Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Rolando Berlinguer-Palmini is active.

Publication


Featured researches published by Rolando Berlinguer-Palmini.


Visual Neuroscience | 2014

Optogenetic approaches to retinal prosthesis

John Martin Barrett; Rolando Berlinguer-Palmini; Patrick Degenaar

The concept of visual restoration via retinal prosthesis arguably started in 1992 with the discovery that some of the retinal cells were still intact in those with the retinitis pigmentosa disease. Two decades later, the first commercially available devices have the capability to allow users to identify basic shapes. Such devices are still very far from returning vision beyond the legal blindness. Thus, there is considerable continued development of electrode materials, and structures and electronic control mechanisms to increase both resolution and contrast. In parallel, the field of optogenetics—the genetic photosensitization of neural tissue holds particular promise for new approaches. Given that the eye is transparent, photosensitizing remaining neural layers of the eye and illuminating from the outside could prove to be less invasive, cheaper, and more effective than present approaches. As we move toward human trials in the coming years, this review explores the core technological and biological challenges related to the gene therapy and the high radiance optical stimulation requirement.


PLOS ONE | 2013

GPR35 Activation Reduces Ca2+ Transients and Contributes to the Kynurenic Acid-Dependent Reduction of Synaptic Activity at CA3-CA1 Synapses

Rolando Berlinguer-Palmini; Alessio Masi; Roberto Narducci; Leonardo Cavone; Dario Maratea; Andrea Cozzi; Maria Sili; Flavio Moroni; Guido Mannaioni

Limited information is available on the brain expression and role of GPR35, a Gi/o coupled receptor activated by kynurenic acid (KYNA). In mouse cultured astrocytes, we detected GPR35 transcript using RT-PCR and we found that KYNA (0.1 to 100 µM) decreased forskolin (FRSK)-induced cAMP production (p<0.05). Both CID2745687 (3 µM, CID), a recently described GPR35 antagonist, and GPR35 gene silencing significantly prevented the action of KYNA on FRSK-induced cAMP production. In these cultures, we then evaluated whether GPR35 activation was able to modulate intracellular Ca2+ concentration ([Ca2+]i ) and [Ca2+]i fluxes. We found that both KYNA and zaprinast, a phosphodiesterase (PDE) inhibitor and GPR35 agonist, did not modify either basal or peaks of [Ca2+]i induced by challenging the cells with ATP (30 µM). However, the [Ca2+]i plateau phase following peak was significantly attenuated by these compounds in a store-operated Ca2+ channel (SOC)-independent manner. The activation of GPR35 by KYNA and zaprinast was also studied at the CA3-CA1 synapse in the rat hippocampus. Evoked excitatory post synaptic currents (eEPSCs) were recorded from CA1 pyramidal neurons in acute brain slices. The action of KYNA on GPR35 was pharmacologically isolated by using NMDA and α7 nicotinic receptor blockers and resulted in a significant reduction of eEPSC amplitude. This effect was prevented in the presence of CID. Moreover, zaprinast reduced eEPSC amplitude in a PDE5- and cGMP-independent mechanism, thus suggesting that glutamatergic transmission in this area is modulated by GPR35. In conclusion, GPR35 is expressed in cultured astrocytes and its activation modulates cAMP production and [Ca2+]i. GPR35 activation may contribute to KYNA effects on the previously reported decrease of brain extracellular glutamate levels and reduction of excitatory transmission.


IEEE Transactions on Biomedical Engineering | 2013

A Processing Platform for Optoelectronic/Optogenetic Retinal Prosthesis

Walid Al-Atabany; Brian McGovern; Kamyar Mehran; Rolando Berlinguer-Palmini; Patrick Degenaar

The field of retinal prosthesis has been steadily developing over the last two decades. Despite the many obstacles, clinical trials for electronic approaches are in progress and already demonstrating some success. Optogenetic/optoelectronic retinal prosthesis may prove to have even greater capabilities. Although resolutions are now moving beyond recognition of simple shapes, it will nevertheless be poor compared to normal vision. If we define the aim to be to return mobility and natural scene recognition to the patient, it is important to maximize the useful visual information we attempt to transfer. In this paper, we highlight a method to simplify the scene, perform spatial image compression, and then apply spike coding. We then show the potential for translation on standard consumer processors. The algorithms are applicable to all forms of visual prosthesis, but we particularly focus on optogenetic approaches.


