Ensino de ciências sob a óptica do programa de ação interdisciplinar: práticas para uma aprendizagem significativa/ Teaching of sciences under the perspective of the interdisciplinary action program: practices for meaningful learning

O presente trabalho teve como objetivo relatar as principais contribuições do Programa de Ação Interdisciplinar (PAI) na educação científica de estudantes durante o estágio em docência do Programa de Pós-graduação em Biociências (PPGBIO) da Universidade Federal do Oeste do Pará (UFOPA). Foram realizadas 10 atividades científicas com os estudantes, entre elas: 2 encontros de trabalho, 7 aulas práticas e 3 eventos científicos. O PAI proporcionou uma educação científica de qualidade e o fortalecimento da relação professor-aluno. Os resultados alcançados levam-nos a inferir sobre o potencial que o PAI possui como abordagem de ensino-aprendizagem que pode ser reproduzida com relativa facilidade para que possamos avançar na tão necessária educação científica de jovens estudantes brasileiros

Adenosine A1 receptor-mediated inhibition of in vitro prolactin secretion from the rat anterior pituitary

In previous studies, we demonstrated biphasic purinergic effects on prolactin (PRL) secretion stimulated by an adenosine A2 agonist. In the present study, we investigated the role of the activation of adenosine A1 receptors by (R)-N6-(2-phenylisopropyl)adenosine (R-PIA) at the pituitary level in in vitro PRL secretion. Hemipituitaries (one per cuvette in five replicates) from adult male rats were incubated. Administration of R-PIA (0.001, 0.01, 0.1, 1, and 10 µM) induced a reduction of PRL secretion into the medium in a U-shaped dose-response curve. The maximal reduction was obtained with 0.1 µM R-PIA (mean ± SEM, 36.01 ± 5.53 ng/mg tissue weight (t.w.)) treatment compared to control (264.56 ± 15.46 ng/mg t.w.). R-PIA inhibition (0.01 µM = 141.97 ± 15.79 vs control = 244.77 ± 13.79 ng/mg t.w.) of PRL release was blocked by 1 µM cyclopentyltheophylline, a specific A1 receptor antagonist (1 µM = 212.360 ± 26.560 ng/mg t.w.), whereas cyclopentyltheophylline alone (0.01, 0.1, 1 µM) had no effect. R-PIA (0.001, 0.01, 0.1, 1 µM) produced inhibition of PRL secretion stimulated by both phospholipase C (0.5 IU/mL; 977.44 ± 76.17 ng/mg t.w.) and dibutyryl cAMP (1 mM; 415.93 ± 37.66 ng/mg t.w.) with nadir established at the dose of 0.1 µM (225.55 ± 71.42 and 201.9 ± 19.08 ng/mg t.w., respectively). Similarly, R-PIA (0.01 µM) decreased (242.00 ± 24.00 ng/mg t.w.) the PRL secretion stimulated by cholera toxin (0.5 mg/mL; 1050.00 ± 70.00 ng/mg t.w.). In contrast, R-PIA had no effect (468.00 ± 34.00 ng/mg t.w.) on PRL secretion stimulation by pertussis toxin (0.5 mg/mL; 430.00 ± 26.00 ng/mg t.w.). These results suggest that inhibition of PRL secretion after A1 receptor activation by R-PIA is mediated by a Gi protein-dependent mechanism

Stimulatory effects of adenosine on prolactin secretion in the pituitary gland of the rat

We investigated the effects of adenosine on prolactin (PRL) secretion from rat anterior pituitaries incubated in vitro. The administration of 5-N- methylcarboxamidoadenosine (MECA), an analog agonist that preferentially activates A2 receptors, induced a dose-dependent (1 nM to 1 µM) increase in the levels of PRL released, an effect abolished by 1,3-dipropyl-7-methylxanthine, an antagonist of A2 adenosine receptors. In addition, the basal levels of PRL secretion were decreased by the blockade of cyclooxygenase or lipoxygenase pathways, with indomethacin and nordihydroguaiaretic acid (NDGA), respectively. The stimulatory effects of MECA on PRL secretion persisted even after the addition of indomethacin, but not of NDGA, to the medium. MECA was unable to stimulate PRL secretion in the presence of dopamine, the strongest inhibitor of PRL release that works by inducing a decrease in adenylyl cyclase activity. Furthermore, the addition of adenosine (10 nM) mimicked the effects of MECA on PRL secretion, an effect that persisted regardless of the presence of LiCl (5 mM). The basal secretion of PRL was significatively reduced by LiCl, and restored by the concomitant addition of both LiCl and myo-inositol. These results indicate that PRL secretion is under a multifactorial regulatory mechanism, with the participation of different enzymes, including adenylyl cyclase, inositol-1-phosphatase, cyclooxygenase, and lipoxygenase. However, the increase in PRL secretion observed in the lactotroph in response to A2 adenosine receptor activation probably was mediated by mechanisms involving regulation of adenylyl cyclase, independent of membrane phosphoinositide synthesis or cyclooxygenase activity and partially dependent on lipoxygenase arachidonic acid-derived substances

