The anomaly that Anopheles culicifacies (Diptera: Culicidae) species B is a major vector of malaria in Sri Lanka, but a non-vector in India, has been noted for several years. In 1999, a Y chromosome dimorphism associated with Plasmodium vivax infectivity within the Indian A. culicifacies species B suggested that this was itself a complex of two sibling species, B and E. A recent cytogenetic analysis shows the sympatric presence of these sibling species in Sri Lanka, a situation similar to that reported from nearby Rameshwaram Island, India. Species E, with a submetacentric Y chromosome, is a more effective vector of P. vivax than species B with an acrocentric Y chromosome. Larval karyotyping, however, is time-consuming and labour-intensive. Recently, the development of a PCR-RFLP assay distinguishing species B and E of A. culicifacies from India, based on differences in one region of the cytochrome oxidase subunit II (COII) gene, was reported. Here we show that whilst this diagnostic approach reveals polymorphism in Sri Lankan A. culicifacies, this variation is not correlated with Y chromosome karyotype. Hence this assay will not be useful for distinguishing species B and E in Sri Lanka. Further, we found no difference between the sequences of Sri Lankan specimens in any of three other regions (ITS2, D3 region of 28S rDNA, and guanylate cyclase intron) often used for species discrimination.
The effects of nitric oxide on evoked acetylcholine (ACh) release were studied at two identified cholinergic neuro-neuronal synapses of the nervous system of the mollusc Aplysia californica. The NO- donor, 3-morpholinosydnonimine (SIN-1), decreased the amplitude of evoked inhibitory postsynaptic currents (buccal ganglion) and potentiated that of evoked excitatory postsynaptic currents (abdominal ganglion). SIN-1 acted by modulating the number of ACh quanta released. 8Br-cGMP mimicked the effects of NO on ACh release in both types of synapses thus pointing to the involvement of a NO- sensitive guanylate cyclase. Presynaptic voltage-dependent Ca2+ and K+ (Ia and late outward rectifier) currents were not modified by SIN-1 suggesting another final target for NO/cGMP. The labelling of a NO-synthase by immunostaining in several neurones as well as the modulation of ACh release by L-arginine indicate that an endogenous NO-synthase is involved in the modulation of synaptic efficacy in both buccal and abdominal ganglia.