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  • 1
    Electronic Resource
    Electronic Resource
    Reversibility of Nimodipine Binding to Brain in Transient Cerebral Ischemia (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Using autoradiography, we have measured the in vivo binding of [3H]nimodipine to brain in a rat model of reversible cerebral ischemia. Ischemia was induced by simultaneous occlusion of the middle cerebral artery (MCA) and ipsilateral common carotid artery by microaneurysm clips. Rats were studied after 15 min of ischemia (ischemic group) or after 45 min of reperfusion following 15 min of ischemia (reperfused group). Regional cerebral blood flow (CBF) was determined autoradiographically using [14C]iodoantipyrine in both ischemic (n = 6) and reperfused (n = 6) groups. During ischemia blood flow in the territory of the MCA was depressed and recovered to normal only in the distal territory of the MCA following reperfusion. [3H]Nimodipine binding in the ischemic group (n = 12) was elevated in ischemic brain regions and declined significantly (p 〈 0.01) in these regions in the reperfused group (n = 11). The ratio of the volume of cortex showing increased binding to the total volume of the forebrain was 0.113 pmn 0.025 (mean pmn SD) in the ischemic group and declined to 0.080 pmn 0.027 following reperfusion (p 〈 0.005). In general, infarct was only observed in regions showing persistent elevation of nimodipine binding following reperfusion as determined by histology performed in a separate group of rats (n = 8) after 24 h of reperfusion. We conclude that increased nimodipine binding to ischemic tissue is initially reversible with prompt reestablishment of CBF and is a sensitive indicator of early and reversible ischemia-induced cerebral dysfunction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11006.x
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of Nimodipine on the Regional Cerebral Acidosis Accompanying Thiamine Deficiency in the Rat (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 51 (1988), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of the calcium channel blocker nimodipine on the previously described regional cerebral acidosis accompanying thiamine deficiency was investigated. Local cerebral pH (LCpH) and blood flow (LCBF) were separately determined autoradiographically in normal and 16-day thia-mine-deficient rats administered the calcium antagonist drug and compared to appropriate controls. Nimodipine did not modify LCpH in normal brain. In thiamine deficiency, nimodipine significantly raised LCpH in 5 of 17 structures evaluated, two of which, the medial dorsal nucleus of the thalamus and the mammillary body, are vulnerable to the development of histological lesions in this condition. Although the calcium blocker augmented LCBF in normal brain, it had no effect on the hyperperfusion already present by day 16 of thiamine deprivation. Thus, the pH changes we are reporting are probably not related to an effect on cerebral perfusion, but could have resulted from an improved ability of the brain to reduce its proton load in the presence of nimodipine. These results may have wider therapeutic implications than in thiamine deficiency alone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1988.tb03074.x
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  • 3
    Electronic Resource
    Electronic Resource
    Cerebral Vulnerability Is Associated with Selective Increase in Extracellular Glutamate Concentration in Experimental Thiamine Deficiency (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Microdialysis in the awake, freely moving rat was used to determine the effect of pyrithiamine-induced thiamine deficiency on the levels of amino acids in the brain. Studies were carried out on (a) presymptomatic animals immediately before the development of behavioral changes and (b) acute symptomatic animals within 6 h following loss of righting reflexes. This latter stage precedes the appearance of histological lesions. The results were compared with pair-fed controls. Dialysis probes were implanted in one vulnerable structure [ventral posterior medial thalamus (VPMT)] and one nonvulnerable area [frontal parietal cortex (FPC)] on the contralateral side. In VPMT of acute symptomatic animals, the glutamate concentration was significantly increased (3.37 ± 0.64 μM; p 〈 0.005) compared with control values (0.93 ± 0.09 μM), whereas in FPC no change in glutamate content was evident. These results suggest that glutamate plays a significant role in the development of central thiamine deficiency lesions. The absence of any increase in glutamate levels in the nonvulnerable FPC suggests that a glutamate-mediated excitotoxic mechanism may be responsible for the selective cerebral vulnerability in thiamine deficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb03635.x
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  • 4
    Electronic Resource
    Electronic Resource
