RESUMO
In 1915 the Rockefeller Foundation took its hookworm eradication campaign to Suriname, but was soon disappointed because of opposition from its main target group: the Javanese. Moreover, authorities and planters objected to the construction of latrines because of the costs and their belief that the Javanese were “unhygienic”. In describing the labor migration from Java to Suriname, I show that this “lack of hygiene” was closely related to the system’s organization. I argue that uncleanliness was the consequence of harmful socio-economic and ecological conditions. Secondly I suggest that even though the Foundation did not manage to cleanse Suriname of hookworm, its educational efforts, its emphasis on prevention, and its training of local health workers probably had more impact than Rockefeller officials thought.
Em 1915, a Fundação Rockefeller levou sua campanha de erradicação da ancilostomíase ao Suriname, logo sofrendo a oposição de seu principal alvo, os javaneses. Autoridades e proprietários rurais também reagiram à instalação de latrinas devido aos custos implicados e à crença de que os javaneses eram “anti-higiênicos”. Ao descrever a migração de trabalhadores de Java para o Suriname, mostro que a “falta de higiene” ligava-se à organização do sistema. Argumento que a sujeira era consequência de condições ecológicas e socioeconômicas danosas. Sugiro ainda que, embora a Fundação não tenha livrado o Suriname da anciolostomíase, seus esforços educacionais, sua ênfase na prevenção e o treinamento de profissionais de saúde locais tiveram maior impacto do que o imaginado pelos funcionários da agência norte-americana.
Assuntos
Animais , Masculino , Camundongos , Ratos , Analgésicos/farmacologia , Dimaprit/análogos & derivados , Inibidores Enzimáticos/farmacologia , Antagonistas do Ácido Fólico/farmacologia , Agonistas dos Receptores Histamínicos/farmacologia , Histamina N-Metiltransferase/antagonistas & inibidores , Pirimidinas/farmacologia , Analgésicos/administração & dosagem , Relação Dose-Resposta a Droga , Dimaprit/administração & dosagem , Dimaprit/farmacologia , Inibidores Enzimáticos/administração & dosagem , Antagonistas do Ácido Fólico/administração & dosagem , Agonistas dos Receptores Histamínicos/administração & dosagem , Injeções Intraventriculares , Metilistaminas/farmacologia , Contração Muscular/efeitos dos fármacos , Medição da Dor/efeitos dos fármacos , Equilíbrio Postural/efeitos dos fármacos , Desempenho Psicomotor/efeitos dos fármacos , Pirimidinas/administração & dosagem , Pirimidinas/antagonistas & inibidores , Ratos WistarRESUMO
The role of the basolateral amygdala (BLA) in the consolidation of aversive memory is well established. Here we investigate the involvement of the histaminergic system in BLA on this variable. Rats were chronically implanted with bilateral cannulae in the BLA and after recovery were trained in a one-trial step-down inhibitory avoidance task. Immediately after training histaminergic compounds either alone or in combination were infused through the cannulae. Memory was assessed in test sessions carried out 24 h after the training session. Post-training histamine (1-10 nmol; 0.5 µl/side) enhanced consolidation and the histamine H3 receptor antagonist thioperamide (50 nmol; 0.5 µl/side) impaired memory consolidation. The effect was shared by the histamine N-methyltransferase inhibitor SKF-91844 (50 nmol; 0.5 µl/side) as well as by the H3 receptor agonist imetit (10 nmol; 0.5 µl/side). The promnesic action of histamine was unaffected by the H1 receptor antagonist pyrilamine (50 nmol; 0.5 µl/side). The H1 receptor agonist pyridylethylamine (10 nmol; 0.5 µl/side), the H2 agonist dimaprit (10 nmol; 0.5 µl/side) and the H2 antagonist ranitidine (50 nmol; 0.5 µl/side) were ineffective. Histaminergic compounds infused into the BLA had no effect on open-field or elevated plus-maze behaviour. The data show that histamine induces a dose-dependent mnemonic effect in rats and indicate that this reflects a role of endogenous histamine in the BLA mediated by H3 receptors.
