The anticonvulsant action of 1,5-benzodiazepine clobazam was studied in 12-, 18-, and 25-day-old rats. Cortical epileptic afterdischarges (ADs) elicited by rhythmic electrical stimulation of the sensorimotor cortical area were used as a model in animals with implanted electrodes. As far as the duration of ADs is concerned, clobazam in doses of 1 or 5 mg/kg i.p. blocked the progressive increase with repeated stimulations in all age groups and the higher dose significantly shortened ADs in 25-day-old rats. The intensity of movements accompanying stimulation was decreased only by the 5 mg/kg dose in 25-day-old animals, whereas clonic seizures were less intense after both doses in 12- and 25-day-old rat pups. Clobazam exerted an anticonvulsant action at all the developmental stages studied; the lower efficacy in 18-day-old rats (described also for clonazepam) remains to be analyzed.
Activation of GABAB receptors leads to longer inhibitory postsynaptic potentials than activation of GABAA receptors. Therefore GABAB receptors may be a target for anticonvulsant therapy. The present study examined possible effects of GABAB receptor agonist SKF97541 on cortical and hippocampal epileptic afterdischarges (ADs). Epileptic ADs elicited by electrical stimulation of sensorimotor cortex or dorsal hippocampus were studied in adult male Wistar rats. Stimulation series were applied 6 times with 10- or 20-min interval. Either interval was efficient for reliable elicitation of cortical ADs but stimulation at 10-min intervals did not reliably elicit hippocampal ADs, many stimulations were without effect. SKF97541 in dose 1 mg/kg significantly prolonged cortical ADs. Duration of hippocampal ADs was not significantly changed by either dose of SKF97541 in spite of a marked myorelaxant effect of the higher dose. Our present data demonstrated that neither cortical nor hippocampal ADs in adult rats were suppressed by GABAB receptor agonist SKF97541. Proconvulsant effect on cortical ADs indicates a different role in these two brain structures. In addition, duration of refractory period for electrically-induced ADs in these two structures in adult rats is different., P. Fábera, P. Mares., and Obsahuje bibliografii
Recent reports have indicated a considerably inactivated PSII in twig cortices, in spite of the low light transmittance of overlying periderms. Corresponding information for more deeply located and less illuminated tissues like xylem rays and pith are lacking. In this investigation we aimed to characterize the efficiency of PSII and its light sensitivity along twig depth, in conjunction with the prevailing light quantity and quality. To that aim, optical methods (spectral reflectance and transmittance, chlorophyll fluorescence imaging, low temperature fluorescence spectra) and photoinhibitory treatments were applied in cut twig sections of four tree species, while corresponding leaves served as controls. Compared to leaves, twig tissues displayed lower chlorophyll (Chl) levels and dark-adapted PSII efficiency, with strong decreasing gradients towards the twig center. The low PSII efficiencies in the inner stem were not an artifact due to an actinic effect of measuring beam or to an enhanced contribution of PSI fluorescence. In fact, the PSII/PSI ratios in cortices were higher and those in the xylem rays similar to that of leaves. Inner twig tissues were quite resistant to photoinhibitory treatments, tolerating irradiation levels several-fold higher than those encountered in their microenvironment. Moreover, the extent of high light tolerance was similar in naturally exposed and shaded twig sides. The results indicate an increasing, inherent and light-independent inactivation of PSII along twig depth. The findings are discussed on the basis of a recently proposed model for photosynthetic electron flow in twigs, taking into account the specific atmospheric and light microenvironment as well as the possible metabolic needs of such bulky organs. and C. Yiotis, Y. Petropoulou, Y. Manetas.
Five-sixths nephrectomy is a widely used experimental model of chronic kidney disease (CKD) that is associated with severe mitochondrial dysfunction of the remnant tissue. In this study, we assessed the effect of CKD on mitochondrial respiration separately in the rat kidney cortex and medulla 10 weeks after induction of CKD by subtotal 5/6 nephrectomy (SNX). Mitochondrial oxygen consumption was evaluated on mechanically permeabilized samples of kidney cortex and medulla using high-resolution respirometry and expressed per mg of tissue wet weight or IU citrate synthase (CS) activity. Mitochondrial respiration in the renal cortex of SNX rats was significantly reduced in all measured respiratory states if expressed per unit wet weight and remained lower if recalculated per IU citrate synthase activity, i.e. per mitochondrial mass. In contrast, the profound decrease in the activity of CS in SNX medulla resulted in significantly elevated respiratory states expressing the OXPHOS capacity when Complexes I and II or II only are provided with electrons, LEAK respiration after oligomycin injection, and Complex IV-linked oxygen consumption per unit CS activity suggesting compensatory hypermetabolic state in remaining functional mitochondria that is not sufficient to fully compensate for respiratory deficit expressed per tissue mass. The results document that CKD induced by 5/6 nephrectomy in the rat is likely to cause not only mitochondrial respiratory dysfunction (in the kidney cortex), but also adaptive changes in the medulla that tend to at least partially compensate for mitochondria loss.