Possible involvement of A1 receptors in the inhibition of gonadotropin secretion induced by adenosine in rat hemipituitaries in vitro

We investigated the participation of A1 or A2 receptors in the gonadotrope and their role in the regulation of LH and FSH secretion in adult rat hemipituitary preparations, using adenosine analogues. A dose-dependent inhibition of LH and FSH secretion was observed after the administration of graded doses of the R-isomer of phenylisopropyladenosine (R-PIA; 1 nM, 10 nM, 100 nM, 1 µM and 10 µM). The effect of R-PIA (10 nM) was blocked by the addition of 8-cyclopentyltheophylline (CPT), a selective A1 adenosine receptor antagonist, at the dose of 1 µM. The addition of an A2 receptor-specific agonist, 5-N-methylcarboxamidoadenosine (MECA), at the doses of 1 nM to 1 µM had no significant effect on LH or FSH secretion, suggesting the absence of this receptor subtype in the gonadotrope. However, a sharp inhibition of the basal secretion of these gonadotropins was observed after the administration of 10 µM MECA. This effect mimicked the inhibition induced by R-PIA, supporting the hypothesis of the presence of A1 receptors in the gonadotrope. R-PIA (1 nM to 1 µM) also inhibited the secretion of LH and FSH induced by phospholipase C (0.5 IU/ml) in a dose-dependent manner. These results suggest the presence of A1 receptors and the absence of A2 receptors in the gonadotrope. It is possible that the inhibition of LH and FSH secretion resulting from the activation of A1 receptors may have occurred independently of the increase in membrane phosphoinositide synthesis

Does plasma ANP participate in natriuresis induced by a-MSH?

-Melanocyte-stimulating hormone (-MSH; 0.6 and 3 nmol) microinjected into the anteroventral region of the third ventricle (AV3V) induced a significant increase in diuresis without modifying natriuresis or kaliuresis. Intraperitoneal (ip) injection of -MSH (3 and 9.6 nmol) induced a significant increase in urinary sodium, potassium and water excretion. Intraperitoneal (3 and 4.8 nmol) or iv (3 and 9.6 nmol) administration of -MSH did not induce any significant changes in plasma atrial natriuretic peptide (ANP), suggesting that the natriuresis, kaliuresis and diuresis induced by the systemic action of -MSH can be dissociated from the increase in plasma ANP. These preliminary results suggest that -MSH may be involved in a -MSHindependent mechanism of regulation of hydromineral metabolism

Methylmercury inhibits prolactin release in a cell line of pituitary origin

Heavy metals, such as methylmercury, are key environmental pollutants that easily reach human beings by bioaccumulation through the food chain. Several reports have demonstrated that endocrine organs, and especially the pituitary gland, are potential targets for mercury accumulation; however, the effects on the regulation of hormonal release are unclear. It has been suggested that serum prolactin could represent a biomarker of heavy metal exposure. The aim of this study was to evaluate the effect of methylmercury on prolactin release and the role of the nitrergic system using prolactin secretory cells (the mammosomatotroph cell line, GH3B6). Exposure to methylmercury (0-100 μM) was cytotoxic in a time- and concentration-dependent manner, with an LC50 higher than described for cells of neuronal origin, suggesting GH3B6 cells have a relative resistance. Methylmercury (at exposures as low as 1 μM for 2 h) also decreased prolactin release. Interestingly, inhibition of nitric oxide synthase by N-nitro-L-arginine completely prevented the decrease in prolactin release without acute neurotoxic effects of methylmercury. These data indicate that the decrease in prolactin production occurs via activation of the nitrergic system and is an early effect of methylmercury in cells of pituitary origin.MAUÉS, L. A. L. Dr. Docente da Universidade Federal do Pará, Campus Universitário de AltamiraMACCHI, B. de M. Dr. Docente da Universidade Federal do Pará, Instituto de Ciências BiológicasCRESPO LÓPEZ, M. E. Dr. Docente da Universidade Federal do Pará, Insituto de Ciências Biológica

Fingerprinting of psychoactive drugs in zebrafish anxiety-like behaviors.