Assuntos
Tonsila do Cerebelo/efeitos dos fármacos , Aprendizagem da Esquiva/efeitos dos fármacos , Agonistas dos Receptores Histamínicos/farmacologia , Histamina/farmacologia , Memória/efeitos dos fármacos , Tonsila do Cerebelo/fisiologia , Análise de Variância , Animais , Dimaprit/análogos & derivados , Dimaprit/farmacologia , Comportamento Exploratório/efeitos dos fármacos , Antagonistas dos Receptores Histamínicos/farmacologia , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Ratos , Ratos Wistar , Tempo de Reação/efeitos dos fármacos , Estatísticas não ParamétricasRESUMO
Electrical and chemical stimulation of the dorsal periaqueductal gray matter (dPAG) and the inferior colliculus (IC) induces escape behavior, usually accompanied by autonomic responses and antinociception. Recently, we presented evidence for a tonic inhibitory control exerted by H(2) histamine receptors on defensive behaviors generated in these midbrain tectum sites. Since treatments of these areas that elicit the defensive behavior repertoire frequently also have anxiogenic effects, we here used the elevated plus-maze (EPM) test for assessing the effects of microinjections of histamine (5-40 nmol), dimaprit (5-10 nmol) and ranitidine (10-30 nmol) into either dPAG or IC, which have a relative abundance of histamine-containing cells and histaminergic receptors. Dimaprit is an agonist and ranitidine is an antagonist of H(2) histamine receptors. Immediately after the injections, the animals were submitted to the EPM test. Whereas dPAG injections of dimaprit had no behavioral effects, histamine (40 nmol) caused a significant reduction in exploratory activity. On the other hand, ranitidine alone or following saline had aversive-like effects in both structures, i.e. reduced open arm, but not closed arm, entries. This pattern is usually interpreted as representing an anxiogenic effect. These effects were more pronounced after injection into dPAG than into IC. Freezing, the most prominent effect produced by ranitidine, was significantly inhibited by histamine as well as dimaprit. Thus, H(2) receptor blockade has fear-like action in the midbrain tectum with predominance in the dPAG. Such an action can be understood as a concomitant of defensive behavior, which has been shown to be a consequence of H(2) receptor antagonism in both dPAG and IC. The functional significance of the different effects of H(2) receptor blockade in dPAG and IC is discussed in the light of the probable distinct roles of these structures in the organization of defensive behavior.
Assuntos
Comportamento Animal/efeitos dos fármacos , Medo/efeitos dos fármacos , Medo/psicologia , Antagonistas dos Receptores H2 da Histamina/farmacologia , Colículos Inferiores/efeitos dos fármacos , Substância Cinzenta Periaquedutal/efeitos dos fármacos , Animais , Dimaprit/administração & dosagem , Dimaprit/farmacologia , Comportamento Exploratório/efeitos dos fármacos , Histamina/administração & dosagem , Histamina/farmacologia , Agonistas dos Receptores Histamínicos/administração & dosagem , Agonistas dos Receptores Histamínicos/farmacologia , Antagonistas dos Receptores H2 da Histamina/administração & dosagem , Masculino , Mesencéfalo/fisiologia , Microinjeções , Ranitidina/administração & dosagem , Ranitidina/farmacologia , Ratos , Ratos WistarRESUMO
The dorsal periaqueductal grey matter (dPAG) and inferior colliculus (IC) have been implicated in the control of defence reactions. Electrical and chemical stimulation of these structures induces escape behaviour, usually accompanied by autonomic responses and decreased pain sensitivity. Recently, we presented evidence for an involvement of histamine in the generation and organization of such defensive reactions in the midbrain tectum. In this study we have used the open field test to assess the effects of microinjections of histamine (40 nmol), dimaprit (10 nmol) and ranitidine (50 nmol) into the midbrain tectum of rats. Dimaprit is an agonist and ranitidine an antagonist of H2 histamine receptors. Immediately after the injections the animals were tested in an open field for 60 min. In an additional groups of rats, dimaprit was injected 15 min before the microinjections of ranitidine into either the dPAG or the IC. The results show that whereas histamine preceded by saline did not cause any apparent behavioural changes, ranitidine led to a behavioural reaction, with clear signs of fear, which was blocked by previous injection of dimaprit. Injections of only dimaprit had no apparent effects. The present results suggest that H2 receptors may be involved in the control of defensive behaviour following activation of the neural substrates of fear in the dPAG and IC.