This article presents the perspective of both non-disabled and developmentally disabled people working together in a research project on poverty and disability. Our study used a participatory action research approach that challenges the norm of exclusion in the research process. Control of the research agenda has been inclusive and shared to varying degrees in accordance with the needs and desires of the members of an advisory committee of developmentally disabled people living with low income. We reflect on our process of working together according to four principles of participatory action research with disabled people. We discuss our successes and challenges enacting these principles in the hopes that future researchers can build upon our experience to be more inclusive of developmentally disabled people in their work.
Points of interest• This article presents the perspective of both non-disabled and developmentally disabled people working together in a research project on poverty and disability. • Our study aimed to help raise the voices of developmentally disabled people living with low income and support the development of poverty-reduction strategies to meet their needs and priorities. • In this paper we discuss how we worked together to develop the research project, conduct focus groups, analyze results and use what we have learned to raise awareness and help make change in relation to poverty and disability issues. • We reflect on our process of working together according to four principles of participatory action research with disabled people to describe our successes and challenges.
Administration of the serotonin-releasing drug fenfluramine to male rats caused a dose-dependent increase in both plasma prolactin and corticosterone levels. The effect of fenfluramine on prolactin was maximal at 30 min after injection, whereas the effect on plasma corticosterone levels reached a maximum 2 h after injection. In order to determine if the effect of fenfluramine on both hormones was mediated via serotonin release, rats were pretreated with the serotonin uptake inhibitors fluoxetine (10 mg/kg i.p.) or indalpine (10 mg/kg i.p.) 30 min prior to administration of fenfluramine (5 mg/kg i.p.). Both fluoxetine and indalpine inhibited the effect of fenfluramine on plasma prolactin levels, but did not modify the effect of fenfluramine on plasma corticosterone levels. Pretreatment of rats with the serotonin precursor L· tryptophan (100 mg/kg i.p.) potentiated the effect of a submaximal dose of fenfluramine (2 mg/kg i.p.) on plasma prolactin levels, but did not affect the corticosterone response. Depletion of serotonin stores by pretreatment with the serotonin inhibitor p-chlorophenylalanine (300 mg/kg i.p.; 72 h) did not significantly prevent the effect of fenfluramine on either hormone. There was a 34% inhibition of the effect of fenfluramine on plasma prolactin levels, but this effect was not statistically significant. The results of the experiments suggest that the effect of fenfluramine on prolactin secretion is mediated, at least in part, by a serotoninergic mechanism, but the effect on corticosterone secretion is not mediated via serotonin release.
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