Cuerpos, género y violencia: construcciones y deconstrucciones

The paper aims to develop a reflection on gender violence from an interdisciplinary perspective. Moving from tasks and positions of philosophical and psychoanalytic matrix , the authors bring into discussion the notion of gender based violence as a monolithic entity. After drawing a short theoretical trajectory on gender, sex and identity, the different meanings of the violence as social phenomenon are highlighted from a critical reflection on interpretative paradigms so far suggested. The main reference will be the difficulty associated with concepts such as heterosexual norm, required identity, performative gender, exclusionary effects associated with it, in order to analyze the rhetoric that act as guidance/ ordering in the speeches on gender based violence.Género, sexualidad e identidad son tres puntos clave de una discusión, en la que desde cualquier perspectiva que se quiera abordar no dejan de contribuir a la discusión de las y los académicos que trabajan en diversas disciplinas. Sea desde la teoría psicoanalítica, en la post-estructuralista y en la tradición filosófica de los estudios emprendidos por Butler (1990), nos encontramos con una actitud crítica frente al común binario sexo-género. En el marco de referencia, evitando así seguir la lógica del pensamiento único, abordamos el concepto de violencia basada en el género, como el conjunto de actos de abuso, acoso y otras agresiones ciegas procedentes de la necesidad de mantener cada ser humano dentro de la matriz heterosexual dicotómica, con el fin de preservar su identidad calmante y oficial. Mostramos como la violencia puede responder a un intento de aprovechar lo que está presente fuera de la "norma" y amenaza con desafiar la ley ordena toda relación interhumana

Die Zwischenebene der Fachkommunikation. Wissenstransfer in Lehrtexten der Neurologie

This paper focuses a genre belonging to a complex level of LSP communication which can be defined as “intermediate”, i.e. the academic textbook. This level plays a central role in granting the continuity of specialised scientific knowledge, as the fundamental requirement for the survival of each scientific field lies in the possibility of recruiting new members through formal (academic) education. Since this latter largely makes use of (and often depends on) this genre, a description of its linguistic features, internal structure, and the way it presents scientific knowledge should necessarily fall within the research trends in LSP communication. The aims of this paper are therefore twofold: 1. to determine the levels of analysis required for the description of this genre and to describe the characteristics of the (neurological) textbook according to those levels, and 2. to interpret such features and thereby investigate whether they may be classified exclusively as didactic or whether other categories are necessary to interpret them. The assumption arising from the analysis is that only some functional aspects can be regarded as didactic while others can only be interpreted as serving the (socially determined) function that this text fulfils in its context of use. The analysis also offers insight into of the differences existing among the various types of textbooks. These can in fact be connected to the way the two functional features of the texts are balanced depending on the specific needs of the addressees.

Endocannabinoid activation of CB1 receptors contributes to long-lasting reversal of neuropathic pain by repetitive spinal cord stimulation

BACKGROUND: Spinal cord stimulation (SCS) has been shown to be effective in the management of certain neuropathic pain conditions, however, the underlying mechanisms are incompletely understood. In this study, we investigated repetitive SCS in a rodent neuropathic pain model, revealing long-lasting and incremental attenuation of hyperalgesia and a mechanism of action involving endocannabinoids. METHOD: Animals were implanted with monopolar electrodes at the time of partial sciatic nerve injury. Dorsal columns at spinal segments T12/13 were stimulated 3 days later (early SCS), and again at day 7 (late SCS) using low-frequency parameters. Hypersensitivity to cutaneous mechanical stimuli was assessed using von Frey filaments. Pharmacological agents, selected to identify endocannabinoid and opioid involvement, were administered intraperitoneally, 10 min before SCS. RESULTS: Early SCS caused partial reversal of mechanical hypersensitivity with corresponding changes in the biomarker of central sensitization, [phospho-Tyr1472 ]-GluN2B. The partial reversal of hyperalgesia by early SCS was amplified by co-administration of LY 2183240, an inhibitor of endocannabinoid reuptake/breakdown. This amplification was inhibited by a CB1 R antagonist, AM251, but not by a CB2 R antagonist, AM630. Early SCS-induced reversal of hyperalgesia was attenuated by naloxone, indicating a role for opioids. Late SCS resulted in an incremental level of reversal of hyperalgesia, which was inhibited by AM251, but not by CB2 or opioid receptor antagonists. CONCLUSION: The endocannabinoid system, and in particular the CB1 R, plays a pivotal role in the long-lasting and incremental reversal of hyperalgesia induced by repetitive SCS in a neuropathic pain model

