Cellular and molecular neurobiology
-
Cell. Mol. Neurobiol. · Sep 2009
Serum neuron specific enolase and malondialdehyde in patients after out-of-hospital cardiac arrest.
Sudden cardiac arrest (CA) is a leading cause of death in Europe. The victims of CA need immediate cardiopulmonary resuscitation (CPR). Patients resuscitated due to CA have high mortality rate. Prognostic evaluation based on clinical observation is uncertain and would benefit from the use of biochemical markers of hypoxic brain damage. Multiple factors of brain origin can be measured in blood. ⋯ Estimation serum concentrations of NSE but not MDA seems to be a predictor of fate of patients after CA. The exact nature of oxidative stress can only be resolved by further studies.
-
Cell. Mol. Neurobiol. · Sep 2009
Spinal cord transection significantly influences nNOS-IR in neuronal circuitry that underlies the tail-flick reflex activity.
Spinal cord transection interrupts supraspinal input and leads to the development of prominent spasticity. In this study, we investigated the effect of rat spinal cord transection performed at low thoracic level on changes in (i) neuronal nitric oxide synthase immunoreactivity (nNOS-IR), and (ii) the level of neuronal nitric oxide synthase (nNOS) protein in the neuronal circuitry that underlies tail-flick reflex. ⋯ These data indicate that transection of the spinal cord significantly influences nNOS-IR in neuronal circuitry that underlies the tail-flick reflex activity.
-
Cell. Mol. Neurobiol. · Jul 2009
Differential regulation of CuZnSOD expression in rat brain by acute and/or chronic stress.
Neuroendocrine stress (NES) causes increase of glucocorticoids and alters physiological levels of reactive oxygen species production in cells, which might involve modifications in the antioxidant defense system. We investigated the hypothesis that acute, chronic, or combined stress alters copper-zinc superoxide dismutase (CuZnSOD) expression pattern at both, mRNA and subcellular protein level in the cerebral cortex and hippocampus of rats and that there may be a relationship between stress-induced corticosterone and CuZnSOD expression. The most effective stress model which led to the most pronounced changes in CuZnSOD expression patterns was also investigated. ⋯ Chronic isolation compromises CuZnSOD protein expression, which may lead to the inefficient defense against reactive oxygen species (ROS). The stress-triggered CuZnSOD protein expression was not correlated by the corresponding mRNA. The results suggest that different stress models exert a different degree of influence on mRNA and protein level of CuZnSOD in both brain structures as well as serum corticosterone.
-
Cell. Mol. Neurobiol. · Mar 2009
Dynamic alterations of cerebral pial microcirculation during experimental subarachnoid hemorrhage.
The study aimed to investigate the involvement of cerebral microcirculation turbulence after subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH and SAH groups. Autologous arterial hemolysate was injected into rat's cisterna magna to induce SAH. ⋯ Decreased flow velocity of venules was found from 5 to 90 min after induction of SAH. Spasm of the basilar artery and increased brain malondialdehyde were also found after SAH. We concluded that cerebral microcirculation turbulence plays an important role in the development of secondary cerebral ischemia following SAH.
-
Cell. Mol. Neurobiol. · Nov 2008
Local loperamide inhibits thermal hyperalgesia but not mechanical allodynia induced by intratibial inoculation of melanoma cells in mice.
The stimulation of peripheral opioid receptors counteracts thermal hyperalgesia produced by the intratibial inoculation of NCTC 2472 cells in mice, through the activation of the nitric oxide/cGMP/ATP-sensitive K+-channels (NO/cGMP/K(+) (ATP)) cascade (Menéndez et al. 2007, Neuropharmacology 53:71-80). We aimed to elucidate whether this peripheral opioid antihyperalgesic effect is exclusive to this model or might also occur in other types of bone neoplastic processes. In C57BL/6 mice intratibially inoculated with B16-F10 melanoma cells, the progressive tumoral damage was accompanied by the establishment of thermal hyperalgesia (unilateral hot plate test) and mechanical allodynia (von Frey test). ⋯ The fact that the coadministration of naloxone-methiodide (5 microg) completely suppressed the thermal antihyperalgesic effect induced by loperamide indicates its production through the stimulation of peripheral opioid receptors. Furthermore, its prevention by the coadministration of the non-selective inhibitor of the NO synthase, N(G)-monomethyl-L-arginine (L-NMMA, 10 microg), the selective inhibitor of neural NOS, N-omega-propyl-L-arginine (1-10 microg), or the K+ (ATP) channel blocker, glibenclamide (10 microg) demonstrated the involvement of the NO/cGMP/K(+) (ATP) pathway in the antihyperalgesic effect induced by loperamide. Overall, the present results show that the intratibial inoculation of B16-F10 cells to C57BL/6 mice evokes thermal hyperalgesia and mechanical allodynia and that, as occurred in the osteosarcoma model, the stimulation of peripheral opioid receptors is not effective in modifying neoplastic allodynia but completely inhibits thermal hyperalgesia through the activation of the NO/cGMP/K+ (ATP) cascade.