We developed an experimental setup for selective infrared (IR) stimulation of an isolated porcine vagus nerve. The system consists of an infrared IR diode (IR diode), providing an optical power of 6.5 W at [lambda] = 1937 nm, high-quality fibre optic multimode patch cables, an optical pulse shaper, and a custom made experimental chamber. The system allows researchers to vary: the radiant exposure from 0 to 2.3 Jcm-2, vertical displacement of the IR aperture, nominal pulse duration that could be set at 250, 500, and 800 [micro]s, and frequency of IR pulses between 15 and 50 Hz, enabling the assessment of the relationship between different patterns of IR pulses and the elicited nerve response (NR). The main contribution resulting from the study is an optical pulse shaper, which generates IR pulses with a rise-time of approximately 100 ns, and facilitatesan appropriate coupling efficiency via a Grin Lens Fibre Coupler/Fibre Optic Positioner. Another novelty is the 3D positioning device of the experimental chamber, which enables the ex-vivo assessment of spatial and fibre-type selectivity.
COBISS.SI-ID: 34307289
Ibogaine, administered as a single oral dose (1-25 mg/kg body weight), has been used as an addiction-interrupting agent. Its effects persist for up to 72 h. Ex vivo results showed that ibogaine induced cellular energy consumption and restitution, followed by increased reactive oxygen species production and antioxidant activity. Therefore, the aim of this work was to explore the effect of a single oral dose of ibogaine (1 or 20 mg/kg body weight) on antioxidative defenses in rat liver and erythrocytes. Six and 24 h after ibogaine administration, histological examination showed glycogenolytic activity in hepatocytes, which was highest after 24 h in animals that received 20 mg/kg ibogaine. There were no changes in the activities of superoxide dismutases, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase in the liver and erythrocytes after ibogaine treatment, regardless of the dose. Hepatic xanthine oxidase activity was elevated in rats that received 20 mg/kg compared to the controls (p(0.01), suggesting faster adenosine turnover. TBARS concentration was elevated in the group treated with 1 mg/kg after 24 h compared to the controls (p(0.01), suggesting mild oxidative stress. Our results show that ibogaine treatment influenced hepatic redox homeostasis, but not sufficiently to remodel antioxidant enzyme activities at 6 and 24 h post-ibogaine application. [Project of the Serbian Ministry of Education, Science and Technological Development,...
COBISS.SI-ID: 34217689
Our previous results showed that a single oral dose (1 or 20 mg/kg body weight) of the anti-addiction agent ibogaine induced in rats 6 and 24 h after administration glycogenolytic activity in hepatocytes, followed by a mild oxidative stress. In this work, we examined the in vivo effect of the same doses of ibogaine on rat kidney morphology, antioxidant enzyme (superoxide dismutases (SOD 1 and 2), catalase, glutathione peroxidase (GSH-Px), glutathione reductase (GR) and glutathione-S-transferase) activities, and oxidative stress (TBARS) and redox (-SH groups) parameters. The dose of 1 mg/kg ibogaine induced an elevation in SOD1 activity and decreased GR activity after 6 and 24 h. GR activity was decreased at 6 and 24 h after 20 mg/kg ibogaine administration, suggesting changed redox homeostasis. After 24 h, we observed an increase in moderate morphological changes, without changes in urinalyses, indicating that kidney function was not measurably affected. Nevertheless, kidney-function monitoring during and following ibogaine use in human subjects is advisable. [Project of the Serbian Ministry of Education, Science and Technological Development, Grant no.173014: Molecular mechanisms of redox signaling in homeostasis, adaptation and pathology]
COBISS.SI-ID: 34217945
Neuroinflammation is an important factor in pathogenesis of neurodegenerative diseases. Microglia-derived lysosomal cathepsins have been increasingly recognized as important inflammatory mediators that trigger signalling pathways that aggravate neuroinflammation. In vitro, a contribution to neuroinflammation processes has been shown for cathepsin X, however; the expression patterns and functional roles of cathepsin X in neuroinflammatory brain pathology remain elusive. In this study, we analyzed the expression, activity, regional distribution and cellular localization of cathepsin X in the rat brain with neuroinflammation-induced neurodegeneration. Unilateral injection of LPS induced strong upregulation of cathepsin X expression and its activity in the ipsilateral striatum. In addition to the striatum, cathepsin X overexpression was detected in other brain areas such as cerebral cortex, corpus callosum, subventricular zone and external globus pallidus, whereas the upregulation was mainly restricted to activated microglia and reactive astrocytes. Continuous administration of the cathepsin X inhibitor AMS36 indicated protective effects against LPS-induced striatal degeneration, as seen by the attenuated the LPS-mediated dilation of the lateral ventricles and partial decreased extent of striatal lesion. Taken together, our results indicate that cathepsin X plays a role as a pathogenic factor in neuroinflammation-induced neurodegeneration.
COBISS.SI-ID: 36086275
We hypothesised that if pathophysiology differs between sexes in PD, this will be reflected in differences of motor cortex measurements with transcranial magnetic stimulation. The study provides one of the first neurophysiological evidences of sex differences in early PD. Female patients have a more favorable profile of transcranial magnetic stimulation measures, possibly reflecting a more successful cortical compensation or delayed maladaptive changes in the sensorimotor cortex.
COBISS.SI-ID: 6593452