Molecular Brain | 2015

Channel-mediated astrocytic glutamate modulates hippocampal synaptic plasticity by activating postsynaptic NMDA receptors

Hyungju Park; Kyung Seok Han; Jinsoo Seo; Jaekwang Lee; Shashank M. Dravid; Junsung Woo; Heejung Chun; Sukhee Cho; Jin Young Bae; Heeyoung An; Woohyun Koh; Bo Eun Yoon; Rolando Berlinguer-Palmini; Guido Mannaioni; Stephen F. Traynelis; Yong Chul Bae; Se-Young Choi; C. Justin Lee

BackgroundActivation of G protein coupled receptor (GPCR) in astrocytes leads to Ca2+-dependent glutamate release via Bestrophin 1 (Best1) channel. Whether receptor-mediated glutamate release from astrocytes can regulate synaptic plasticity remains to be fully understood.ResultsWe show here that Best1-mediated astrocytic glutamate activates the synaptic N-methyl-D-aspartate receptor (NMDAR) and modulates NMDAR-dependent synaptic plasticity. Our data show that activation of the protease-activated receptor 1 (PAR1) in hippocampal CA1 astrocytes elevates the glutamate concentration at Schaffer collateral-CA1 (SC-CA1) synapses, resulting in activation of GluN2A-containing NMDARs and NMDAR-dependent potentiation of synaptic responses. Furthermore, the threshold for inducing NMDAR-dependent long-term potentiation (LTP) is lowered when astrocytic glutamate release accompanied LTP induction, suggesting that astrocytic glutamate is significant in modulating synaptic plasticity.ConclusionsOur results provide direct evidence for the physiological importance of channel-mediated astrocytic glutamate in modulating neural circuit functions.


Molecular Pharmacology | 2015

Pharmacological NAD-Boosting Strategies Improve Mitochondrial Homeostasis in Human Complex I-Mutant Fibroblasts

Roberta Felici; Andrea Lapucci; Leonardo Cavone; Sara Pratesi; Rolando Berlinguer-Palmini; Alberto Chiarugi

Mitochondrial disorders are devastating genetic diseases for which efficacious therapies are still an unmet need. Recent studies report that increased availability of intracellular NAD obtained by inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation with the NAD-precursor nicotinamide riboside (NR) ameliorates energetic derangement and symptoms in mouse models of mitochondrial disorders. Whether these pharmacological approaches also improve bioenergetics of human cells harboring mitochondrial defects is unknown. It is also unclear whether the same signaling cascade is prompted by PARP-1 inhibitors and NR supplementation to improve mitochondrial homeostasis. Here, we show that human fibroblasts mutant for the NADH dehydrogenase (ubiquinone) Fe-S protein 1 (NDUFS1) subunit of respiratory complex I have similar ATP, NAD, and mitochondrial content compared with control cells, but show reduced mitochondrial membrane potential. Interestingly, mutant cells also show increased transcript levels of mitochondrial DNA but not nuclear DNA respiratory complex subunits, suggesting activation of a compensatory response. At variance with prior work in mice, however, NR supplementation, but not PARP-1 inhibition, increased intracellular NAD content in NDUFS1 mutant human fibroblasts. Conversely, PARP-1 inhibitors, but not NR supplementation, increased transcription of mitochondrial transcription factor A and mitochondrial DNA–encoded respiratory complexes constitutively induced in mutant cells. Still, both NR and PARP-1 inhibitors restored mitochondrial membrane potential and increased organelle content as well as oxidative activity of NDUFS1-deficient fibroblasts. Overall, data provide the first evidence that in human cells harboring a mitochondrial respiratory defect exposure to NR or PARP-1, inhibitors activate different signaling pathways that are not invariantly prompted by NAD increases, but equally able to improve energetic derangement.


