Loss of the central rachis and synaptonemal complexes during meiotic prophase in female Ascaris lumbricoides var. suum after exposure to albendazole

Albendazole, a benzimidazole anthelmintic, interferes with the formation of microtubules and inhibits meiosis in the nematode Ascaris lumbricoides var. suum. Pigs treated with albendazole had worms in their uteri that had a severely deteriorated central rachis, complete loss of synaptonemal complexes and irregular oocytes at meiotic prophase I. The nuclear matrix and envelope were poorly formed and there was formation of accessory nuclei. This study represents the first examination of the changes in meiotic nuclear architecture and meiotic chromosomes after exposure to albendazole. These results provide the basis for the loss of fecundity in A. suum after exposure to albendazole resulting in control in the population of the parasitic nematode.

Expression of RESP18 in Peptidergic and Catecholaminergic Neurons

We examined the expression of regulated endocrine-specific protein of 18-kD (RESP18) in selected peptidergic and catecholaminergic neurons of adult rat brain. In the hypothalamic paraventricular, supraoptic, and accessory nuclei, RESP18 mRNA was highly expressed in neurons immunostained for oxytocin and vasopressin. RESP18 mRNA was also highly expressed in paraventricular nucleus neurons immunostained for corticotropin-releasing hormone, thyrotropin-releasing hormone, and somatostatin. RESP18 mRNA was expressed in POMC cells of the arcuate nucleus, in neuropeptide Y cells of the dorsal teg-mental nucleus, lateral reticular nucleus, and hippocampus, and in brainstem catechola-minergic neurons. RESP18 mRNA expression was high in all paraventricular and arcuate neurons, but RESP18 protein was detectable in the perikarya of a subset of these neurons, suggesting an important post-transcriptional component to the regulation of RESP18 expression. RESP18 antisera immunostained perikarya but not axon fibers or terminals. Sub-cellular fractionation of homogenates of several hypothalamic nuclei identified RESP18 protein in fractions enriched in endoplasmic reticulum. The presence of 22- and 24-kD RESP18 isoforms in the neural lobe of the pituitary indicated that some RESP18 protein exited the endoplasmic reticulum. The post-transcriptional regulation of RESP18 expression and localization of RESP18 protein primarily to the endoplasmic reticulum suggests that RESP18 plays a regulatory role in peptidergic neurons.