    In Vivo Distribution of CGS-19755 Within Brain in a Model of Focal Cerebral Ischemia (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The blood–brain barrier permeability of the competitive N-methyl-D-aspartate receptor antagonist CGS-19755 [cis-4-(phosphonomethyl)-2-piperidine carboxylic acid] was assessed in normal and ischemic rat brain. The brain uptake index of CGS-19755 relative to iodoantipyrine was assessed using the Oldendorf technique in normal brain. The average brain uptake index in brain regions supplied by the middle cerebral artery was 0.15 ± 0.35% (mean ± SEM). The unidirectional clearance of CGS-19755 from plasma across the blood–brain barrier was determined from measurements of the volume of distribution of CGS-19755 in brain. These studies were performed in normal rats and in rats with focal cerebral ischemia produced by combined occlusion of the proximal middle cerebral artery and ipsilateral common carotid artery. In normal rats the regional plasma clearance across the blood–brain barrier was low, averaging 0.015 ml 100 g−1 min−1. In ischemic rats this clearance value averaged 0.019 ml 100 g−1 min−1 in the ischemic hemisphere and 0.009 ml 100 g−1 min−1 in the nonischemic hemisphere. No significant regional differences in plasma clearance of CGS-19755 were observed in either normal or ischemic rats except in cortex injured by electrocautery where a 14-fold increase in clearance across the blood–brain barrier was measured. We conclude that CGS-19755 crosses the blood–brain barrier very slowly, even in acutely ischemic tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09294.x
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  • 5
    Electronic Resource
    Electronic Resource
    Attenuation of neurotoxicity in cortical cultures and hippocampal slices from E2F1 knockout mice (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The E2F1 transcription factor modulates neuronal apoptosis induced by staurosporine, DNA damage and β-amyloid. We demonstrate E2F1 involvement in neuronal death induced by the more physiological oxygen-glucose deprivation (OGD) in mouse cortical cultures and by anoxia in mouse hippocampal slices. E2F1(+/+) and (−/−) cultures were comparable, in that they contained similar neuronal densities, responded with similar increases in intracellular calcium concentration ([Ca2+]i) to glutamate receptor agonists, and showed similar NMDA receptor subunit mRNA expression levels for NR1, NR2A and NR2B. Despite these similarities, E2F1(−/−) cultures were significantly less susceptible to neuronal death than E2F1(+/+) cultures 24 and 48 h following 120–180 min of OGD. Furthermore, the absence of E2F1 significantly improved the ability of CA1 neurons in hippocampal slices to recover synaptic transmission following a transient anoxic insult in vitro. These results, along with our finding that E2F1 mRNA levels are significantly increased following OGD, support a role for E2F1 in the modulation of OGD- and anoxia-induced neuronal death. These findings are consistent with studies showing that overexpression of E2F1 in postmitotic neurons causes neuronal degeneration and the absence of E2F1 decreases infarct volume following cerebral ischemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00423.x
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  • 6
    Electronic Resource
    Electronic Resource
    Preconditioning with Cortical Spreading Depression Decreases Intraischemic Cerebral Glutamate Levels and Down-Regulates Excitatory Amino Acid Transporters EAAT1 and EAAT2 from Rat Cerebal Cortex Plasma Membranes (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: We previously reported a 50% reduction in cortical infarct volume following transient focal cerebral ischemia in rats preconditioned 3 days earlier with cortical spreading depression (CSD). The mechanism of the protective effect of prior CSD remains unknown. Recent studies demonstrate reversal of excitatory amino acid transporters (EAATs) to be a principal cause for elevated extracellular glutamate levels during cerebral ischemia. The present study measured the effect of CSD preconditioning on (a) intraischemic glutamate levels and (b) regulation of glutamate transporters within the ischemic cortex of the rat. Three days following either CSD or sham preconditioning, rats were subjected to 200 min of focal cerebral ischemia, and extracellular glutamate concentration was measured by in vivo microdialysis. Cortical glutamate exposure decreased 70% from 1,772.4 ± 1,469.2 μM-min in sham-treated (n = 8) to 569.0 ± 707.8 μM-min in CSD-treated (n = 13) rats (p 〈0.05). The effect of CSD preconditioning on glutamate transporter levels in plasma membranes (PMs) prepared from rat cerebral cortex was assessed by western blot analysis. Down-regulation of the glial glutamate transporter isoforms EAAT2 and EAAT1 from the PM fraction was observed at 1, 3, and 7 days but not at 0 or 21 days after CSD. Semiquantitative lane analysis showed a maximal decrease of 90% for EAAT2 and 50% for EAAT1 at 3 days post-CSD. The neuronal isoform EAAT3 was unaffected by CSD. This period of down-regulation coincides with the time frame reported for induced ischemic tolerance. These data are consistent with reversal of glutamate transporter function contributing to glutamate release during ischemia and suggest that down-regulation of these transporters may contribute to ischemic tolerance induced by CSD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0750812.x