Proceedings of SPIE | 2013

Development of optics with micro-LED arrays for improved opto-electronic neural stimulation

Lionel Chaudet; Mark A. A. Neil; Patrick Degenaar; Kamyar Mehran; Rolando Berlinguer-Palmini; Brian Corbet; Pleun Maaskant; David Rogerson; Peter M. P. Lanigan; Ernst Bamberg; Botond Roska

The breakthrough discovery of a nanoscale optically gated ion channel protein, Channelrhodopsin 2 (ChR2), and its combination with a genetically expressed ion pump, Halorhodopsin, allowed the direct stimulation and inhibition of individual action potentials with light alone. This work reports developments of ultra-bright elec tronically controlled optical array sources with enhanced light gated ion channels and pumps for use in systems to further our understanding of both brain and visual function. This work is undertaken as part of the European project, OptoNeuro. Micro-LED arrays permit spatio-temporal control of neuron stimulation on sub-millisecond timescales. However they are disadvantaged by their broad spatial light emission distribution and low fill factor. We present the design and implementation of a projection and micro-optics system for use with a micro-LED array consisting of a 16x16 matrix of 25 μm diameter micro-LEDs with 150 μm centre-to-centre spacing and an emission spectrum centred at 470 nm overlapping the peak sensitivity of ChR2 and its testing on biological samples. The projection system images the micro-LED array onto micro-optics to improve the fill-factor from ~2% to more than 78% by capturing a larger fraction of the LED emission and directing it correctly to the sample plane. This approach allows low fill factor arrays to be used effectively, which in turn has benefits in terms of thermal management and electrical drive from CMOS backplane electronics. The entire projection system is integrated into a microscope prototype to provide stimulation spots at the same size as the neuron cell body (μ10 pm).


PLOS ONE | 2014

Arrays of MicroLEDs and Astrocytes: Biological Amplifiers to Optogenetically Modulate Neuronal Networks Reducing Light Requirement

Rolando Berlinguer-Palmini; Roberto Narducci; Kamyar Merhan; Arianna Dilaghi; Flavio Moroni; Alessio Masi; Tania Scartabelli; Elisa Landucci; Maria Sili; Antonio Schettini; Brian McGovern; Pleun Maskaant; Patrick Degenaar; Guido Mannaioni

In the modern view of synaptic transmission, astrocytes are no longer confined to the role of merely supportive cells. Although they do not generate action potentials, they nonetheless exhibit electrical activity and can influence surrounding neurons through gliotransmitter release. In this work, we explored whether optogenetic activation of glial cells could act as an amplification mechanism to optical neural stimulation via gliotransmission to the neural network. We studied the modulation of gliotransmission by selective photo-activation of channelrhodopsin-2 (ChR2) and by means of a matrix of individually addressable super-bright microLEDs (μLEDs) with an excitation peak at 470 nm. We combined Ca2+ imaging techniques and concurrent patch-clamp electrophysiology to obtain subsequent glia/neural activity. First, we tested the μLEDs efficacy in stimulating ChR2-transfected astrocyte. ChR2-induced astrocytic current did not desensitize overtime, and was linearly increased and prolonged by increasing μLED irradiance in terms of intensity and surface illumination. Subsequently, ChR2 astrocytic stimulation by broad-field LED illumination with the same spectral profile, increased both glial cells and neuronal calcium transient frequency and sEPSCs suggesting that few ChR2-transfected astrocytes were able to excite surrounding not-ChR2-transfected astrocytes and neurons. Finally, by using the μLEDs array to selectively light stimulate ChR2 positive astrocytes we were able to increase the synaptic activity of single neurons surrounding it. In conclusion, ChR2-transfected astrocytes and μLEDs system were shown to be an amplifier of synaptic activity in mixed corticalneuronal and glial cells culture.


Journal of Biophotonics | 2018

Opto-electro-thermal optimization of photonic probes for optogenetic neural stimulation

Na Dong; Rolando Berlinguer-Palmini; Ahmed Soltan; Nikhil K. Ponon; Anthony O'Neil; Andrew Travelyan; Pleun Maaskant; Patrick Degenaar; Xiaohan Sun

Implantable photonic probes are of increasing interest to the field of biophotonics and in particular, optogenetic neural stimulation. Active probes with onboard light emissive elements allow for electronic multiplexing and can be manufactured through existing microelectronics methods. However, as the optogenetics field moves towards clinical practice, an important question arises as to whether such probes will cause excessive thermal heating of the surrounding tissue. Light emitting diodes typically produce more heat than light. The resultant temperature rise of the probe surface therefore needs to be maintained under the regulatory limit of 2°C. This work combines optical and thermal modelling, which have been experimental verified. Analysis has been performed on the effect of probe/emitter geometries, emitter, and radiance requirements. Finally, the effective illumination volume has been calculated within thermal limits for different probe emitter types and required thresholds.


