IRET Foundation

Ozzano dell'Emilia, Italy

IRET Foundation

Ozzano dell'Emilia, Italy

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Beggiato S.,University of Ferrara | Giuliani A.,University of Bologna | Sivilia S.,University of Bologna | Lorenzini L.,University of Bologna | And 8 more authors.
Neuroscience | Year: 2014

CHF5074 is a nonsteroidal anti-inflammatory derivative that has been shown to inhibit β-amyloid plaque deposition and to reverse memory deficit in vivo in transgenic mouse models of Alzheimer's disease (AD).In the present in vivo study we used pre-plaque Tg2576 mice showing cognitive impairments to investigate the effects of a sub-acute treatment with CHF5074 on prefrontal cortex dialysate glutamate levels. Furthermore, the effects of CHF5074 have been compared with those induced, under the same experimental conditions, by LY450139, a potent γ-secretase inhibitor, that has been shown to inhibit brain β-amyloid production. No differences in prefrontal cortex dialysate glutamate levels were observed between control Tg2576 and wild-type animals. A sub-acute (8. days) treatment with CHF5074 (30. mg/kg, s.c.), LY450139 (3. mg/kg, s.c.) or their respective vehicles did not modify prefrontal cortex dialysate glutamate levels. After these treatments, the injection of CHF5074 reduced, while LY450139 increased, prefrontal cortex dialysate glutamate levels in Tg2576 mice, but not in wild-type animals. These results suggest that at the dose tested CHF5074 and LY450139 differently affect cortical glutamate transmission in pre-plaque Tg2576 mice. This different neurochemical profile could be involved in the different ability of the two drugs in improving early cognitive performance in this animal model of AD. © 2014 IBRO.

Ferraro L.,University of Ferrara | Beggiato S.,University of Ferrara | Marcellino D.,Karolinska Institutet | Frankowska M.,Karolinska Institutet | And 8 more authors.
Journal of Neural Transmission | Year: 2010

Previous studies have indicated that cocaine binding sites contain both high- and low-affinity binding components and have actions not related to dopamine uptake inhibition. Therefore, it has been studied if concentrations of cocaine in the range of 0.1-100 nM can affect not only dopamine uptake but also the quinpirole-induced inhibition of the K+-evoked [ 3H]-dopamine efflux from rat striatal synaptosomes. It was found that quinpirole-induced inhibition of K+-evoked [3H]-dopamine efflux was significantly enhanced by cocaine at 1 and 10 nM but not at 0.1 nM with cocaine alone being inactive and 1 nM cocaine lacking effects on [ 3H]-dopamine uptake in rat striatal synaptosomes. The results indicate the existence of a novel allosteric agonist action of cocaine in low concentrations, not affecting dopamine uptake, at striatal D2 autoreceptors modulating striatal dopamine transmission. © 2010 Springer-Verlag.

Beggiato S.,University of Ferrara | Beggiato S.,IRET Foundation | Antonelli T.,University of Ferrara | Antonelli T.,IRET Foundation | And 9 more authors.
Current Protein and Peptide Science | Year: 2014

Striatal dopamine adenosine A2A and D2 receptors interact to modulate some aspects of motor and motivational function. The demonstration of A2A/D2 receptor heteromerization in living cells constituted a progress for understanding the neurobiology of dopamine D2 and adenosine A2A receptors. In fact, the existence of putative striatalA2A/D2 receptor heteromers has been suggested to be important for striatal function under both normal and pathological conditions, such as Parkinson’s disease. Consequently, the antagonistic A2A-D2 receptor interactions in a putative striatal receptor heteromer on striato-pallidal GABA neuron led to the introduction of A2A receptor antagonists as possible anti- Parkinsonian drugs. The present mini-review briefly summarizes the main findings supporting the presence of antagonistic A2A-D2 receptor interactions in putative receptor heteromers in the basal ganglia. Special emphasis is given to in vivo microdialysis findings demonstrating the functional role putative A2A/D2 heteromers on striato-pallidal GABA neurons play in the modulation of this pathway, in which A2A receptors inhibit D2 receptor signaling. The possible relevance of compounds targeting the putative striatal A2A/D2 heteromer in the Parkinson’s disease pharmacological treatment is also discussed. © 2014 Bentham Science Publishers

PubMed | Karolinska Institutet, University of Ferrara and IRET Foundation
Type: Journal Article | Journal: Journal of neurochemistry | Year: 2016

