An immunogold investigation of the distribution of GABA and glycine in nerve terminals on the somata of spherical bushy cells in the anteroventral cochlear nucleus of guinea pig.

Spherical bushy neurons in the anteroventral cochlear nucleus receive glutamatergic primary terminals from the cochlear nerve and terminals of noncochlear (i.e. nonprimary) origin, many of which colocalize gamma-aminobutyric acid (GABA) and glycine. Here the relationship between GABA and glycine in these terminals has been investigated using postembedding immunogold labelling. A significant negative correlation was found between the density of terminal labelling for GABA and for glycine in four guinea pigs. Terminals could be divided into three categories, GABA-only, glycine-only, or colocalizing depending on whether they had a significantly higher labelling density for either amino acid than the primary terminals. The overall labelling density in all four animals was significantly greater for GABA in GABA-only terminals than colocalizing ones but similar for glycine in both. Within the terminals, the labelling density over synaptic vesicles, nonvesicular regions of cytoplasm and mitochondria was also investigated. No significant difference was detected in the labelling density of vesicles compared with nonvesicular regions for either amino acid. However, a significant difference was found between the overall labelling density over mitochondria and nonvesicular regions for both. There was also significantly more mitochondrial GABA labelling in GABA-only terminals compared to colocalizing terminals but mitochondrial glycine labelling was similar in glycine-only and colocalizing terminals. Thus the level of GABA is higher in single than in colocalizing terminals, particularly in the mitochondria, but similar for glycine in both. It is possible therefore that the presence of glycine affects the level of GABA in the nonprimary terminals but that the presence of GABA does not affect the level of glycine.

Enhanced sandfly attraction to Leishmania-infected hosts.

We report that hamsters infected with Leishmania infantum are more attractive to female sandflies in bioassays. Entrained odours from infected animals were shown by gas chromatography to contain peaks absent from uninfected individuals. Implications of enhanced transmission, potential for developing novel diagnoses and the significance to epidemiological models are discussed.

Malaria-induced apoptosis in mosquito ovaries: a mechanism to control vector egg production.

Many insects are able to adjust their egg production according to physiological conditions such as nutrient supply and mating success. One way in which this is achieved is by resorption of some, or all, of the ovarian follicles at some stage during oogenesis. We have shown that the mosquito Anopheles stephensi responds in this manner when ookinetes of the malaria parasite Plasmodium yoelii nigeriensis first begin to invade the midgut. Little is known about the initiation and regulation of follicle resorption in any insect. Here, we demonstrate that there is a significant positive correlation between follicle resorption and the presence of follicular epithelial cells that are undergoing apoptosis. The parasite causes significantly more follicles to contain apoptotic cells from 16h post-infection onwards. Injection of a caspase inhibitor immediately after feeding on an infective blood meal prevents parasite-induced resorption of follicles and thus demonstrates that apoptosis precedes resorption. Ultrastructural studies show that patches of follicular epithelial cells contain condensed nuclear chromatin, a characteristic of apoptosis, and that no patency develops in these cells. Our work suggests that apoptosis plays a role in malaria-initiated inhibition of mosquito oogenesis and that caspase is central to this process. Follicle resorption is one of the main factors contributing to malaria-induced fecundity reduction in mosquitoes.

A parasite that increases host lifespan.

Tenebrio molitor is an intermediate host for the rat tapeworm, Hymenolepis diminuta. Parasite oncospheres hatch in the beetle midgut and burrow through into the haemocoel, where they rapidly grow and mature into metacestodes. Repair of damage incurred during invasion and the nutritional demands of the parasites are likely to impose costs on the host. Despite these costs, there is an overall very highly significant difference in survival time (p < 0.001) between infected and control populations of beetles, with a hazard ratio of 2.35 (control versus infected). Infected females showed a 40% increase in survival time to 50% mortality and males showed a 25% increase in survival time to 50% mortality. This parasite-induced increase in host longevity is discussed in the light of changes in resource allocation that may occur in infected beetles. Previous findings have demonstrated that reproductive success is significantly reduced in infected females. The outcome of changes in the reproductive effort made by male beetles is less clear. We suggest that the optimum trade-off between reproduction and longevity may be altered to favour longer host survivorship, which is likely to enhance parasite transmission.