1,721,125 research outputs found
Le tecniche teatrali sono in grado di influenzare positivamente il cervello umano?
No full textThe special issue of the journal «Biblioteca Teatrale», devoted to the subject of “Theatre as Enriched Environment”, is the result of an international conference held at Sapienza University of Rome in June 2015. In a multidisciplinary perspective (human and social sciences, cognitive and medical sciences), the contributions are experience proofs, and theoretical and methodological reflections about the value and the role that theatre can get in certain situations of uneasiness and deprivation. Essay: Laura Maggi, Sergio Fucile, “Are Theatrical Techniques Able to Positively Influence Human Brain?
Regulation of GABA release by nicotinic acetylcholine receptors in the neonatal rat hippocampus
No full text1. The whole-cell configuration of the patch-clamp technique was used to study the modulation of giant depolarizing potentials (GDPs) by nicotinic acetylcholine receptors (nAChRs) in CA3 hippocampal neurons in slices from postnatal day (P) 2-6 rats. 2. Bath application of nicotine increased GDP frequency in a concentration-dependent manner. For example, nicotine (0.5-1 μM) enhanced GDP frequency from 0.05 ± 0.04 to 0.17 ± 0.04 Hz. This effect was prevented by the broad-spectrum nicotinic receptor antagonist dihydro-β-erythtroidine (DHβE, 50 μM) and partially antagonized by methyllycaconitine (MLA, 50 nM) a competitive antagonist of α7 nAChRs. GDP frequency was also enhanced by AR-17779 (100 μM), a selective agonist of α7 nAChRs. 3. The GABAA receptor antagonist bicuculline (10 μM) and the non-NMDA glutamate receptor antagonist DNQX (20 μM) blocked GDPs and prevented the effects of nicotine on GDPs. In the presence of DNQX, nicotine increased GABA-mediated synaptic noise, indicating that this drug may have a direct effect on GABAergic interneurons. 4. Bath application of edrophonium (20 μM), a cholinesterase inhibitor, in the presence of atropine (1 μM), increased GDP frequency, indicating that nAChRs can be activated by ACh released from the septo-hippocampal fibres. This effect was prevented by DHβE (50 μM). 5. In the majority of neurons tested, MLA (50 nM) and DHβE (50 μM) reduced the frequency of GDPs with different efficacy: a reduction of 98 ± 11 and 61 ± 29% was observed with DHβE and MLA, respectively. In a subset of cells (40% in the case of MLA and 17% in the case of DHβE) these drugs induced a twofold increase in GDP frequency. 6. It is suggested that, during development, nAChRs modulate the release of GABA, assessed as GDPs, through distinct nAChRs. The rise of intracellular calcium via nAChRs would further strengthen GABA-mediated oscillatory activity. This can be crucial for consolidation of synaptic contacts and for the fine-tuning of the developing hippocampus
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Editorial: Cytokines as players of neuronal plasticity and sensitivity to environment in healthy and pathological brain
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Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Effects of Zn2+ on wild and mutant neuronal alpha7 nicotinic receptors
No full textZn2+ is a key structural/functional component of many proteins and is present at high concentrations in the brain and retina, where it modulates ligand-gated receptors. Therefore, a study was made of the effects of zinc on homomeric neuronal nicotinic receptors expressed in Xenopus oocytes after injection of cDNAs encoding the chicken wild or mutant alpha7 subunits. In oocytes expressing wild-type receptors, Zn2+ alone did not elicit appreciable membrane currents. Acetylcholine (AcCho) elicited large currents (IAcCho) that were reduced by Zn2+ in a reversible and dose-dependent manner, with an IC50 of 27 microM and a Hill coefficient of 0.4. The inhibition of IAcCho by Zn2+ was competitive and voltage-independent, a behavior incompatible with a channel blockade mechanism. In sharp contrast, in oocytes expressing a receptor mutant, with a threonine-for-leucine 247 substitution (L247Talpha7), subnanomolar concentrations of Zn2+ elicited membrane currents (IZn) that were reversibly inhibited by the nicotinic receptor blockers methyllycaconitine and alpha-bungarotoxin. Cell-attached single-channel recordings showed that Zn2+ opened channels that had a mean open time of 5 ms and a conductance of 48 pS. At millimolar concentrations Zn2+ reduced IAcCho and the block became stronger with cell hyperpolarization. Thus, Zn2+ is a reversible blocker of wild-type alpha7 receptors, but becomes an agonist, as well as an antagonist, following mutation of the highly conserved leucine residue 247 located in the M2 channel domain. We conclude that Zn2+ is a modulator as well as an activator of homomeric nicotinic alpha7 receptors
Effects of fluoxetine (Prozac) on wild and mutant neuronal alpha7 nicotinic receptors
No full textFluoxetine is used in the treatment of a variety of clinical disorders including depression and obesity, and of cocaine detoxification or alcoholism. It is generally believed that fluoxetine exerts its clinical effects because it selectively blocks 5-hydroxytryptamine (5HT) reuptake into nerve terminals. In here we describe that fluoxetine antagonized the neuronal homomeric alpha(7) nicotinic acetylcholine receptors (nAChR) expressed in Xenopus oocytes, with an IC50 of 43 mu M, when fluoxetine was coapplied with ACh, and of 1.6 mu M when the oocytes were pretreated briefly with fluoxetine. A similar block occurred in oocytes expressing L247T alpha(7) mutant nAChR. Furthermore, blockage of mutant alpha(7) receptors appeared non-competitive and was stronger with cell membrane hyperpolarization. Cell-attached single channel recordings in oocytes expressing L247T alpha(7) mutant nAChR showed that the voltage-dependence of the blockage by fluoxetine could be due to a drastic decrease in channel opening frequency accompanied by marked channel flickering and reduced channel conductance. We conclude that fluoxetine behaves as a reversible blocker of both wild and mutant alpha(7) receptors; and that the Leu-247T mutation in the channel domain renders the blockage of alpha(7) nAChR by fluoxetine voltage-dependent. These effects of fluoxetine on alpha(7) receptors may be clinically importan
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