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Field experiments with manually defoliated black alders ( Alnus glutinosa ) showed that defoliation affected herbivory by the major alder antagonist, the leaf beetle Agelastica alni . Herbivore damage increased with increasing distance to the defoliated tree, suggesting induced resistance not only on the damaged tree, but also on the neighbouring trees. The beetles also avoided leaves from the nearest neighbours for both feeding and oviposition in a laboratory assay, so the alders showed interplant resistance transfer. Natural enemies did not appear to shape this pattern, because the number of entomophagous arthropods and predator–prey ratios even increased with increasing distance to the defoliated tree. The numbers of all specialist, but not the generalist, herbivore species paralleled the increase in the attack of the specialist A. alni , supporting the view that specialists are more affected by plant resistance than generalists. Mechanisms causing this pattern, found in the field, were studied in more detail using biochemical analyses and further bioassays. Responses of alder leaves to herbivory of A. alni were shown to include ethylene emission and the release of a blend of volatiles with mono-, sesqui- and homoterpenes. Changes in leaf chemistry after herbivory included increases in the activity of oxidative enzymes (polyphenoloxidase, PPO, lipoxygenase, LOX, and peroxidase, POD) and proteinase inhibitors (PIs), and an increase in the phenolic contents of the leaves. Quantification of the endogenous jasmonic acid (JA) showed the activation of the octadecanoid pathway following herbivory. The active components in mediating a possible interplant signal transfer via airborne volatiles may have included ethylene, β -ocimene, 4,8-dimethylnona-1,3,7-triene (DMNT), and 4,8,12-trimethyltrideca-1,3,7,11-tetraene (TMTT). The incubation with volatiles resulted in an increase in the activity of catalase (CAT) and PIs (after MeJA application) and in an increase in the content of phenolics and PI activity (after ethylene application). Further evidence that airborne interplant communication may be important in the response of alder trees to beetle attack came from container experiments. In airtight chambers, unattacked leaves significantly increased the activity of proteinase inhibitors when they were associated with leaves previously attacked by beetle larvae. In conclusion, field experiments, bioassays in the laboratory as well as biochemical analyses suggest the existence of interplant resistance transfer in A. glutinosa , with airborne volatiles as a possible mechanism. However, the relative importance of airborne and possible soil-borne signals as well as unknown effects of intensified nutrient absorption of defoliated trees, possibly reducing foliage quality of undamaged neighbours, remains to be shown.

Primary cultures of pituitary cells from adult female rats were exposed to increasing concentrations (10(-13) to 10(-6)M) of selected prostaglandins (PGE2, PGF2 alpha, PGI2, 6-keto-PGF1 alpha, and sulproston). The release of luteinizing hormone (LH) by the pituicytes was monitored. In a second series of experiments, pituitary cells were treated with prostaglandins as described above and additionally challenged with a submaximal stimulus of gonadotrophin-releasing hormone (GnRH; 10(-9) M). The spontaneous LH-release in all prostaglandin treated cultures did not differ from the controls. When stimulated with 10(-9) M GnRH, the LH-release increased approx. six-fold in all cultures, with no difference between prostaglandin treated cells and the respective controls. Thus, the prostaglandins tested - at least at concentrations less than or equal to 10(-6) M - have neither a direct positive or negative effect on pituitary LH-release, nor do they enhance or decrease the LH-releasing effect of GnRH. These prostaglandins are probably not involved in the cellular regulation of LH-release by the pituicyte.

Primary pituitary cell cultures from adult female rats were incubated for 4 or 24 h with various concentrations of estradiol (E2) or the antiestrogens (AE) tamoxifen (TMX), 4-hydroxytamoxifen (OH-TMX), and clomiphene citrate (CC). The luteinizing hormone (LH)-response of these cultures to gonadotrophin releasing hormone (GnRH) was monitored. Treatment for 4 or 24 h with high concentrations (10(-5) M) of the AE significantly decreased the GnRH-induced LH-release by the gonadotrophs. The negative E2-effect, which is observed in this model after 4 h was enhanced and the positive E2-effect, which occurs after 24 h, was completely reversed into a negative effect by these high AE-concentrations. Treatment of pituitary cells with increasing concentrations of E2 (10(-13)-10(-6) M) or AE (10(-12)-10(-5) M) for 24 h led first to a dose dependent increase of the LH-response to 5 X 10(-10) M GnRH. At higher E2- or AE-concentrations this positive effect was lost, resulting in bell shaped dose-response curves. The following maximal effective concentrations (EDmax) were found: E2 = 10(-10) M, OH-TMX = 10(-9) M, CC = 10(-7) M, TMX = 10(-6) M. Incubation of pituitary cells for 24 h with concentrations of AE near their EDmax and stimulation with increasing concentrations (10(-11)-10(-7) M) of GnRH resulted in significant increases of LH-secretion over a wide range of GnRH-concentrations. It is concluded that AE possess marked intrinsic activities on pituitary LH-secretion: at extremely high concentrations they suppress the GnRH-induced release of the gonadotrophin. At lower concentrations they increase the pituitary LH-response to GnRH in a manner which is qualitatively indistinguishable from that of E2.