Correlation Between Hippocampal Neuronal Damage and Spatial Learning Deficit Due to Global Ischemia

Block, F.; Schwarz, Michael

doi:10.1016/s0091-3057(96)00484-4

Cited by 45 publications

(30 citation statements)

References 36 publications

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“…Previous experiments showed that various types of cerebral ischemia in humans and animals are accompanied by hippocampal neuronal damage (major generator of τ-waves) [1,3,11] and decrease in τ-activity [3,12]. The hippocampus has a key role in higher nervous functions (e.g., orientation-and-exploratory behavior, attention, memory, learning, etc.)…”

Section: Resultsmentioning

confidence: 99%

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Multiparameter Analysis of EEG in Old Wistar Rats after Bilateral Carotid Artery Ligation

2009

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We showed that 302 of 840 EEG parameters in old Wistar rats significantly change 3 h after bilateral carotid artery ligation. All animals (n=7) died 250+/-47 min after ligation. EEG power spectra had signs of suppression (increased d-activity, decreased t-activity, and increased low-frequency alpha-activity) or activation of CNS (decreased high-frequency alpha-activity and paroxysmal increase in beta-activity). The coherence, synchrony, and entropy of potentials were reduced in the majority of brain regions. This method and scheme of experiments are suitable for the search and study of anti-stroke drugs.

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Section: Resultsmentioning

confidence: 99%

“…The hippocampus has a key role in higher nervous functions (e.g., orientation-and-exploratory behavior, attention, memory, learning, etc.) [1]. Damage or destruction of the hippocampus is followed by cognitive deficit, memory disorders (in humans) [6], and impairment of learning (in rats) [11].…”

Section: Resultsmentioning

confidence: 99%

Multiparameter Analysis of EEG in Old Wistar Rats after Bilateral Carotid Artery Ligation

2009

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“…N-2-MPG may also confer some neuroprotective effects by scavenging free radicals and replenishing glutathione supplies (31,32). A free radical cytoprotective mechanism is unlikely, however, because 3-aminopropanal cytotoxicity to glial cell cultures in vitro is not attenuated by other known free radical scavengers such as ascorbate and butylated hydroxytoluene (16,33,34). In addition to direct inactivation of 3-aminopropanal, replenishment of reduced glutathione levels by N-2-MPG remains a plausible potential mechanism for the cytoprotective effects of this drug (31).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection in cerebral ischemia by neutralization of 3-aminopropanal

Ivanova

Batliwalla

Mocco

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Cerebral ischemia stimulates increased activity of polyamine oxidase, a ubiquitous enzyme that catabolizes polyamines to produce 3-aminopropanal. 3-Aminopropanal is a reactive aldehyde that mediates progressive neuronal necrosis and glial apoptosis. Here we report that increased levels of 3-aminopropanal-modified protein levels in humans after aneurysmal subarachnoid hemorrhage correlate with the degree of cerebral injury as measured by admission Hunt͞Hess grade. In vitro screening of clinically approved drugs reveals that N-2-mercaptopropionyl glycine (N-2-MPG), an agent clinically approved for prevention of renal stones in patients with cysteinuria, significantly inhibits the cytotoxicity of 3-aminopropanal. N-2-MPG reacts with 3-aminopropanal to yield a nontoxic thioacetal adduct, as confirmed by electrospray ionization mass spectroscopy. Administration of N-2-MPG in clinically relevant doses to rats significantly reduces cerebral 3-aminopropanal-modified protein immunoreactivity and infarct volume in a standardized model of middle cerebral artery occlusion, even when the agent is administered after the onset of ischemia. These results implicate 3-aminopropanal as a therapeutic target for cerebral ischemia.

