Decreased neuronal excitability in hippocampal neurons of mice exposed to cyclic hypoxia.
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To study the physiological effects of chronic intermittent hypoxia on neuronal excitability and function in mice, we exposed animals to cyclic hypoxia for 8 h daily (12 cycles/h) for approximately 4 wk, starting at 2-3 days of age, and examined the properties of freshly dissociated hippocampal neurons in vitro. Compared with control (Con) hippocampal CA1 neurons, exposed (Cyc) neurons showed action potentials (AP) with a smaller amplitude and a longer duration and a more depolarized resting membrane potential. They also have a lower rate of spontaneous firing of AP and a higher rheobase. Furthermore, there was downregulation of the Na(+) current density in Cyc compared with Con neurons (356.09 +/- 54.03 pA/pF in Cyc neurons vs. 508.48 +/- 67.30 pA/pF in Con, P < 0.04). Na(+) channel characteristics, including activation, steady-state inactivation, and recovery from inactivation, were similar in both groups. The deactivation rate, however, was much larger in Cyc than in Con (at -100 mV, time constant for deactivation = 0.37 +/- 0.04 ms in Cyc neurons and 0.18 +/- 0.01 ms in Con neurons). We conclude that the decreased neuronal excitability in mice neurons treated with cyclic hypoxia is due, at least in part, to differences in passive properties (e.g., resting membrane potential) and in Na(+) channel expression and/or regulation. We hypothesize that this decreased excitability is an adaptive response that attempts to decrease the energy expenditure that is used for adjusting disturbances in ionic homeostasis in low-O(2) conditions. (+info)
Growth and mitochondrial respiration of mungbeans (Phaseolus aureus Roxb.) germinated at low pressure.
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Mungbean (Phaseolus aureus Roxb.) seedlings were grown hypobarically to assess the effects of low pressure (21-24 kilopascals) on growth and mitochondrial respiration. Control seedlings grown at ambient pressure (101 kilopascals) were provided amounts of O2 equivalent to those provided experimental seedlings at reduced pressure to factor out responses to O2 concentration and to total pressure. Respiration was assayed using washed mitochondria, and was found to respond only to O2 concentration. Regardless of total pressure, seedlings grown at 2 millimoles O2 per liter had higher state 3 respiration rates and decreased percentages of alternative respiration compared to ambient (8.4 millimoles O2 per liter) controls. In contrast, seedling growth responded to total pressure but not to O2 concentration. Seedlings were significantly larger when grown under low pressure. While low O2 (2 millimoles O2 per liter) diminished growth at ambient pressure, growth at low pressure in the same oxygen concentration was enhanced. Respiratory development and growth of mungbean seedlings under low pressure is unimpaired whether oxygen or air is used as the chamber gas, and further, low pressure can improve growth under conditions of poor aeration. (+info)
Carnitine pretreatment can partially change the excitability of the immature nervous tissue.
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The possible protective action of L-carnitine on neuronal excitability was studied in 21-day-old male Wistar rats with implanted electrodes. Administration of L-carnitine did not change the elicitation and duration of the epileptic seizures (cortical afterdischarges, ADs) in rats under normobaric oxygen atmosphere conditions. However, in animals exposed to 30 min hypobaric hypoxia the duration of the ADs was shortened after the second, fourth and sixth stimulation (in comparison with the first evoked ADs) while carnitine-treated rats retained their neuronal excitability and the duration of ADs was shortened only after the third stimulation. (+info)
Effect of C-fiber-mediated, ozone-induced rapid shallow breathing on airway epithelial injury in rats.
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We examined the relationship between C-fiber-mediated, ozone-induced rapid shallow breathing and airway epithelial cell injury at different airway sites within the lower respiratory tract of conscious Wistar rats (n = 24). We combined an acute 8-h ozone inhalation with vagal perineural capsaicin treatment, a selective C-fiber conduction block, and 5-bromo-2'-deoxyuridine (BrdU) labeling as an index of epithelial injury. Vehicle-treated rats that inhaled ozone developed a rapid shallow breathing pattern during ozone inhalation, whereas the capsaicin-treated rats that inhaled ozone showed no changes in respiratory frequency. In vehicle-treated, ozone-exposed rats that developed rapid shallow breathing, a progressive increase in BrdU-labeling density (no. of BrdU-labeled cells/mm(2) airway) was observed starting at the bifurcation of the left main stem bronchi (central airway) and going down either a short or long airway path. In vehicle-treated, ozone-exposed rats, terminal bronchioles supplied by short and long airway paths had a similar degree of BrdU-labeling density that was significantly (P < 0.05) greater than the BrdU-labeling density of the proximal airways that supply them. In contrast, the attenuation of rapid shallow breathing produced by capsaicin treatment resulted in a significantly reduced BrdU-labeling density in the terminal bronchioles supplied by short airway paths compared with the terminal bronchioles supplied by long airway paths. Our data indicate that ozone-induced rapid shallow breathing protects large conducting airways while producing a more even distribution of injury to terminal bronchioles. (+info)
Contribution of the 5-HT(1B) receptor to hypoxia-induced pulmonary hypertension: converging evidence using 5-HT(1B)-receptor knockout mice and the 5-HT(1B/1D)-receptor antagonist GR127935.
