higher in the cerebral cortex than in the hypothalamus and AP. After ME lesions, there was an increment of [3H]GABA binding in AP and hypothalamus and a reduction in cerebral cortex. The data indicate that the ME participates in the regulation of [3H]GABA binding in AP and also suggest that it plays a role in regulating GABA receptors in various regions of the brain.

Pharmacological manipulation of H1 and H2 histamine receptors clearly indicates their participation in control of anterior pituitary secretion by the brain. Of particular interest is the PRL-releasing effect of H2 histamine receptor blocking agents like metiamide and cimetidine. The aim of the present study was to determine whether serotoninergic pathways, which exert a well known releasing effect on PRL secretion, were involved in the PRL-releasing action of cimetidine. As our first approach, the PRL-releasing effect of cimetidine was determined in developing male and female rats. Cimetidine failed to increase PRL in rats of 1 and 4 days of age. From 12 days onwards, the drug was able to cause a PRL increment in both sexes. There was a significant release of PRL at 20 and 28 days of age, and the response was greater in male than in female rats. The ontogeny of the cimetidine action, both in timing and sex differences, showed a close similarity with the development of the serotoninergic control of PRL secretion, and it was in clear contrast with the maturation of other controlling mechanisms, dopaminergic and TRH. In a second set of experiments, adult male rats were used. Methysergide, a serotonin receptor blocker, used in a dose and given by a route so that it did not modify the basal level of PRL, was able to completely prevent the PRL release evoked by cimetidine. Administration of p-chlorophenylalanine, a drug which reduces serotonin synthesis, was followed by a significant decline in the indole content of a portion of the brain which included the brain stem, the hypothalamus, and the preopticsuprachiasmatic area; and by a blockade of the PRL-releasing effect of cimetidine. Treatment of adult male rats with cimetidine, methysergide, or serotonin did not modify serum LH. It is concluded that a major serotoninergic input is involved in the PRL-releasing effect of cimetidine.

The effect of the opiate antagonist naloxone on serum prolactin after treatment with serotonin, arginine vasotocin (AVT) or melatonin was studied in prepubertal and adult unanesthetized rats. Prolactin was quantified in blood samples withdrawn through an intrajugular silastic cannula from undisturbed ovariectomized adult rats. After taking a basal sample, animals were injected through the cannula with naloxone (0.8 mg/kg) and 5 min later with serotonin creatine sulphate (6.4 mg/kg), AVT (20 micrograms/kg), melatonin (4 mg/kg) or saline; new samples were taken 15 and 30 min thereafter. Injection of serotonin was followed by a 10-fold increase of prolactin levels 15 min later; this increase was drastically reduced, although not abolished, by pretreatment with naloxone. In animals injected with saline, AVT or melatonin, no significant changes in serum prolactin were observed. In a second group of experiments, 30 day-old female rats injected with serotonin creatinine sulphate (10 mg/kg, i.p.) exhibited a 6-fold increase in serum prolactin 15 min after injection; this increment was reduced but not abolished by pretreatment with naloxone (5 mg/kg, i.p.). It is postulated that the prolactin releasing effect of serotonin is mediated, at least in part, by an opioid receptor.