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“…Similar correlation in hippocampal cell damage and spatial learning deficit has also been reported. 27,28) Neuroprotective effect of trolox is further supported by its protective effect in amyloid b-mediated neurotoxicity, 29) and interleukin (IL-1b) induced neurodegeneration. 30) In addition to protective effects in neurotoxicity models, trolox counteracted the toxic effects of S-morpholinosydnonimine (SIN-1), a peroxynitrite donor in lung epithelial cells, 31) and in arrhythmias in isolated heart preparations.…”

Section: Discussionmentioning

confidence: 96%

“…Similar correlation in hippocampal cell damage and spatial learning deficit has also been reported. 27,28) Neuroprotective effect of trolox is further supported by its …”

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confidence: 92%

Neuroprotective Effects of Trolox in Global Cerebral Ischemia in Gerbils

Gupta

Sharma

2006

Biological & Pharmaceutical Bulletin

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Stroke is the third leading cause of death and a major cause of long-term disability in industrialized countries. Dramatic reduction of oxygen in stroke may lead to ischemia of the whole brain (global ischemia) or of defined cerebral territories (focal ischemia) depending on the cerebral artery occluded.1) Global cerebral ischemia is commonly an outcome of a range of clinical conditions, which comprises cardiac arrest, closed head injury, coronary artery bypass surgery etc. The most affected brain area as a consequence of global ischemia is CA1 neurons of the hippocampus. Neuronal death in global ischemia precedes 1-3 d after insult, a process referred as delayed neuronal death. 2-4)The pathophysiological mechanisms leading to neuronal injury in ischemic stroke are complex and multifactorial. Ischemia induced brain damages are accompanied by biochemical alterations and neurological sequelae.1) There are substantial experimental evidences that reactive oxygen species (ROS) are produced in the brain during ischemia and reperfusion injury.5) ROS such as superoxide radical, hydroxyl radical and hydrogen peroxide contributes to ischemic brain damage.5) Superoxide can react with nitric oxide to form peroxynitrite, a potent oxidant. It has been proposed that many of the toxic effects of nitric oxide are due to the generation of peroxynitrite. Peroxynitrite can directly react with target biomolecules like DNA, protein, via one or two electron oxidations. 5-7)Antioxidants such as (Ϫ)-epigallocatechin gallate, melatonin, curcumin, FeTMPyP and FeTPPS have been demonstrated to ameliorate neuronal damage in cerebral ischemic reperfusion injury. 3,[8][9][10][11] Antioxidant activity of trolox (6-hydroxy-2,5,7,8-tetramethyl chroman-2-carboxylic acid) a cellpermeable, water-soluble derivative of vitamin E has been established in vitro and in vivo conditions. 12-15) However its neuroprotective effects have not been investigated in global cerebral ischemia. Therefore, in the present study, the neuroprotective potential of trolox was investigated in bilateral carotid artery occlusion induced global cerebral ischemia in Mongolian gerbils. MATERIALS AND METHODS AnimalsAdult male Mongolian gerbils (Meriones unguiculatus) weighing 60-80 g were obtained from Central Animal Facility (CAF), NIPER for this study. They were provided with standard diet and water ad libitum and were maintained at 22Ϯ2°C and a 12 : 12 h light : dark cycle. All the procedures used in this study were approved by Institutional Animal Ethics Committee (IAEC), NIPER.Materials Trolox was purchased from Calbiochem Inc., U.S.A. Cresyl violet and malondialdehyde were purchased from Sigma Chemical Company, U.S.A. Rest of the chemicals were of analytical grade and were purchased from commercial suppliers.Treatment Schedule Gerbils were divided into sham, vehicle-treated ischemic and trolox-treated (3, 10, 30 mg/kg i.p.) ischemic groups. Phosphate buffer saline (pH 7.4) was used as a vehicle for trolox. Trolox was administered 30 min before occlusion.Induction of Transie...

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Correlation Between Hippocampal Neuronal Damage and Spatial Learning Deficit Due to Global Ischemia

Cited by 45 publications

References 36 publications

Multiparameter Analysis of EEG in Old Wistar Rats after Bilateral Carotid Artery Ligation

Multiparameter Analysis of EEG in Old Wistar Rats after Bilateral Carotid Artery Ligation

Neuroprotection in cerebral ischemia by neutralization of 3-aminopropanal

Neuroprotective Effects of Trolox in Global Cerebral Ischemia in Gerbils

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