In this study, the functional role of individual striatal receptors for adenosine (A2AR), dopamine (D2R), and the metabotropic glutamate receptor mGlu5R in regulating rat basal ganglia activity was characterized invivo using dual-probe microdialysis in freely moving rats. In particular, intrastriatal perfusion with the D2R agonist quinpirole (10M, 60min) decreased ipsilateral pallidal GABA and glutamate levels, whereas intrastriatal CGS21680 (A2AR agonist; 1M, 60min) was ineffective on either pallidal GABA and glutamate levels or the quinpirole-induced effects. Intrastriatal perfusion with the mGlu5R agonist (RS)-2-chloro-5-hydroxyphenylglycine (600M, 60min), by itself ineffective on pallidal GABA and glutamate levels, partially counteracted the effects of quinpirole. When combined with CGS21680 (1M, 60min), (RS)-2-chloro-5-hydroxyphenylglycine (CHPG; 600M, 60min) fully counteracted the quinpirole (10M, 60min)-induced reduction in ipsilateral pallidal GABA and glutamate levels. These effects were fully counteracted by local perfusion with the mGlu5R antagonist MPEP (300M) or the A2AR antagonist ZM 241385 (100 nM). These results suggest that A2ARs and mGlu5Rs interact synergistically in modulating the D2R-mediated control of striatopallidal GABA neurons. Using dual-probe microdialysis, we characterized the functional role of striatal adenosine A2A receptor (A2AR), dopamine D2 receptor (D2R), and metabotropic glutamate receptor 5 (mGluR5) interactions in regulating rat basal ganglia activity. The results suggest the possible usefulness of using an A2AR antagonist and mGluR5 antagonist combination in the treatment of Parkinsons disease to increase the inhibitory D2 signaling on striatopallidal GABA neurons.

Baratto L.,La Colletta Bioengineering Center | Calza L.,IRET Foundation | Calza L.,University of Bologna | Capra R.,La Colletta Bioengineering Center | And 5 more authors.
Lasers in Medical Science | Year: 2011

A growing number of laboratory and clinical studies over the past 10 years have shown that low-level laser stimulation (633 or 670 nm) at extremely low power densities (about 0.15 mW/cm2), when administered through a particular emission mode, is capable of eliciting significant biological effects. Studies on cell cultures and animal models as well as clinical trials give support to a novel therapeutic modality, which may be referred to as ultra low level laser therapy (ULLLT). In cultured neural cells, pulsed irradiation (670 nm, 0.45 mJ/cm2) has shown to stimulate NGF-induced neurite elongation and to protect cells against oxidative stress. In rats, anti-edema and antihyperalgesia effects following ULLL irradiation were found. Clinical studies have reported beneficial effects (also revealed through sonography) in the treatment of musculoskeletal disorders. The present paper reviews the existing experimental evidence available on ULLLT. Furthermore, the puzzling issue of the biophysical mechanisms that lie at the basis of the method is explored and some hypotheses are proposed. Besides presenting the state-ofthe-art about this novel photobiostimulation therapy, the present paper aims to open up an interdisciplinary discussion and stimulate new research on this subject. © Springer-Verlag London Ltd 2010.

Rinaldi S.,Rinaldi Fontani Foundation | Rinaldi S.,Rinaldi Fontani Institute | Calza L.,IRET Foundation | Calza L.,University of Bologna | And 6 more authors.
Frontiers in Psychiatry | Year: 2015

Global research in the field of pharmacology has not yet found effective drugs to treat Alzheimer's disease (AD). Thus, alternative therapeutic strategies are under investigation, such as neurostimulation by physical means. Radio electric asymmetric conveyer (REAC) is one of these technologies and has, until now, been used in clinical studies on several psychiatric and neurological disorders with encouraging results in the absence of side effects. Moreover, studies at the cellular level have shown that REAC technology, with the appropriate protocols, is able to induce neuronal differentiation both in murine embryonic cells and in human adult differentiated cells. Other studies have shown that REAC technology is able to positively influence senescence processes. Studies conducted on AD patients and in transgenic mouse models have shown promising results, suggesting REAC could be a useful therapy for certain components of AD. © 2015 Rinaldi, Calzà, Giardino, Biella, Zippo and Fontani.

Calza L.,University of Bologna | Calza L.,IRET Foundation | Fernandez M.,University of Bologna | Giardino L.,University of Bologna | Giardino L.,IRET Foundation
Comprehensive Physiology | Year: 2015

The role of thyroid hormone on brain development is dramatically illustrated by "cretinism," a severe mental retardation due to iodine deficiency and maternal hypothyroidism during gestation. In the last decades, the molecular bases of the cellular action of thyroid hormone in the nervous tissue have been at least partially elucidated, and the emerged picture is much more complex than expected. In this article, the main mechanisms determining thyroid hormone availability, nuclear and membrane receptor occupancy and downstream action, gene expression, and nongenomic mechanism are reviewed, focusing on myelination and myelin turnover. © 2015 American Physiological Society.

