Our data suggest that a genetic approach could be useful in providing molecular support to the hypothesis that hypersensitivity of the dopaminergic system may represent the pathophysiologic basis of migraine, at least in a subgroup of patients.

No abstract

Genetic variation within triatomine bugs was investigated by amplification of a 400 bp portion of the mitochondrial 16S ribosomal RNA gene by polymerase chain reaction (PCR), using evolutionarily conserved primers, from a selection of species representative of the genera Rhodnius, Triatoma and Panstrongylus. Amplification products were subsequently screened for sequence variation using single strand conformational polymorphism analysis (SSCP) and also subjected to direct sequencing. Single strand conformational polymorphism analysis could detect variation within and between genera; intraspecific variation was also detected and SSCP profiles appear to be useful for identification purposes at the inter-and intraspecific levels. A 290 bp multiple alignment of 15 sequences obtained from nine species was generated, phylogenetic inference subsequently used three methods; a distance estimate, maximum parsimony and maximum likelihood. This 16S region exhibited considerable variation which ranged from intergeneric to intraspecific levels. Phylogenies from these three methods of inference were in broad agreement. Triatoma and Panstrongylus were more closely related to each other than either was to Rhodnius, in keeping with the current taxonomic appraisal.

The aim of this study was to test genetic differences in the clinical response to rizatriptan in patients affected by migraine without aura. These genetic differences could be explained by various genes, the HTR1B, encoding the 5-HT1 receptor subtype, MAO-A gene that encodes the monoamino-oxidase, the main metabolic enzyme of this triptan, SLC6A4 (gene encoding the serotonin transporter) and DRD2 (gene encoding the D2 receptor), both involved in the pathogenesis of migraine. Fifty unrelated patients affected by migraine without aura (IHS) were included. Patients were divided into two groups (responders and non-responders) according to clinical response. Thirty-one out of fifty patients responded to rizatriptan. A significant difference among the two groups was observed in both allele (p=0.02) and genotype distribution (p=0.03) of DRD2/NcoI. The significant association with the DRD2/NcoI polymorphism in responders suggested that the DRD2/NcoI C allele may be considered a susceptibility factor heralding a good response to rizatriptan.