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5-Hydroxytryptamine (5-HT)(1B) receptors mediate contraction in human pulmonary arteries, and 5-HT(1B) receptor-mediated contraction is enhanced in pulmonary arteries from hypoxic rats. Here we further examine the role of this receptor in the development of pulmonary hypertension (PHT) by examining (1) the effects of a 5-HT(1B/1D)-receptor antagonist (GR127935) on hypoxia-induced PHT (CHPHT) in rats and (2) CHPHT in 5-HT(1B)-receptor knockout mice. In rats, hypoxia increased right ventricular pressure and right ventricular hypertrophy and induced pulmonary vascular remodeling associated with an increase in pulmonary arterial wall thickness. GR127935 (3 mg. kg(-1). d(-1)) reduced all of these indices. 5-HT(1)-mediated contraction was enhanced in pulmonary arteries of the CHPHT rats. The effects of GR127935 on PHT indices were associated with an attenuation of the enhanced contractile responses to 5-HT and the 5-HT(1)-receptor agonist, 5-carboxamidotryptamine (5-CT), in isolated pulmonary arteries. In wild-type mice, hypoxia increased right ventricular hypertrophy, which was absent in 5-HT(1B)-receptor knockout mice. Hypoxia increased pulmonary vascular remodeling in wild-type mice, and this was reduced in the 5-HT(1B)-receptor knockout mice. Hypoxia increased 5-HT(1)-mediated contraction in pulmonary arteries from the wild-type mice and this was attenuated in the 5-HT(1B)-receptor knockout mice. In conclusion, the 5-HT(1B) receptor plays a role in the development of CHPHT. One possible mechanism may be via enhanced 5-HT(1) receptor-mediated contraction of the pulmonary arterial circulation. (+info)
Experimental toxicology of pyrolysis and combustion hazards.
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Data are presented on the acute toxicity (mortality only) of the thermal degradation products of polymers obtained by two methods of degradation. One system utilized a slowly increasing temperature (5 degrees C/min) and gradual degradation of the polymer with the rats being exposed to degradation products as they were evolved. In this system the more toxic polymers included wool, polypropylene, poly(vinyl chloride), and urethane foam. The second system utilized conditions of rapid combustion and exposure of rats to the total products of combustion for a period of 4 hr. In this system the more toxic materials included red oak, cotton, acrylonitrile-butadiene-styrene (ABS), and styrene-acrylonitrile. It is of interest to note that the natural product wool is among the least toxic under these rapid combustion conditions and among the most toxic under slow pyrolysis conditions. Other materials also vary in the comparative toxicity of their thermal degradation products, depending upon the conditions of degradation and animal exposure. The two experimental techniques presented here may well represent the two extreme conditions of rapid combustion versus slow pyrolysis. Intermediate types of fire situations might be expected to result in relative acute toxicities somewhere between these two extremes. This report deals with acute toxicity on the basis of mortality data only and does not include other parameters of toxicity such as organ weights and histopathology. (+info)
Selective vulnerability of late oligodendrocyte progenitors to hypoxia-ischemia.
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In the premature infant, hypoxic-ischemic damage to the cerebral white matter [periventricular leukomalacia (PVL)] is a common and leading cause of brain injury that often results in chronic neurologic disability from cerebral palsy. The cellular basis for the propensity of white matter injury to occur in the developing brain and the greater resistance of the adult white matter to similar injury remains unknown. By using a neonatal rat model of hypoxic-ischemic injury, we found that the mechanism of perinatal white matter injury involved maturation-dependent vulnerability in the oligodendroctye (OL) lineage. The timing of appearance of late OL progenitors was the major developmental factor that accounted for the susceptibility of the neonatal white matter to injury. Late OL progenitors were the major OL lineage stage killed by apoptosis, whereas early OL progenitors and more mature OLs were highly resistant. The density of pyknotic late OL progenitors was significantly increased in the ischemic hemisphere (67 +/- 31 cells/mm2) versus the control hemisphere (2.2 +/- 0.4 cells/mm2; mean +/- SEM; p = 0.05), which resulted in the death of 72 +/- 6% of this OL stage. Surviving late OL progenitors displayed a reactive response in which an increase in cell density was accompanied by accelerated maturation to a P27/kip1-positive oligodendrocyte. Because we showed recently that late OL progenitors populate human cerebral white matter during the high risk period for PVL (Back et al., 2001), maturation-dependent vulnerability of OL progenitors to hypoxia-ischemia may underlie the selective vulnerability to PVL of the white matter in the premature infant. (+info)
Impact of elevated CO(2) and O(3) on gas exchange parameters and epidermal characteristics in potato (Solanum tuberosum L.).
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Potato plants (Solanum tuberosum L. cv. Bintje) were grown in open-top chambers (OTCs) under three CO(2) levels (ambient and 24 h d(-1) seasonal mean concentrations of 550 and 680 micromol mol(-1)) and two O(3) levels (ambient and a seasonal mean 8 h d(-1) concentration of 50 nmol mol(-1)). The objectives were to determine the effects of season-long exposure to these key climate change gases on gas exchange, leaf thickness and epidermal characteristics. The experimental design also provided an ideal opportunity to examine within-leaf variation in epidermal characteristics at the whole-leaf level. Stomatal and epidermal cell density and stomatal index were measured at specific locations on the youngest fully expanded leaf (centre of lamina, mid-way between tip and base) and representative whole leaves from each treatment. Effects on leaf conductance, assimilation rate and instantaneous transpiration efficiency were determined by infrared gas analysis, while anatomical characteristics were examined using a combination of leaf impressions and thin sections. Exposure to elevated CO(2) or O(3) generally increased leaf thickness, leaf area, stomatal density, and assimilation rate, but reduced leaf conductance. The irregular stomatal distribution within leaves resulted from a combination of uneven differentiation and expansion of the epidermal cells. The results are discussed with reference to sampling protocols and the need to account for within-leaf variation when examining the impact of climate change or other environmental factors on epidermal characteristics. (+info)