The effect of herbicides applied to V3 soybeans on race 3 soybean cyst nematode (SCN) reproduction and glyceollin production in roots was measured. Soybeans were treated postemergence with 1 × and 2 × rates of herbicides plus adjuvants or with adjuvants alone, and SCN development was measured. Acifluorfen, bentazon, lactofen, crop oil concentrate (COC), and nonionic surfactant (NIS) applications reduced SCN egg population densities 50 to 60% compared with the untreated control 4 and 8 wk after application. The SCN reproduction on plants treated with fluazifop-P, sethoxydim, and imazethapyr was similar to the untreated control. Crop oil concentrate or NIS applications alone were as effective as acifluorfen, bentazon, or lactofen applications for reducing SCN reproduction. However, no additive effect of adjuvant-herbicide combinations was observed, nor did herbicide rate affect SCN reproduction. Treatments reduced SCN reproduction only when applied to soybeans and had no effect on SCN reproduction when applied directly to the soil. No treatment stimulated SCN reproduction relative to the untreated control. Soybeans treated with COC, NIS, acifluorfen, and bentazon also had more glyceollin detected than the untreated control. Herbicide-induced glyceollin production may have increased the resistance of soybean to SCN.

Electrical stimulation in pigeons of the input from the medial subdivision of the nucleus of Edinger-Westphal (EWM) to the choroidal neurons of the ipsilateral ciliary ganglion, which themselves have input to the choroidal blood vessels of the ipsilateral eye, increases choroidal blood flow (ChBF). Since the EWM receives input from the contralateral suprachiasmatic nucleus (SCN), which in turn receives contralateral retinal input, the present study sought to determine if activation of the SCN by microstimulation or by retinal illumination of the contralateral eye would also yield increases in ChBF in that same eye. Using laser Doppler flowmetry (LDF) to measure ChBF, we found that electrical activation of the contralateral SCN by 100-Hz anodal pulse trains yielded increases in ChBF that were stimulus related and proportional to the stimulating current. These increases in ChBF elicited by the SCN stimulation were accompanied by increases in choroidal volume (vasodilation), but not by increases in systemic blood pressure. Furthermore, the increases could be blocked reversibly by lidocaine injection into the EWM. These results suggest that the increases in ChBF in the eye contralateral to the SCN stimulation were specifically mediated by the SCN-EWM pathway. Retinal illumination with a fiber optic light source was also found to increase ChBF in the illuminated eye, and these effects too could be blocked reversibly with lidocaine injection into the EWM or permanently by the EWM lesion. Control studies confirmed that the light-elicited increases were mediated by increases in choroidal volume (i.e. vasodilation), were not accompanied by systemic blood pressure increases, and were not artifactually generated by transocular illumination of the LDF probe. Thus, the SCN-EWM circuit may be involved in regulating ChBF in response to the level of retinal illumination and/or the visual patterns falling on the retina.