Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Influence of hyperglycemia and of hypercapnia on cellular calcium transients during reversible brain ischemia (1995)
    Springer
    Experimental brain research 104 (1995), S. 462-466 
    Details
    ISSN: 1432-1106
    Keywords: Transient ischemia ; Extracellular calcium ; Acidosis ; Brain ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The object of the study was to find out how preischemic hyperglycemia (in normocapnic animals) or excessive hypercapnia (in normoglycemic animals) affect the calcium transient during ischemia, as this can be assessed by measurements of the extracellular calcium concentration ([Ca2+]e). To that extent, normocapnic-normoglycemic control animals were compared with animals with induced hyperglycemia or hypercapnia, all being subjected to 10 min of forebrain ischemia, the [Ca2+]e and d.c. potential being measured with ion-sensitive glass microelectrodes. Hyperglycemia and hypercapnia delayed the loss of ion homeostasis following induction of ischemia. Furthermore, both hyperglycemia and hypercapnia reduced the delay of Ca2+ extrusion upon recirculation. As a result, both hyperglycemia and hypercapnia significantly reduced the ischemic calcium transient, as this was assessed by calculating the duration of maximal calcium load of cells. The results make it less likely that aggravation of brain damage by hyperglycemia or excessive hypercapnia is related to a further derangement of cell calcium homeostasis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00231980
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    The influence of insulin-induced hypoglycemia on the calcium transients accompanying reversible forebrain ischemia in the rat (1990)
    Springer
    Experimental brain research 105 (1990), S. 363-369 
    Details
    ISSN: 1432-1106
    Keywords: Ischemia ; Hypoglycemia ; Calcium transient ; Insulin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The primary objective of this study was to explore why preischemic hypoglycemia, which restricts tissue acidosis during the ischemic insult, does not ameliorate cell damage incurred as a result of transient ischemia. The question arose whether hypoglycemia (plasma glucose concentration 2–3 mM) delays resumption of extrusion of Ca2+ from cells during recirculation. Measurements of extracellular Ca2+ concentration during forebrain ischemia of 15 min duration proved that this was the case. Thus, normoglycemic animals resumed Ca2+ extrusion upon recirculation after a delay of 1.5–2.0 min, and hypoglycemic ones after an additional delay which could amount to 3–4 min. We attempted to explore the cause of this delay. At first sight, the results suggested that resumption of oxidative phosphorylation upon recirculation was substrate limited. However, glucose infusion during ischemia or just after recirculation failed to accelerate Ca2+ extrusion from the cells. A comparison between non-injected and insulin-injected animals at equal plasma glucose concentrations suggested that insulin was responsible for the delay. On analysis, the delay proved to be related to a sluggish recovery of cerebral blood flow. The results suggest that when cell damage is evaluated after transient ischemia in hypo- and normoglycemic subjects, attention should be directed to the period of cell calcium ‘overload’. Unobserved differences in the duration of the calcium transient may also confound interpretation of data on the effects of insulin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233036
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Calcium-dependent dephosphorylation of brain mitochondrial calcium/cAMP response element binding protein (CREB) (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 92 (2005), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Calcium-mediated signaling regulates nuclear gene transcription by calcium/cAMP response element binding protein (CREB) via calcium-dependent kinases and phosphatases. This study tested the hypothesis that CREB is also present in mitochondria and subject to dynamic calcium-dependent modulation of its phosphorylation state. Antibodies to CREB and phosphorylated CREB (pCREB) were used to demonstrate the presence of both forms in isolated mitochondria and mitoplasts from rat brain. When energized mitochondria were exposed to increasing concentrations of Ca2+ in the physiological range, pCREB was lost while total CREB remained constant. In the presence of Ru360, an inhibitor of the mitochondrial Ca2+ uptake uniporter, calcium-dependent loss of pCREB levels was attenuated, suggesting that intramitochondrial calcium plays an important role in pCREB dephosphorylation. pCREB dephosphorylation was not, however, inhibited by the phosphatase inhibitors okadaic acid and Tacrolimus. In the absence of Ca2+, CREB phosphorylation was elevated by the addition of ATP to the mitochondrial suspension. Exposure of mitochondria to the pore-forming molecule alamethicin that causes osmotic swelling and release of intermembrane proteins enriched mitochondrial pCREB immunoreactivity. These results further suggest that mitochondrial CREB is located in the matrix or inner membrane and that a kinase and a calcium-dependent phosphatase regulate its phosphorylation state.