Search

Background Oxidative stress plays an important role in neurodegeneration, pain and inflammation. (R)-(-)-linalool (LIN) is endowed with neuroprotective, anti-nociceptive and anti-inflammatory properties. Purpose The present study aims at investigating the hypothesis that LIN's neuroprotective, antinociceptive and anti-inflammatory properties descend from its ability to act as antioxidant. The study challenges this hypothesis by verifying whether LIN may counteract hydrogen peroxide (H2O2)-induced oxidative stress in PC12 cells. Methods In H2O2-exposed PC12 cells, LIN was tested on a) cell viability, measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), b) damage of plasma membrane, measured by lactate dehydrogenase (LDH) release, c) intracellular levels of reactive-oxygen-species (ROS), d) apoptosis and e) cell cycle distribution. Results Under H2O2-induced cell viability reduction, LIN protects PC12 cells. Likewise, LIN protects cells from oxidative damage by preventing the H2O2-dependent increase of LDH release, counteracts intracellular ROS overproduction and reduces H2O2-induced apoptosis. Finally, the results of the cell cycle analysis from cells exposed to H2O2 indicate that LIN incubation reduces the number of cells induced into quiescence by H2O2 in the G2/M phase. Conclusions These findings indicate that LIN protects PC12 cells from H2O2-induced oxidative stress. This mechanism could justify the neuroprotective, anti-nociceptive and anti-inflammatory effects of this compound and suggest LIN as a potential therapeutic agent for the management oxidative stress-mediated pain.

The Ca2+ sensitizer levosimendan (LEV) improves myocardial contractility by enhancing the sensitivity of the contractile apparatus to Ca2+. In addition, LEV promotes Ca2+ entry through L-type channels in human cardiac myocytes. In this study, which was performed using microdialysis, infusion of LEV at 0.25 μM for 160 min increased dopamine (DA) concentrations (up to fivefold baseline) in dialysates from the striatum of freely moving rats. Ca2+ omission from the perfusion fluid abolished baseline DA release and greatly decreased LEV-induced DA release. Reintroduction of Ca2+ in the perfusion fluid restored LEV-induced DA release. Chelation of intracellular Ca2+ by co-infusing 1,2-bis (o-amino-phenoxy)ethane-N,N,N′,N′-tetraacetic acid tetra (acetoxymethyl) ester (BAPTA-AM, 0.2 mM) did not affect basal DA release and scarcely affected LEV-induced increases in dialysate DA. In addition, co-infusion of the L-type (Cav 1.1 – 1.3) voltage-sensitive Ca2+-channel inhibitor nifedipine failed to inhibit LEV-induced increases in dialysate DA, which, in contrast, was inhibited by co-infusion of the N-type (Cav 2.2) voltage-sensitive Ca2+-channel inhibitor ω-conotoxin GVIA. We conclude that LEV promotes striatal extracellular Ca2+ entry through N-type Ca2+ channels with a consequent increase in DA release. Keywords:: levosimendan, microdialysis, striatal dopamine, calcium entry

Corrigendum to “Reactive astrocytes and Wnt/β-catenin signaling link nigrostriatal injury to repair in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease” [Neurobiol. Dis. 41/2 (2011) 508–527] F. L'Episcopo , C. Tirolo , N. Testa , S. Caniglia , M.C. Morale , C. Cossetti , P. D'Adamo , E. Zardini , L. Andreoni , A.E.C. Ihekwaba , P.A. Serra , D. Franciotta , G. Martino , S. Pluchino , B. Marchetti a,g,h,⁎

A new bidirectional telemetry system for amperometric sensor applications has been developed. A fully automated peripheral unit (PU), constituted by a potentiostat, a two-channel I/V converter, a microcontroller unit (MCU) and a signal transmitter, was designed, constructed, and tested. A peripheral interface controller (PIC) MCU drives a digital-to-analog converter (DAC), which polarized the sensor, while the resulting anodic current is converted to a digital value by an analog-to-digital converter (ADC). The PIC firmware is developed in assembly and transferred to the MCU through a bootloader algorithm. The digital data are sent to a personal computer using a 4-byte packet protocol by means of a miniaturized 433 MHz frequency modulation (FM) transceiver with a linear range up to 200 m. The central unit (CU) is connected to a PC via Universal Serial Bus (USB). Custom developed software, implemented in Basic and C, allows the PC to control several PUs and record, plot and handle received data. The development and operation of the hardware and software are described. The system performance was evaluated using an automated dummy cell connected to the PU. The amperometric response of nitric oxide (NO), dopamine (DA) microsensors and a glucose biosensor was determined in vitro. This apparatus serves as a basic model to realize an in vivo bidirectional telemetry system built with standard components readily available at low cost.

A new embedded telemetry system for amperometric biosensor application is presented. The device consists of a single-supply miniature potentiostat-I/V converter, a microcontroller unit (MCU), a signal transmitter, and a stabilized power supply. The sensor current is converted to a digital value using a peripheral interface controller (PIC) MCU with an integrated analog-to-digital converter (ADC). The PIC firmware is developed in assembly and transferred to the MCU through an in-circuit-serial-programmer (ICSP). The digital data are sent to a personal computer using a miniaturized 433.92 MHz amplitude modulation (AM) transmitter with a linear range up to 30 m. The radio receiver is connected to a PC via a Universal Serial Bus (USB). Custom developed software, written in C and Basic, allows the PC to record, plot and handle the received data. The design, construction and operation of the hardware and software are described. The system performance was evaluated in vitro using a dummy cell and a platinum (Pt) amperometric glucose biosensor. This device serves as a basic model to realize an in vivo, low-cost, miniaturized telemetry system built with standard hardware components readily available.