Regulation of Kir4.1 expression in astrocytes and astrocytic tumors: a role for interleukin-1 beta

<p>Abstract</p> <p>Objective</p> <p>Decreased expression of inwardly rectifying potassium (Kir) channels in astrocytes and glioma cells may contribute to impaired K⁺ buffering and increased propensity for seizures. Here, we evaluated the potential effect of inflammatory molecules, such as interleukin-1β (IL-1β) on Kir4.1 mRNA and protein expression.</p> <p>Methods</p> <p>We investigated Kir4.1 (Kcnj10) and IL-1β mRNA expression in the temporal cortex in a rat model of temporal lobe epilepsy 24 h and 1 week after induction of status epilepticus (SE), using real-time PCR and western blot analysis. The U373 glioblastoma cell line and human fetal astrocytes were used to study the regulation of Kir4.1 expression in response to pro-inflammatory cytokines. Expression of Kir4.1 protein was also evaluated by means of immunohistochemistry in surgical specimens of patients with astrocytic tumors (<it>n</it> = 64), comparing the expression in tumor patients with (<it>n</it> = 38) and without epilepsy (<it>n</it> = 26).</p> <p>Results</p> <p>Twenty-four hours after onset of SE, Kir4.1 mRNA and protein were significantly down-regulated in temporal cortex of epileptic rats. This decrease in expression was followed by a return to control level at 1 week after SE. The transient downregulation of Kir4.1 corresponded to the time of prominent upregulation of IL-1β mRNA. Expression of Kir4.1 mRNA and protein in glial cells in culture was downregulated after exposure to IL-1β. Evaluation of Kir4.1 in tumor specimens showed a significantly lower Kir4.1 expression in the specimens of patients with epilepsy compared to patients without epilepsy. This paralleled the increased presence of activated microglial cells, as well as the increased expression of IL-1β and the cytoplasmic translocation of high mobility group box 1 (HMGB1).</p> <p>Conclusions</p> <p>Taken together, these findings indicate that alterations in expression of Kir4.1 occurring in epilepsy-associated lesions are possibly influenced by the local inflammatory environment and in particular by the inflammatory cytokine IL-1β.</p

Developmental regulation of CB1-mediated spike-time dependent depression at immature mossy fiber-CA3 synapses

Early in postnatal life, mossy fibres (MF), the axons of granule cells in the dentate gyrus, release GABA which is depolarizing and excitatory. Synaptic currents undergo spike-time dependent long-term depression (STD-LTD) regardless of the temporal order of stimulation (pre versus post and viceversa). Here we show that at P3 but not at P21, STD-LTD, induced by negative pairing, is mediated by endocannabinoids mobilized from the postsynaptic cell during spiking-induced membrane depolarization. By diffusing backward, endocannabinoids activate cannabinoid type-1 (CB1) receptors probably expressed on MF. Thus, STD-LTD was prevented by CB1 receptor antagonists and was absent in CB1-KO mice. Consistent with these data, in situ hybridization experiments revealed detectable level of CB1 mRNA in the granule cell layer at P3 but not at P21. These results indicate that CB1 receptors are transiently expressed on immature MF terminals where they counteract the enhanced neuronal excitability induced by the excitatory action of GABA

Defective microglial development in the hippocampus of Cx3cr1 deficient mice

Microglial cells participate in brain development and influence neuronal loss and synaptic maturation. Fractalkine is an important neuronal chemokine whose expression increases during development and that can influence microglia function via the fractalkine receptor, CX3CR1. Mice lacking Cx3cr1 show a variety of neuronal defects thought to be the result of deficient microglia function. Activation of CX3CR1 is important for the proper migration of microglia to sites of injury and into the brain during development. However, little is known about how fractalkine modulates microglial properties during development. Here we examined microglial morphology, response to ATP, and K(+) current properties in acute brain slices from Cx3cr1 knockout mice across postnatal hippocampal development. We found that fractalkine signaling is necessary for the development of several morphological and physiological features of microglia. Specifically, we found that the occurrence of an outward rectifying K(+) current, typical of activated microglia, that peaked during the second and third postnatal week, was reduced in Cx3cr1 knockout mice. Fractalkine signaling also influenced microglial morphology and ability to extend processes in response to ATP following its focal application to the slice. Our results reveal the developmental profile of several morphological and physiological properties of microglia and demonstrate that these processes are modulated by fractalkine signaling