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2004.02873.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Heterogeneity of the calcium-induced permeability transition in isolated non-synaptic brain mitochondria (2002)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 83 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Calcium overload of neural cell mitochondria plays a key role in excitotoxic and ischemic brain injury. This study tested the hypothesis that brain mitochondria consist of subpopulations with differential sensitivity to calcium-induced inner membrane permeability transition, and that this sensitivity is greatly reduced by physiological levels of adenine nucleotides. Isolated non-synaptosomal rat brain mitochondria were incubated in a potassium-based medium in the absence or presence of ATP or ADP. Measurements were made of medium and intramitochondrial free calcium, light scattering, mitochondrial ultrastructure, and the elemental composition of electron-opaque deposits within mitochondria treated with calcium. In the absence of adenine nucleotides, calcium induced a partial decrease in light scattering, accompanied by three distinct ultrastructural morphologies, including large-amplitude swelling, matrix vacuolization and a normal appearance. In the presence of ATP or ADP the mitochondrial calcium uptake capacity was greatly enhanced and calcium induced an increase rather than a decrease in mitochondrial light scattering. Approximately 10% of the mitochondria appeared damaged and the rest contained electron-dense precipitates that contained calcium, as determined by electron-energy loss spectroscopy. These results indicate that brain mitochondria are heterogeneous in their response to calcium. In the absence of adenine nucleotides, approximately 20% of the mitochondrial population exhibit morphological alterations consistent with activation of the permeability transition, but less than 10% exhibit evidence of osmotic swelling and membrane disruption in the presence of ATP or ADP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2002.01238.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Alterations in Lipid and Calcium Metabolism Associated with Seizure Activity in the Postischemic Brain (2000)
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 75 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Transient ischemia is known to lead to a long-lastingdepression of cerebral metabolic rate and blood flow and to an attenuatedmetabolic and circulatory response to physiological stimuli. However, thecorresponding responses to induced seizures are retained, demonstratingpreserved metabolic and circulatory capacity. The objective of the presentstudy was to explore how a preceding period of ischemia (15 min) alters therelease of free fatty acids (FFAs) and diacylglycerides (DAGs), the formationof cyclic nucleotides, and the influx/efflux of Ca2+, followingintense neuronal stimulation. For that purpose, seizure activity was inducedwith bicuculline for 30 s or 5 min at 6 h after the ischemia. ExtracellularCa2+ concentration (Ca2+e) was recorded, andthe tissue was frozen in situ for measurements of levels of FFAs, DAGs, andcyclic nucleotides. Six hours after ischemia, the FFA concentrations werenormalized, but there was a lowering of the content of 20:4 in the DAGfraction. Cyclic AMP levels returned to normal values, but cyclic GMP contentwas reduced. Seizures induced in postischemic animals showed similar changesin Ca2+e, as well as in levels of FFAs, DAGs, and cyclicnucleotides, as did seizures induced in nonischemic control animals, with theexception of an attenuated rise in 20:4 content in the DAG fraction. Weconclude that, at least in the neocortex, seizure-induced phospholipidhydrolysis and cyclic cAMP/cyclic GMP formation are not altered by a precedingperiod of ischemia, nor is there a change in the influx/efflux ofCa2+ during seizure discharge or in associated spreadingdepression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0752521.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Characteristics of the Calcium-Triggered Mitochondrial Permeability Transition in Nonsynaptic Brain Mitochondria (2000)