Tomasini M.C.,University of Ferrara | Tomasini M.C.,IRET Foundation | Beggiato S.,University of Ferrara | Beggiato S.,IRET Foundation | And 8 more authors.
Neurochemistry International | Year: 2012

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is considered one of the most toxic dioxin-like compounds. It is ubiquitous in foodstuffs of animal origin and accumulates in the fatty tissues of animals and humans. Prenatal TCDD exposure has been associated, beside other effects, with persistent impaired cognitive development. In the present study, the effects of maternal exposure to TCDD during pregnancy on cortical neuron development at birth and cortical glutamate transmission in new-born, 14- and 60-day-old rat offspring, were investigated. A single dose (0.7 μg/kg) of TCDD dissolved in corn oil was orally administrated to the dams on gestational day 18; controls dams were treated with the vehicle. All the experiments have been performed on the male offspring from vehicle-treated (i.e. control group) and TCDD-treated dams. Primary cultures of cerebral cortical neurons obtained from 1-day-old rats born from mothers exposed to TCDD displayed a reduction in cell viability (MTT assay) and an increase in the number of apoptotic nuclei (nuclear staining with Hoechst 33258) possibly associated with altered dendrite outgrowth (MAP2-immunoreactivity) with respect to control cell cultures. These changes were associated with impairment in cortical glutamate transmission, characterized by a reduction in basal and K+-evoked outflow as well as a decrease in [ 3H]glutamate uptake. Interestingly, the prenatal TCDD-induced alteration of cortical glutamate signaling is persistent since it was also present in 14- and 60-day-old offspring. Taken together, these results suggest that a single prenatal exposure to TCDD produces alterations in cortical neuron development associated with a long-term dysfunction of glutamate transmission in rat cerebral cortex. The possible relevance of these findings for the understanding of the long-lasting cognitive deficit observed in the offspring from mothers exposed to the toxicant during pregnancy, is discussed. © 2012 Elsevier Ltd. All rights reserved.

Giuliani A.,University of Bologna | Lorenzini L.,University of Bologna | Alessandri M.,University of Bologna | Torricella R.,University of Bologna | And 5 more authors.
BMC Complementary and Alternative Medicine | Year: 2015

Background: Low-level lasers working at 633 or 670 nm and emitting extremely low power densities (Ultra Low Level Lasers - ULLL) exert an overall effect of photobiostimulation on cellular metabolism and energy balance. In previous studies, it was demonstrated that ULLL pulsed emission mode regulates neurite elongation in vitro and exerts protective action against oxidative stress. Methods: In this study the action of ULLL supplied in both pulsed and continuous mode vs continuous LLL on fibroblast cultures (Mouse Embryonic Fibroblast-MEF) was tested, focusing on mitochondria network and the expression level of mRNA encoding for proteins involved in the cell-matrix adhesion. Results: It was shown that ULLL at 670 nm, at extremely low average power output (0.21 mW/ cm2) and dose (4.3 mJ/ cm2), when dispensed in pulsed mode (PW), but not in continuous mode (CW) supplied at both at very low (0.21 mW/cm2) and low levels (500 mW/cm2), modifies mitochondria network dynamics, as well as expression level of mRNA encoding for selective matrix proteins in MEF, e.g. collagen type 1α1 and integrin α5. Conclusions: We suggest that pulsatility, but not energy density, is crucial in regulating expression level of collagen I and integrin α5 in fibroblasts by ULLL. © Giuliani et al.

PubMed | University of Foggia, University of Ferrara and IRET Foundation
Type: Journal Article | Journal: Journal of Alzheimer's disease : JAD | Year: 2015

Considering the heterogeneity of pathological changes occurring in Alzheimers disease (AD), a therapeutic approach aimed both to neuroprotection and to neuroinflammation reduction may prove effective. Palmitoylethanolamide (PEA) has attracted attention for its anti-inflammatory/neuroprotective properties observed in AD animal models.We evaluated the protective role of PEA against amyloid- (A) toxicity on cell viability and glutamatergic transmission in primary cultures of cerebral cortex neurons and astrocytes from the triple-transgenic murine model of AD (3xTg-AD) and their wild-type littermates (non-Tg) mice.A (0.5 M; 24 h) affects the cell viability in cultured cortical neurons and astrocytes from non-Tg mice, but not in those from 3xTg-AD mice. These effects were counteracted by the pretreatment with PEA (0.1 M). Basal glutamate levels in cultured neurons and astrocytes from 3xTg-AD mice were lower than those observed in cultured cells from non-Tg mice. A-exposure reduced and increased glutamate levels in non-Tg mouse cortical neurons and astrocytes, respectively. These effects were counteracted by the pretreatment with PEA. By itself, PEA did not affect cell viability and glutamate levels in cultured cortical neurons and astrocytes from non-Tg or 3xTg-AD mice.The exposure to A induced toxic effects on cultured cortical neurons and astrocytes from non-Tg mice, but not in those from 3xTg-AD mice. Furthermore, PEA exerts differential effects against A-induced toxicity in primary cultures of cortical neurons and astrocytes from non-Tg and 3xTg-AD mice. In particular, PEA displays protective properties in non-Tg but not in 3xTg-AD mouse neuronal cultured cells overexpressing A.

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