Vibrational and Photoluminescence Properties of Composites Based on Double-Walled Carbon Nanotubes, Poly(o-phenylenediamine) and Poly(ethylene oxide).

Chemical polymerization of o-phenylenediamine (OPD) in the presence of poly(ethylene oxide), double-wall carbon nanotubes (DWNTs) and ferric chloride is carried out in order to obtain composites based on the poly(o-phenylenediamine)-poly(ethylene oxide) (POPD-PEO) fibres covered and interconnected with DWNTs. Vibrational and photoluminescence properties of these composite materials as well as their morphologies are shown by infrared (IR) spectroscopy, Raman scattering, photoluminescence (PL) and scanning electron microscopy (SEM). An adsorption of DWNTs onto the POPD rods surface in the absence and in the presence of PEO is highlighted by SEM. The vibrational changes reported by Raman scattering and IR spectroscopy prove a covalent functionalization of DWNTs with the macromolecular compound POPD which is doped with FeCl-4 ions. New hydrogen bonds are generated between POPD covalently functionalized DWNTs and hydroxyl groups of PEO according to IR spectroscopic studies. The two macromolecular compounds, POPD and POPD-PEO, show a complex emission band with maxima at 572 and 566 nm, having a shoulder at 667 nm. A significant change in the profile of the PL bands of POPD and POPD-PEO is induced in the DWNTs presence. We show that DWNTs induce (i) a diminution in the POPD PL band intensity peaked between 525-600 nm simultaneous with the increase in the intensity of the PL band situated in the 600-800 nm spectral range and (ii) an enhancement process of the emission band localized in the 475-800 nm spectral range in the case of POPD-PEO.

Studies on brain volume, Alzheimer-related proteins and cytokines in mice with chronic overexpression of IL-1 receptor antagonist.

Inflammation is associated with both acute and chronic neurological disorders, including stroke and Alzheimer's disease (AD). Cytokines such as interleukin (IL)-1 have several activities in the brain both under physiological and pathophysiological conditions. The objective of this study was to evaluate consequences of the central blockade of IL-1 transmission in a previously developed transgenic mouse strain with brain-directed overexpression of human soluble IL-1 receptor antagonist (Tg hsIL-1ra). Effects on brain morphology and brain levels of the AD-related proteins beta-amyloid precursor protein (APP) and presenilin 1(PS1), as well as the levels of IL-1beta, IL-6 and tumour necrosis factor-alpha (TNF-alpha) were analysed in homozygotic and heterozygotic mice and wild type (WT) controls, of both genders and of young (30-40 days) and adult (13-14 months) age. A marked reduction in brain volume was observed in transgenic mice as determined by volumetry. Western blot analysis showed higher levels of APP, but lower levels of PS1, in adult animals than in young ones. In the cerebellum, heterozygotic (Tg hsIL-1ra(+/-)) mice had lower levels of APP and PS1 than WT mice. With one exception, there were no genotypic differences in the levels of IL-1beta, IL-6 and TNF-alpha. The cytokine levels were generally higher in adult than in young mice. In conclusion, the chronic blockade of IL-1 signalling in the brain was associated with an atrophic phenotype of the brain, and with modified levels of APP and PS1. Brain-directed overexpression of hsIL-1ra was not followed by major compensatory changes in the levels of pro-inflammatory cytokines.

Inflammatory mechanisms associated with brain damage induced by kainic acid with special reference to the interleukin-1 system.

The evidence of inflammatory processes in the clinical manifestations and neuropathological sequelae of epilepsy have accumulated in the last decade. Administration of kainic acid, an analogue of the excitatory amino acid glutamate, induces a characteristic behavioural syndrome and a reproducible pattern of neurodegeneration in several brain areas, closely resembling human temporal lobe epilepsy. Results from studies using the kainic acid model indicate that manipulation of pro- and anti-inflammatory cytokines can modify the outcome with regard to the behavioural syndrome as well as the neuropathological consequences. Interleukin-1 is one of the most important cytokines and has several actions in the brain that are critical for the host defense against injury and infection, and it is involved in the initiation of early stages of inflammation. It is believed that interleukin-1 plays a pivotal role in the neuroinflammation associated with certain forms of neurodegeneration, including cerebral ischemia, trauma and excitotoxic brain injury. In this review, we have summarized the experimental data available with regard to the involvement of the interleukin-1 system in kainic acid-induced changes in the brain and emphasized the modulatory role of interleukin-1beta in this model of epilepsy

Effects of kainic acid on rat body temperature: unmasking by dizocilpine.