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 74 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The objective of the present study was to assess the capacity of nonsynaptic brain mitochondria to accumulate Ca2+ when subjected to repeated Ca2+ loads, and to explore under what conditions a mitochondrial permeability transition (MPT) pore is assembled. The effects of cyclosporin A (CsA) on Ca2+ accumulation and MPT pore assembly were compared with those obtained with ubiquinone 0 (Ub0), a quinone that is a stronger MPT blocker than CsA, when tested on muscle and liver mitochondria. When suspended in a solution containing phosphate (2 mM) and Mg2+ (1 mM), but no ATP or ADP, the brain mitochondria had a limited capacity to accumulate Ca2+ (210 nmol/mg of mitochondrial protein). Furthermore, when repeated Ca2+ pulses (40 nmol/mg of protein each) saturated the uptake system, the mitochondria failed to release the Ca2+ accumulated. However, in each instance, the first Ca2+ pulse was accompanied by a moderate release of Ca2+, a release that was not observed during the subsequent pulses. The initial release was accompanied by a relatively marked depolarization, and by swelling, as assessed by light-scattering measurements. However, as the swelling was 〈50% of that observed following addition of alamethicin, it is concluded that the first Ca2+ pulse gives rise to an MPT in a subfraction of the mitochondrial population. CsA, an avid blocker of the MPT pore, only marginally increased the Ca2+-sequestrating capacity of the mitochondria. However, CsA eliminated the Ca2+ release accompanying the first Ca2+ pulse. The effects of CsA were shared by Ub0, but when the concentration of Ub0 exceeded 20 μM, it proved toxic. The results thus suggest that brain mitochondria are different from those derived from a variety of other sources. The major difference is that a fraction of the brain mitochondria, studied presently, depolarized and showed signs of an MPT. This fraction, but not the remaining ones, contributed to the chemically and electron microscopically verified mitochondrial swelling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0741999.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    The influence of repeated spreading depression-induced calcium transients on neuronal viability in moderately hypoglycemic rats (1994)
    Springer
    Experimental brain research 97 (1994), S. 397-403 
    Details
    ISSN: 1432-1106
    Keywords: Spreading depression ; Hypoglycemia ; Neuronal damage ; [Ca2+]e ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The calcium transients which are associated with spreading depression (SD) do not lead to neuronal necrosis, even if the SDs are repeated over hours. We have previously shown that a restriction of energy production by moderate hypoglycemia prolongs the calcium transients during SD. In the present experiments, we explored whether such prolonged transients lead to neuronal necrosis. To that end, SDs were elicited for 2 h by topical application of KC1 in anesthetized rats at plasma glucose concentrations of 6, 3, and 2 mM. The animals were then allowed to recover, and they were studied histopathologically after 7 days. In two other groups, hypoglycemic coma of 5 min duration (defined in terms of the d.c. potential shift) was induced either without or with a preceding train of SDs. These animals were also evaluated with respect to histopathological alterations. SDs elicited for 2 h did not give rise to neuronal damage when elicited at plasma glucose concentration of 6 mM, and, of the animals maintained at 3 and 2 mM, only a few animals showed (mild) damage. In general, therefore, repeated SDs with calcium transients of normal or increased duration fail to induce neuronal damage. The results suggest that, if calcium transients are responsible for a gradual extension of the infarct into the penumbra zone of a focal ischemie lesion some additional pathophysiological factors must be present, such as overt energy failure, acidosis, or microvascular damage. A hypoglycemia-induced calcium transient of 5 min duration gave no or only moderate neuronal damage. However, if a series of SDs were elicited in the precoma period, the damage was exaggerated. The results demonstrate that, normally, brain tissues can tolerate a hypoglycemic calcium transient of up to 5 min duration without incurring neuronal necrosis. They also demonstrate that calcium transients preceding a subsequent insult involving calcium influx into cells exaggerate the damage incurred. It is tentatively concluded that the “priming” transients alter membrane properties in such a way that cellular calcium homeostasis is perturbed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00241533
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...