49 research outputs found
Reseña Elsa Freire y Paulo Freire: por una pedagogía de la convivencia de Nima Spigolon (2022)
No full textElsa Freire e Paulo Freire: por uma pedagogia da convivência , by Nima Spigolon (2022), is part of the “Elsa Freire Triptych”1, in which the author seeks to demonstrate the true importance and the possibility of inaugurating a feminine political-pedagogical canon in the work of Paulo Freire, based on Elsa Freire’s presence in his productions. Spigolon’s book arises from the research she began in her master’s thesis and continued in her doctoral thesis at the University of Campinhas. In this first part of the triptych, Spigolon will portray the family, love, and professional life of Elsa Costa Freire from the late 1940s until 1964, when she went into exile with her family.
 
Androgen receptor deficiency alters the arginine-vasopressin sexually dimorphic system in Tfm rats
No full textIn rodents as well as in many other mammalian and non-mammalian species, the arginine-vasopressin (AVP) system includes a parvocellular sexually dimorphic portion located within the bed nucleus of the stria terminalis (BST), the medial amygdaloid nucleus (MeA) and the lateral septum. In this system, males have more cells and denser projections than females, neurons show androgen and estrogen receptors, and gonadal hormones are required for the activation. However, the role of these hormones for the differentiation of the system is not clear. Previous studies performed on aromatase knockout mice suggested that estradiol is not necessary for the differentiation of the system, but it is important for its activation in adulthood.To elucidate the role of androgens on differentiation and functioning of AVP parvocellular system, we compared male and female rats with a non-functional mutation of androgen receptor (Tfm, testicular feminization mutation) to their control littermates. Our data show that the lack of a functional androgen receptor significantly decreases the expression of AVP immunoreactivity within the BST and MeA of male Tfm. Thus supporting the hypothesis that androgens, through the action of their receptor, should have a relevant role in the organization and modulation of the AVP parvocellular sexually dimorphic system
Human mesenchymal stromal cell transplantation modulates neuroinflammatory milieu in a mouse model of amyotrophic lateralsclerosis
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c-Jun N-terminal kinase signaling pathway in excitotoxic cell death following kainic acid-induced status epilepticus
No full textSignal transduction in l-DOPA-induced dyskinesia: from receptor sensitization to abnormal gene expression
No full textNMDA Receptor and L-Type Calcium Channel Modulate Prion Formation
No full textTransmissible neurodegenerative prion diseases are characterized by the conversion of the cellular prion protein (PrPC) to misfolded isoforms denoted as prions or PrP^(Sc). Although the conversion can occur in the test tube containing recombinant prion protein or cell lysates, efficient prion formation depends on the integrity of intact cell functions. Since neurons are main targets for prion replication, we asked whether their most specialized function, i.e. synaptic plasticity, could be a factor by which PrP^(Sc) formation can be modulated.
Immortalized gonadotropin-releasing hormone cells infected with the Rocky Mountain Laboratory prion strain were treated with L-type calcium channels (LTCCs) and NMDA receptors (NMDARs) stimulators or inhibitors. Western blotting was used to monitor the effects on PrP^(Sc) formation in relation to ERK signalling.
Infected cells showed enhanced levels of phosphorylated ERK (pERK) compared with uninfected cells. Exposure of infected cells to the LTCC agonist Bay K8644 enhanced pERK and PrP^(Sc) levels. Although treatment with an LTCC blocker (nimodipine) or an NMDAR competitive antagonist (D-AP5) had no effects, their combination reduced both pERK and PrP^(Sc) levels. Treatment with the non-competitive NMDAR channel blocker MK-801 markedly reduced pERK and PrP^(Sc) levels.
Our study shows that changes in LTCCs and NMDARs activities can modulate PrP^(Sc) formation through ERK signalling. During synaptic plasticity, while ERK signalling promotes long-term potentiation accompanied by expansion of post-synaptic lipid rafts, other NMDA receptor-depending signalling pathways, p38-JNK, have opposing effects. Our findings indicate that contrasting intracellular signals of synaptic plasticity can influence time-dependent prion conversion