The effects of intraperitoneal (i.p.) administration of kainic acid (KA) and dizocilpine, alone or in combination, on body temperature of freely moving rats were examined. Injection of saline or dizocilpine (3.0 or 5.0 mg/kg) was followed after an hour by injection of saline or KA (10 mg/kg) and the body temperature was measured at different time points during the first 5 h. KA alone produced an initial short-lasting hypothermia followed by a longer-lasting hyperthermic effect. Administration of dizocilpine alone produced an early increase in core temperature. Pretreatment of KA-injected rats with dizocilpine potentiated the KA-induced hypothermic effect at 30 min and dose-dependently reduced the temperature measured at 1 h after KA-injection without influencing the ensuing hyperthermia.These data suggest that the KA-induced changes in body temperature do not necessarily involve the activation of NMDA-receptors as opposed to KA-induced behavioural changes that are blocked by dizocilpine in a dose-dependent manner. It is unlikely, therefore, that the KA-induced hyperthermia is a result of the KA-induced seizure motor activity. Furthermore, our findings indicate that KA-induced changes in core temperature may be used as a criterion of drug-responsiveness when the behavioural changes are blocked, e.g. with dizocilpine.

Effects of alpha-MSH on kainic acid induced changes in core temperature in rats.

The effects of intraperitoneal (i.p.) administration of kainic acid (KA) and alpha-melanocyte-stimulating hormone (alpha-MSH) alone or in combination, on core temperature of freely moving rats were examined. KA or saline was administered once (10 mg/kg) and alpha-MSH or saline was given repeatedly i.e. 10 min before and 10, 30 and 60 min after the administration of saline or KA. Two doses of alpha-MSH were used: 0.5 and 2.5 mg/kg. KA alone produced a biphasic effect on core temperature, i.e. an initial short-lasting hypothermia followed by hyperthermia that lasted about 6 h. The higher dose of alpha-MSH had a potentiating effect on KA-induced hypothermia, while the lower dose of alpha-MSH increased the hyperthermia produced by KA. alpha-MSH administered alone produced a late (3 h), dose-dependent increase in core temperature. It is conceivable that repeated administration of alpha-MSH in the doses used in our study may cause a cumulative effect in raising body temperature for a limited period of time. The previously described interactions between KA and alpha-MSH, respectively, with dopaminergic and serotoninergic systems may account for the effects on core temperature in rats observed in our study.

Dantrolene protects neurons against kainic acid induced apoptosis in vitro and in vivo.

Apoptotic cell death induced by kainic acid (KA) in cultures of rat cerebellar granule cells (CGC) and in different brain regions of Wistar rat pups on postnatal day 21 (P21) was studied. In vitro, KA (100-500 microM) induced a concentration-dependent loss of cell viability in MTT assay and cell death had apoptotic morphology as studied by chromatin staining with propidium iodide (PI). In vivo, twenty-four hours after induction of status epilepticus (SE) by an intraperitoneal KA injection (5 mg/kg) we quantified apoptotic cells in hippocampus (CA1 and CA3), parietal cortex and cerebellum using PI staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) technique. We report that dantrolene, a specific ryanodine receptor antagonist, was able to significantly reduce the apoptotic cell death in CGC cultures and in hyppocampal CA1 and parietal cortex regions. Our finding can be valuable for neuroprotective therapy strategies in patients with repeated generalized seizures or status epilepticus.

A comparative study of EEG suppressions induced by global cerebral ischemia and anoxia.

Cerebral ischemia and anoxia induce sequential changes that include ionic redistribution, alteration of enzimatic reactions governing metabolism and intracellular signaling. Despite high technology instrumentation including positron emission, tomography and magnetic resonance imaging used to unravel the intricacies of cerebral blood flow and metabolism, the electroencephalography (EEG) retains a useful place in the evaluation of processes induced by cerebral ischemia, especially in experimental conditions. We have investigated in this study EEG suppression and recovery following global cerebral ischemia, obtained by "four vessel occlusion model", reperfusion and anoxia. Both cerebral ischemia and anoxia have produced a sudden diminution of electrical brain activity and flat line was recorded after 8-10 sec. in the ischemic rats, but after 35-40 sec. in the anoxic rats. After same period of time (2 min) of ischemia and anoxia EEG recovery has been faster in the ischemic rat.

EEG study of kainate-induced epilepsy in non-anaesthetized freely moving rats.

Epileptogenic activity of kainic acid (KA) was examined by a great number of in vitro studies but few in vivo studies were reported. In the present study, we investigated KA-induced epilepsy by clinical observation and EEG recordings in non-anaesthetized freely moving rats.