Temporal changes in extracellular acetylcholine and CA1 pyramidal cells in gerbil hippocampus following transient cerebral ischemia

1994 ◽  
Vol 639 (1) ◽  
pp. 66-72 ◽  
Author(s):  
Hirohisa Ishimaru ◽  
Akira Takahashi ◽  
Yasushi Ikarashi ◽  
Yuji Maruyama
Keyword(s):  
Cerebral Ischemia ◽  
Pyramidal Cells ◽  
Temporal Changes ◽  
Transient Cerebral Ischemia ◽  
Ca1 Pyramidal Cells

scholarly journals The Susceptibility of CA1 Pyramidal Cells to Cerebral Ischemia is Maintained after Neonatal, Lesion-Induced Reorganization of the Hippocampal Circuitry

1994 ◽  
Vol 14 (3) ◽  
pp. 391-396 ◽  
Author(s):  
Niels Tønder ◽  
Flemming F. Johansen ◽  
Jens Zimmer ◽  
Nils H. Diemer
Keyword(s):  
Cerebral Ischemia ◽  
Pyramidal Cell ◽  
Neuronal Degeneration ◽  
Pyramidal Cells ◽  
Cell Loss ◽  
Transient Cerebral Ischemia ◽  
Ca1 Pyramidal Cells ◽  
Neonatal Lesion ◽  
Neonatal Lesions ◽  
Hippocampal Circuitry

Acute lesions of hippocampal pathways have been shown previously to ameliorate CA1 pyramidal cell loss after subsequent transient cerebral ischemia. In this study, we examined the effect of chronic neonatal lesion with reorganization of hippocampal circuitry on adult postischemic neuron loss in the hippocampus. Newborn rats were subjected to unilateral knife-cut lesions at various positions along the trisynaptic entorhino-dentatohippocampal pathway. Seven months later, the rats were subjected to transient cerebral ischemia using the four-vessel occlusion technique. At the time of killing 4 days later, a Nissl stain was used to demonstrate neuronal degeneration, while connective reorganization resulting from the neonatal lesions was monitored by Timm staining. In one group of rats, neonatal lesions had caused severe depletion of entorhinal projections to the septodorsal fascia dentata and hippocampus (CA1 and CA3), without any direct damage to the dorsal hippocampus itself. Another group had extensive damage of the dorsal CA3, with removal of the Schaffer collaterals from these levels to CA1, and variable damage to the entorhinal afferents. In both groups, the extent and pattern of ischemia-induced degeneration of CA1 pyramidal cells were the same on the lesioned and nonlesioned sides of the brain, demonstrating that neonatal lesions and the subsequent connective reorganization did not have a sparing effect. Seen in relationship to previous observations in adult rats of the neuroprotective actions of acute, preischemic lesions of the trisynaptic hippocampal pathway, it is concluded that CA1 pyramidal cell loss requires the presence of intact excitatory afferents rather than an intact hippocampal circuitry.

N--- receptor-mediated, prolonged afterdischarges of CA1 pyramidal cells following transient cerebral ischemia in the rat hippocampus in vivo

1994 ◽  
Vol 657 (1-2) ◽  
pp. 325-329 ◽  
Author(s):  
Shuhei Miyazaki ◽  
Yoichi Katayama ◽  
Makoto Furuichi ◽  
Tsuneo Kano ◽  
Atsuo Yoshino ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Pyramidal Cells ◽  
Transient Cerebral Ischemia ◽  
Rat Hippocampus ◽  
Ca1 Pyramidal Cells

scholarly journals Effects of FK506 on Hippocampal CA1 Cells Following Transient Global Ischemia/Reperfusion in Wistar Rat

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Zahra-Nadia Sharifi ◽  
Farid Abolhassani ◽  
Mohammad Reza Zarrindast ◽  
Shabnam Movassaghi ◽  
Nasrin Rahimian ◽  
...  
Keyword(s):  
Single Dose ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Pyramidal Cells ◽  
Wistar Rat ◽  
Cell Number ◽  
Global Cerebral Ischemia ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Transient Global Cerebral Ischemia

Transient global cerebral ischemia causes loss of pyramidal cells in CA1 region of hippocampus. In this study, we investigated the neurotrophic effect of the immunosuppressant agent FK506 in rat after global cerebral ischemia. Both common carotid arteries were occluded for 20 minutes followed by reperfusion. In experimental group 1, FK506 (6 mg/kg) was given as a single dose exactly at the time of reperfusion. In the second group, FK506 was administered at the beginning of reperfusion, followed by its administration intraperitoneally (IP) 6, 24, 48, and 72 hours after reperfusion. FK506 failed to show neurotrophic effects on CA1 region when applied as a single dose of 6 mg/kg. The cell number and size of the CA1 pyramidal cells were increased, also the number of cell death decreased in this region when FK506 was administrated 48 h after reperfusion. This work supports the possible use of FK506 in treatment of ischemic brain damage.

scholarly journals Effects of the AMPA-Receptor Antagonist, NBQX, on Neuron Loss in Dentate Hilus of the Hippocampal Formation after 8, 10, or 12 Min of Cerebral Ischemia in the Rat

1997 ◽  
Vol 17 (2) ◽  
pp. 147-152 ◽  
Author(s):  
Ping Hu ◽  
Nils Henrik Diemer ◽  
Torben Bruhn ◽  
Flemming Fryd Johansen
Keyword(s):  
Cerebral Ischemia ◽  
Receptor Antagonist ◽  
Ampa Receptor ◽  
Hippocampal Formation ◽  
Neuroprotective Effect ◽  
Pyramidal Cells ◽  
Ca1 Pyramidal Cells ◽  
Ampa Receptor Antagonist ◽  
Hippocampal Ca1 ◽  
Dentate Hilus

The α-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptor antagonist, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo( F)quinoxaline (NBQX), offers protection to hippocampal CA1 pyramidal cells after short episodes of transient cerebral ischemia. Besides CA1 pyramidal cells, neurons containing somatostatin (SS) and located in the dentate hilus of the hippocampal formation are lost after cerebral ischemia. We studied the protective effects of NBQX on SS neurons in the hilus and on hippocampal CA1 pyramidal cells following 8, 10, or 12 min of four-vessel occlusion ischemia during systemic hypotension. NBQX was administered 3 × 30 mg/kg at 0, 10, and 25 after induction of ischemia or sham, and all rats survived for 7 days. NBQX given to control rats without ischemia had no influence on number or morphology of hilar SS neurons and CA1 pyramidal cells. After 8 min of ischemia, NBQX prevented loss of hilar SS neurons. After 10 and 12 min of ischemia, NBQX had no significant effects on loss of SS neurons in the dentate hilus. However, in all ischemic groups, NBQX significantly reduced loss of CA1 pyramidal cells as compared to control rats. This neuroprotective effect decreased gradually and significantly as the time of ischemia increased. Our results support the observation that SS neurons in hilus are among the most ischemia-vulnerable neurons in the brain. We found that administration of NBQX in generally accepted dosages can protect the rapidly dying SS neurons in hilus from only brief episodes of ischemia.

Long-term study of dendritic spines from hippocampal CA1 pyramidal cells, after neuroprotective melatonin treatment following global cerebral ischemia in rats

2007 ◽  
Vol 423 (2) ◽  
pp. 162-166 ◽  
Author(s):  
Ignacio González-Burgos ◽  
Graciela Letechipía-Vallejo ◽  
Elisa López-Loeza ◽  
Gabriela Moralí ◽  
Miguel Cervantes
Keyword(s):  
Cerebral Ischemia ◽  
Dendritic Spines ◽  
Pyramidal Cells ◽  
Global Cerebral Ischemia ◽  
Melatonin Treatment ◽  
Term Study ◽  
Ca1 Pyramidal Cells ◽  
Long Term Study ◽  
Hippocampal Ca1

Diazoxide prevents mitochondrial swelling and Ca 2+ accumulation in CA1 pyramidal cells after cerebral ischemia in newborn pigs

2004 ◽  
Vol 1019 (1-2) ◽  
pp. 97-104 ◽  
Author(s):  
Ferenc Domoki ◽  
Ferenc Bari ◽  
Krisztina Nagy ◽  
David W Busija ◽  
László Siklós
Keyword(s):  
Cerebral Ischemia ◽  
Pyramidal Cells ◽  
Mitochondrial Swelling ◽  
Ca1 Pyramidal Cells ◽  
Newborn Pigs

scholarly journals Impaired Firing and Sodium Channel Function in CA1 Hippocampal Interneurons after Transient Cerebral Ischemia

2007 ◽  
Vol 27 (8) ◽  
pp. 1444-1452 ◽  
Author(s):  
Ren-Zhi Zhan ◽  
J Victor Nadler ◽  
Rochelle D Schwartz-Bloom
Keyword(s):  
Cerebral Ischemia ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Normal Function ◽  
Transient Cerebral Ischemia ◽  
Membrane Properties ◽  
Channel Activation ◽  
Area Ca1

Although interneurons in area CA1 of the hippocampus are less vulnerable to cerebral ischemia than CA1 pyramidal cells, it is not clear whether their relatively intact cellular morphology implies preservation of normal function. As maintenance of cellular excitability and firing properties is essential for interneurons to regulate neural networks, we investigated these aspects of interneuronal function after transient cerebral ischemia in rats. Cerebral ischemia in rats was induced for 8 mins by a combination of bilateral common carotid artery occlusion and hypovolemic hypotension, and whole cell patch clamp recordings were made in hippocampal slices prepared 24 h after reperfusion. Interneurons located within stratum pyramidale of area CA1 exhibited normal membrane properties and action potentials under these conditions. However, their excitability had declined, as evidenced by an increased action potential threshold and a rightward shift in the relationship between injected depolarizing current and firing rate. Voltage–clamp experiments revealed that transient cerebral ischemia reduced the peak Na+ current and shifted Na+ channel activation to more depolarized values, but did not alter steady-state inactivation of the channel. Double immunofluorescence cytochemistry showed that transient cerebral ischemia also reduced Nav1.1 subunit immunoreactivity in interneurons that coexpressed parvalbumin. We conclude that transient cerebral ischemia renders CA1 interneurons less excitable, that depressed excitability involves impaired Na+ channel activation and that Na+ channel dysfunction is explained, at least in part, by reduced expression of the Nav1.1 subunit. These changes may promote interneuron survival, but might also contribute to pyramidal cell death.

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