RESUMO
Echinorhynchus veli (George and Nadakal, 1978), an acanthocephalid worm infesting the estuarine flat fish, Synaptura orientalis, was collected from the Veli lake, Kerala. The parasite was recovered from the intestine of the host fish. The detailed surface morphology was studied with the help of scanning electron microscope. The study revealed a cylindrical, medially swollen proboscis with a flat apex, backward directed hooks, each with smooth surface, broad base, pointed tip and an epidermal elevation at the point of insertion. A pair of sensory pits was seen at the base of the proboscis. The neck was well developed with densely packed epidermal micropores. Paired sensory pits were seen at the base of the neck and a collar between it and the trunk. The epidermis of the trunk has microtriches and micropores. The female genital pore was circular, and terminal in an elevated orifice. In male, the copulatory bursa was directed ventrally, with well-defined rim and several sensory papillae.
RESUMO
Prenatal ethanol exposure is associated with an increased incidence of depressive disorders in patient populations. However, the mechanisms that link prenatal ethanol exposure and depression are unknown. Several recent studies have implicated reduced brain-derived neurotrophic factor (BDNF) levels in the hippocampal formation and frontal cortex as important contributors to the etiology of depression. In the present studies, we sought to determine whether prenatal ethanol exposure is associated with behaviors that model depression, as well as with reduced BDNF levels in the hippocampal formation and/or medial frontal cortex, in a mouse model of fetal alcohol spectrum disorder (FASD). Compared to control adult mice, prenatal ethanol-exposed adult mice displayed increased learned helplessness behavior and increased immobility in the Porsolt forced swim test. Prenatal ethanol exposure was associated with decreased BDNF protein levels in the medial frontal cortex, but not the hippocampal formation, while total BDNF mRNA and BDNF transcripts containing exons III, IV or VI were reduced in both the medial frontal cortex and the hippocampal formation of prenatal ethanol-exposed mice. These results identify reduced BDNF levels in the medial frontal cortex and hippocampal formation as potential mediators of depressive disorders associated with FASD.