A major hindrance for the development of psychiatric drugs is the prediction of how treatments can alter complex behaviors in assays which have good throughput and physiological complexity. Here we report the development of a medium-throughput screen for drugs which alter anxiety-like behavior in adult zebrafish. The observed phenotypes were clustered according to shared behavioral effects. This barcoding procedure revealed conserved functions of anxiolytic, anxiogenic and psychomotor stimulating drugs and predicted effects of poorly characterized compounds on anxiety. Moreover, anxiolytic drugs all decreased, while anxiogenic drugs increased, serotonin turnover. These results underscore the power of behavioral profiling in adult zebrafish as an approach which combines throughput and physiological complexity in the pharmacological dissection of complex behaviors

Environmental enrichment improved learning and memory, increased telencephalic cell proliferation, and induced differential gene expression in Colossoma macropomum

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), the Brazilian Research Council (CNPq) Edital Universal Grant 440722/2014-4 and Grant 302199/2014-4; Fundação Amazônia Paraense de Amparo à Pesquisa (FAPESPA), Grant Centro de Piscicultura do IFPA Campus Bragança and Núcleos Emergentes, Instituto Federal de Educação ciência e Tecnologia do Pará (IFPA), Editais APIPA 2018 e 2019 . DD and CD were supported by Programa PROCAD AMAZÔNIA/CAPES 88887.310939/2018-00.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Universidade Federal do Pará. Instituto de Ciências Biológicas. Hospital Universitário João de Barros Barreto. Laboratório de Investigação em Neurodegeneração e Infecção. Belém, PA, Brazil.Universidade Federal Rural da Amazônia. Instituto Ciências Agrárias. Capitão Poço, PA, Brazil.Universidade Federal do Pará. Instituto de Ciências Biológicas. Hospital Universitário João de Barros Barreto. Laboratório de Investigação em Neurodegeneração e Infecção. Belém, PA, Brazil.Universidade Federal do Pará. Instituto de Ciências Biológicas. Hospital Universitário João de Barros Barreto. Laboratório de Investigação em Neurodegeneração e Infecção. Belém, PA, Brazil.Universidade Federal do Pará. Instituto de Ciências Biológicas. Hospital Universitário João de Barros Barreto. Laboratório de Investigação em Neurodegeneração e Infecção. Belém, PA, Brazil.Universidade Federal do Pará. Instituto de Ciências Biológicas. Hospital Universitário João de Barros Barreto. Laboratório de Investigação em Neurodegeneração e Infecção. Belém, PA, Brazil.Universidade Federal do Pará. Instituto de Ciências Biológicas. Hospital Universitário João de Barros Barreto. Laboratório de Investigação em Neurodegeneração e Infecção. Belém, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Universidade Federal do Oeste do Pará. Laboratório de Fisiologia Ambiental Aplicada. Oriximiná, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Instituto Federal de Educação, Ciência e Tecnologia do Pará. Laboratório de Biologia Molecular e Neuroecologia. Bragança, PA, Brazil.Universidade Federal do Pará. Instituto de Ciências Biológicas. Hospital Universitário João de Barros Barreto. Laboratório de Investigação em Neurodegeneração e Infecção. Belém, PA, Brazil / Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Laboratório de Microscopia Eletrônica. Ananindeua, PA, Brasil.Fish use spatial cognition based on allocentric cues to navigate, but little is known about how environmental enrichment (EE) affects learning and memory in correlation with hematological changes or gene expression in the fish brain. Here we investigated these questions in Colossoma macropomum (Teleostei). Fish were housed for 192 days in either EE or in an impoverished environment (IE) aquarium. EE contained toys, natural plants, and a 12-h/day water stream for voluntary exercise, whereas IE had no toys, plants, or water stream. A third plus maze aquarium was used for spatial and object recognition tests. Compared with IE, the EE fish showed greater learning rates, body length, and body weight. After behavioral tests, whole brain tissue was taken, stored in RNA-later, and then homogenized for DNA sequencing after conversion of isolated RNA. To compare read mapping and gene expression profiles across libraries for neurotranscriptome differential expression, we mapped back RNA-seq reads to the C. macropomum de novo assembled transcriptome. The results showed significant differential behavior, cell counts and gene expression in EE and IE individuals. As compared with IE, we found a greater number of cells in the telencephalon of individuals maintained in EE but no significant difference in the tectum opticum, suggesting differential plasticity in these areas. A total of 107,669 transcripts were found that ultimately yielded 64 differentially expressed transcripts between IE and EE brains. Another group of adult fish growing in aquaculture conditions were either subjected to exercise using running water flow or maintained sedentary. Flow cytometry analysis of peripheral blood showed a significantly higher density of lymphocytes, and platelets but no significant differences in erythrocytes and granulocytes. Thus, under the influence of contrasting environments, our findings showed differential changes at the behavioral, cellular, and molecular levels. We propose that the differential expression of selected transcripts, number of telencephalic cell counts, learning and memory performance, and selective hematological cell changes may be part of Teleostei adaptive physiological responses triggered by EE visuospatial and somatomotor stimulation. Our findings suggest abundant differential gene expression changes depending on environment and provide a basis for exploring gene regulation mechanisms under EE in C. macropomum

Effects of (A) buspirone, (B) diazepam and (C) caffeine on time on white (upper left), risk assessment (upper right), thigmotaxis (lower left), and freezing (lower right).

<p>Bars represent standard error of the mean, and whiskers represent the 2.5 and 97.5 percentile. *, p<0.05; **, p<0.01; ***, p<0.001.</p