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  • 7
    Electronic Resource
    Electronic Resource
    Local Cerebral Glucose Utilization in Two Models of B12 Deficiency (1983)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 40 (1983), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Local cerebral glucose utilization (LCGU), as measured by the 2-deoxy-D-[l-14C]glucose technique, reflects local cerebral functional activity. In an effort to elucidate mechanisms of the encephalopathy associated with deficiency of vitamin B12, LCGU was determined in two recently described models of effective B12 deficiency: exposure of rats to subanesthetic doses of nitrous oxide (N2O) and/or administration of 1-amino-cyclopentane-1-carboxylic acid (cycloleucine). Our results show that exposure of adult rats to N2O depresses LCGU selectively in cortical, auditory, and limbic structures, in association with a depression in whole-brain activities of the vitamin B12-dependent methyltetrahydrofolate-homocysteine methyl-trans-ferase (EC 2.1.1.13, methionine synthetase). Cycloleucine has no discernible effect on LCGU in the adult rat and does not change the cerebral activity of methionine synthetase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1983.tb08107.x
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  • 8
    Electronic Resource
    Electronic Resource
    Effect of Folate Deficiency on Local Cerebral Glucose Utilization in the Rat (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 42 (1984), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: There is considerable debate on the role of folate in CNS function. Recent work indicates that folate deficiency may affect CNS serotonin metabolism, and clinical studies describe many consequences of such a deficiency. On the other hand some workers maintain that folate deficiency alone causes CNS abnormalities. We maintained rats, through dietary deprivation, at folate levels below 4 ng/ml for more than 6 weeks and showed that at that time both their liver and brain folate levels were significantly reduced. We then studied their local cerebral glucose utilization (LCGU) using the [14C]deoxyglucose technique. This method assesses cerebral function by measuring regional metabolic activity. We also determined LCGU in rats given the same diet but replenished with folate (folate control) and in others given free access to commercially available food (normal controls). Our results show that this degree of folate deficiency has no effect on cerebral function. This contrasts with the focal suppression of LCGU we previously reported in a model of vitamin B12 deficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1984.tb12745.x
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  • 9
    Electronic Resource
    Electronic Resource
    A regulated environmental perfusion system for the study of anoxic or hypoxic cultured neurons using microfluorescence imaging and electrophysiology (1998)
    Springer
    Pflügers Archiv 435 (1998), S. 775-780 
    Details
    ISSN: 1432-2013
    Keywords: Key words Perfusion chamber ; Anoxia ; Hypoxia ; Intracellular calcium ; Cultured neurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We describe the design and performance of a newly developed regulated environmental perfusion system (REPS). This system allows study of the effects of anoxia or hypoxia in cultured cells at physiological temperature, without the use of oxygen-scavenging compounds or metabolic inhibitors. The REPS incorporates a ”canoe-shaped” flow-through chamber with access from above to allow positioning of pipettes for patch-clamp, microinjection, rapid-application perfusion, or microprobes for monitoring physical parameters. The combination of laminar flow and complete washout of perfusate within the chamber, and the use of a gas-tight perfusate delivery system and pressurized reservoirs containing media with pre-stabilized oxygen tensions (pO2 values) allow rapid production of accurate perfusate pO2 within the chamber. Perfusate pO2 in the chamber declined monoexponentially with time constants of ≤ 20 s to stable, pre-determined levels of 0 or 2 kPa (15 Torr). Shielding the gas/liquid interface of the chamber with an argon curtain only minimally decreased time constants at flow rates ≥ 2 ml/min. The perfusion chamber of the REPS is easily mounted on the stage of an inverted microscope, for use with fluorescence imaging or electrophysiological studies of cultured cells. In tests with cultured rat cortical neurons, intracellular calcium concentration increased exponentially to values exceeding 1 μM during 10 min of anoxic insult, and returned to baseline values within 1 min after restoring normoxia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050583
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