Effect of in vivo hypoxic preconditioning on changes in intracellular calcium content induced by long-term anoxia in rat brain slices

2004 ◽  
Vol 138 (10) ◽  
pp. 338-340 ◽  
Author(s):  
D. G. Semenov ◽  
O. L. Miller ◽  
M. O. Samoilov
2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S468-S468
Author(s):  
Jennifer K Callaway ◽  
Christine Molnar ◽  
Song T Yao ◽  
Bevyn Jarrott ◽  
R David Andrew

Author(s):  
Chanchanok Chaichim ◽  
Madeleine Jessica Radnan ◽  
Gadiel Dumlao ◽  
John M. Power

Neurons in the lateral septum (LS) integrate glutamatergic synaptic inputs, primarily from hippocampus, and send inhibitory projections to brain regions involved in reward and the generation of motivated behavior. Motivated learning and drugs of abuse have been shown to induce long-term changes in the strength of glutamatergic synapses in the LS, but the cellular mechanisms underlying long-term synaptic modification in the LS are poorly understood. Here we examined synaptic transmission and long-term depression (LTD) in brain slices prepared from male and female C57BL/6 mice. No sex differences were observed in whole-cell patch-clamp recordings of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA-R) and N-methyl-D-aspartate receptor (NMDA-R) mediated currents. Low frequency stimulation of the fimbria fibre bundle (1 Hz 15 min) induced LTD of the LS field excitatory postsynaptic potential (fEPSP). Induction of LTD was blocked by the NMDA-R antagonist APV, but not the selective antagonist of GluN2B-containing NMDA-R ifenprodil. These results demonstrate the NMDA-R dependence of LTD in the LS. The LS is a sexually dimorphic structure and sex differences in glutamatergic transmission have been reported in vivo; our results suggest sex differences observed in vivo result from network activity rather than intrinsic differences in glutamatergic transmission.


1992 ◽  
Vol 70 (S1) ◽  
pp. S269-S277 ◽  
Author(s):  
Joseph C. LaManna ◽  
J. Keven Griffith ◽  
Boris R. Cordisco ◽  
Chii-Wann Lin ◽  
W. David Lust

Intracellular pH can be measured quantitatively in rat brain in vivo and in vitro using spectrophotometric detection of the vital dye neutral red. This method preserves spatial information and is compatible with microhistochemistry. The intracellular pH indicated by this method is in close agreement with that indicated by 31P-NMR spectroscopy. During ischemia, intracellular acidification is correlated with tissue lactate accumulation. The spatial distribution of pH values becomes more heterogeneous as the tissue becomes more acidic. Resuscitation from total cerebral ischemia produced by cardiac arrest results in rapid intracellular realkalinization. This realkalinization is at least partially inhibited by amiloride pretreatment. Some neuronal populations, especially in the hippocampal CA1 and CA4 regions, may become more acidic during ischemia and realkalinize more slowly after reperfusion than other tissue regions. The intracellular pH of hippocampal brain slice preparations is more alkaline than expected from in vivo studies. The intracellular pH of the brain slice can be acidified to near neutrality by specific inhibitors of the sodium/hydrogen ion exchanger.Key words: hippocampal brain slice, intracellular pH, neutral red, cardiac arrest and resuscitation, sodium/hydrogen ion exchanger.


1995 ◽  
Vol 7 (3) ◽  
pp. 385 ◽  
Author(s):  
LD Longo ◽  
S Packianathan

Recent studies in vivo have demonstrated that ornithine decarboxylase (ODC) activity in the fetal rat brain is elevated 4-5-fold by acute maternal hypoxia. This hypoxic-associated increase is seen in the rat brain in both the newborn and the adult. Because of the intimate involvement of ODC in transcription and translation, as well as in growth and development, it is imperative that the manner in which hypoxia affects the regulation of this enzyme be better understood. In order to achieve this, a brain preparation in vitro was required to eliminate the confounding effects of the dam on the fetal and newborn brain ODC activity in vivo. Therefore, brain slices from 3-4-day-old (P-3) newborn rats were utilized to test the hypothesis that ODC activity increases in response to hypoxia in vitro. Cerebral slices from the P-3 rat pups were allowed to equilibrate and recover in artificial cerebrospinal fluid (ACSF) continuously bubbled with a mixture of 95% O2 and 5% CO2 for 1 h before beginning hypoxic exposures. Higher basal ODC activities were obtained by treating the slices with 0.03% fetal bovine serum (FBS) and 0.003% bovine serum albumin (BSA), rather than with ACSF alone. Hypoxia was induced in the slices by replacing the gas with 40%, 21%, 10%, or 5% O2, all with 5% CO2 and balance N2. With FBS and BSA treatment, ODC activity was maintained at about 0.15-0.11 nM CO2 mg-1 protein h-1 throughout the experiment, which was 2-3-fold higher than that without FBS and BSA. ODC activity increased significantly and peaked between 1 h and 2 h after initiation of hypoxia. For instance, with 21% O2, ODC activity increased approximately 1.5-fold at 1 h and approximately 2-fold at 2 h. These studies demonstrate that: (1) the hypoxic-induced increases observed in vivo in the fetal and newborn rat brain ODC activity can be approximated in a newborn rat brain slice preparation in vitro; (2) newborn rat brain slice preparations may provide an alternative to methods in vivo or cell culture methods for studying the regulation of acute hypoxic-induced enzymes; and (3) high, stable baseline ODC activities in brain slices suggest that the cells in the slice are capable of active metabolism if FBS and BSA are available to mimic conditions in vivo.


Neuroscience ◽  
2012 ◽  
Vol 203 ◽  
pp. 244-254 ◽  
Author(s):  
J. Mejía-Toiber ◽  
J.H. Limón-Pacheco ◽  
A. Gonzalez-Gallardo ◽  
M. Giordano
Keyword(s):  

2015 ◽  
Vol 42 (3) ◽  
pp. 202-208 ◽  
Author(s):  
Wen-Jian Jiang ◽  
Yong-Chao Cui ◽  
Jin-Hua Li ◽  
Xiu-Hui Zhang ◽  
Huan-Huan Ding ◽  
...  

Pericardial calcification is detrimental to the long-term durability of valvuloplasty. However, whether calcification susceptibility differs between heterologous and autologous pericardium is unclear. In this study, we compared the progression of calcification in vivo between autologous and heterologous pericardium. We randomly divided 28 rabbits into 4 equal groups. Resected rabbit pericardium served as autologous pericardium, and commercial bovine pericardium served as heterologous pericardium. We subcutaneously embedded one of each pericardial patch in the abdominal walls of 21 of the rabbits. The 7 control rabbits (group A) received no implants. The embedded samples were removed at 2 months in group B, at 4 months in group C, and at 6 months in group D. Each collected sample was divided into 2 parts, one for calcium-content measurement by means of atomic-absorption spectroscopy, and one for morphologic and histopathologic examinations. When compared with the autologous pericardium, calcium levels in the heterologous pericardium were higher in groups B, C, and D (P <0.0001, P <0.0002, and P <0.0006, respectively). As embedding time increased, calcium levels in the heterologous pericardium increased faster than those in the autologous, especially in group D. Disorganized arrangements of collagenous fibers, marked calculus, and ossification were seen in the heterologous pericardium. Inflammatory cells—mainly lymphocytes and small numbers of macrophages—infiltrated the heterologous pericardium. The autologous pericardium showed a stronger ability to resist calcification. Our results indicate that autologous pericardium might be a relatively better choice for valvuloplasty.


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