Immunity | 2018

PD-1 Inhibitory Receptor Downregulates Asparaginyl Endopeptidase and Maintains Foxp3 Transcription Factor Stability in Induced Regulatory T Cells

Chaido Stathopoulou; Arunakumar Gangaplara; Grace Mallett; Francis A. Flomerfelt; Lukasz P. Liniany; David Knight; Leigh Samsel; Rolando Berlinguer-Palmini; Joshua J. Yim; Tania C. Felizardo; Michael A. Eckhaus; Laura E. Edgington-Mitchell; Jonathan Martinez-Fabregas; Daniel H. Fowler; Sander I. van Kasteren; Arian Laurence; Matthew Bogyo; Colin Watts; Ethan M. Shevach; Shoba Amarnath

SUMMARY CD4+ T cell differentiation into multiple T helper (Th) cell lineages is critical for optimal adaptive immune responses. This report identifies an intrinsic mechanism by which programmed death‐1 receptor (PD‐1) signaling imparted regulatory phenotype to Foxp3+ Th1 cells (denoted as Tbet+iTregPDL1 cells) and inducible regulatory T (iTreg) cells. Tbet+iTregPDL1 cells prevented inflammation in murine models of experimental colitis and experimental graft versus host disease (GvHD). Programmed death ligand‐1 (PDL‐1) binding to PD‐1 imparted regulatory function to Tbet+iTregPDL1 cells and iTreg cells by specifically downregulating endo‐lysosomal protease asparaginyl endopeptidase (AEP). AEP regulated Foxp3 stability and blocking AEP imparted regulatory function in Tbet+iTreg cells. Also, Aep−/− iTreg cells significantly inhibited GvHD and maintained Foxp3 expression. PD‐1‐mediated Foxp3 maintenance in Tbet+ Th1 cells occurred both in tumor infiltrating lymphocytes (TILs) and during chronic viral infection. Collectively, this report has identified an intrinsic function for PD‐1 in maintaining Foxp3 through proteolytic pathway. Graphical Abstract Figure. No caption available. HighlightsAsparaginyl endopeptidase (AEP) is expressed in induced regulatory T cellsAEP cleaves Foxp3 and Aep−/− mice have elevated numbers of peripheral Treg cellsAEP deficiency increases Treg cell frequency and numbers in GvHD and melanomaPD‐1 signaling maintains Foxp3 protein expression by inhibiting AEP &NA; Th1 cells are known for their enhanced stability, so mechanisms that mediate their flexibility are poorly studied. Here, Stathopoulou et al. demonstrate that plasticity of Th1 cells to Tbet+iTreg cells is mediated by PD‐1 signaling via asparaginyl endopeptidase (AEP). AEP inhibition enhanced iTreg cells in GvHD and tumor models.


biomedical circuits and systems conference | 2009

Optoelectronic microarrays for retinal prosthesis

Patrick Degenaar; Nir Grossman; Rolando Berlinguer-Palmini; Brian McGovern; V. Pohrer; Emmanuel M. Drakakis; Martin D. Dawson; Christofer Toumazou; Juan Burrone; Konstantin Nikolic; Mark A. A. Neil

In this work we demonstrate the use of optoelectronic Gallium Nitride LED micro arrays for optical neural stimulation. We demonstrate the ability to control these sufficiently to transfer a spike coded ‘image’ to arrays of channelrhodopsin-2 photosensitized cells. We also show how this initial work is scalable from in-vitro towards a long term optoelectronic system for optogenetic retinal prosthesis.

Collaboration


Dive into the Rolando Berlinguer-Palmini's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Nir Grossman

Imperial College London

View shared research outputs
Top Co-Authors

Avatar

V. Pohrer

Imperial College London

View shared research outputs
Top Co-Authors

Avatar

Pleun Maaskant

Tyndall National Institute

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge