Electrophysiological changes of CA3 neurons and dentate granule cells following transient forebrain ischemia

1998 ◽  
Vol 798 (1-2) ◽  
pp. 109-118 ◽  
Author(s):  
Eugene M Howard ◽  
Tian-Ming Gao ◽  
William A Pulsinelli ◽  
Zao C Xu
Keyword(s):  
Granule Cells ◽  
Forebrain Ischemia ◽  
Dentate Granule Cells ◽  
Transient Forebrain Ischemia ◽  
Ca3 Neurons

Transient Neurophysiological Changes in CA3 Neurons and Dentate Granule Cells After Severe Forebrain Ischemia In Vivo

1998 ◽  
Vol 80 (6) ◽  
pp. 2860-2869 ◽  
Author(s):  
T. M. Gao ◽  
E. M. Howard ◽  
Z. C. Xu
Keyword(s):  
Synaptic Transmission ◽  
Neuronal Excitability ◽  
Granule Cells ◽  
Input Resistance ◽  
Cell Types ◽  
Forebrain Ischemia ◽  
Postsynaptic Potentials ◽  
Dentate Granule Cells ◽  
Ca3 Neurons

Gao, T. M., E. M. Howard, and Z. C. Xu. Transient neurophysiological changes in CA3 neurons and dentate granule cells after severe forebrain ischemia in vivo. J. Neurophysiol. 80: 2860–2869, 1998. The spontaneous activities, evoked synaptic responses, and membrane properties of CA3 pyramidal neurons and dentate granule cells in rat hippocampus were compared before ischemia and ≤7 days after reperfusion with intracellular recording and staining techniques in vivo. A four-vessel occlusion method was used to induce ∼14 min of ischemic depolarization. No significant change in spontaneous firing rate was observed in both cell types after reperfusion. The amplitude and slope of excitatory postsynaptic potentials (EPSPs) in CA3 neurons decreased to 50% of control values during the first 12 h reperfusion and returned to preischemic levels 24 h after reperfusion. The amplitude and slope of EPSPs in granule cells slightly decreased 24–36 h after reperfusion. The amplitude of inhibitory postsynaptic potentials in CA3 neurons transiently increased 24 h after reperfusion, whereas that in granule cells showed a transient decrease 24–36 h after reperfusion. The duration of spike width of CA3 and granule cells became longer than that of control values during the first 12 h reperfusion. The spike threshold of both cell types significantly increased 24–36 h after reperfusion, whereas the frequency of repetitive firing evoked by depolarizing current pulse was decreased during this period. No significant change in rheobase and input resistance was observed in CA3 neurons. A transient increase in rheobase and a transient decrease in input resistance were detected in granule cells 24–36 h after reperfusion. The amplitude of fast afterhyperpolarization in both cell types increased for 2 days after ischemia and returned to normal values 7 days after reperfusion. The results from this study indicate that the neuronal excitability and synaptic transmission in CA3 and granule cells are transiently suppressed after severe forebrain ischemia. The depression of synaptic transmission and neuronal excitability may provide protection for neurons after ischemic insult.

scholarly journals Alteration of MAP Kinase Pathways after Transient Forebrain Ischemia

2000 ◽  
Vol 20 (7) ◽  
pp. 1089-1095 ◽  
Author(s):  
Bing R. Hu ◽  
Chun L. Liu ◽  
Darren J. Park
Keyword(s):  
Growth Factor ◽  
Laser Scanning ◽  
Granule Cells ◽  
Regulation Of Gene Expression ◽  
Growth Factor Receptor ◽  
Late Period ◽  
Forebrain Ischemia ◽  
Ca1 Neurons ◽  
Transient Forebrain Ischemia ◽  
Extracellular Regulated Kinase

Extracellular regulated kinase (ERK) transduce growth factor signals while c-Jun NH(2)-terminal kinase (JNK) delivers stress signals into the nuclei for regulation of gene expression. These signaling pathways were studied by laser-scanning confocal microcopy and Western blot analysis using phospho-specific antibodies on rat brains that were subjected to 15 minutes transient forebrain ischemia followed by varied periods of reperfusion. Extracellular regulated kinase was activated at 30 minutes and 4 hours of reperfusion in the nuclei and dendrites of surviving dentate gyrus (DG) cells, but not in dying CA1 neurons after ischemia. Tyrosine phosphorylation of Trk kinase, an ERK upstream growth factor receptor, was elevated in the DG tissue, and to a lesser extent in the CA1 region. In addition, phosphorylation of activating transcription factor-2 (ATF-2) and c-Jun was selectively increased in CA1 dying neurons during the late period of reperfusion. These findings suggested that the Trk-ERK signaling pathway might be neuroprotective for dentate granule cells. The activation of ATF-2 and c-Jun pathways in the late period of reperfusion in CA1 dying neurons might reflect damage signals in these neurons. These results suggested that the lack of protective signals acting in concert with the presence of damage signals in CA1 neurons after ischemia might contribute to delayed neuronal death after transient forebrain ischemia.

scholarly journals Cytotoxic Fragment of Amyloid Precursor Protein Accumulates in Hippocampus after Global Forebrain Ischemia

1996 ◽  
Vol 16 (6) ◽  
pp. 1219-1223 ◽  
Author(s):  
Masayuki Yokota ◽  
Takaomi C. Saido ◽  
Eiichi Tani ◽  
Ikuya Yamaura ◽  
Nobutaka Minami
Keyword(s):  
Amyloid Precursor Protein ◽  
Pyramidal Neurons ◽  
Granule Cells ◽  
Precursor Protein ◽  
Amyloid Peptide ◽  
Forebrain Ischemia ◽  
Ischemic Insult ◽  
Dentate Granule Cells ◽  
Β Amyloid ◽  
Β Amyloid Peptide

We developed an antibody specific to β-amyloid precursor protein (βAPP) fragments possessing the exact amino terminus of the β-amyloid peptide and examined its induction in postischemic hippocampus. In control hippocampus, this APP fragment was lightly observed in pyramidal neurons of CA sectors and dentate granule cells. Transient forebrain ischemia enhanced accumulation of the APP fragment in CA1 pyramidal neurons. Seven days after the ischemia, while the APP fragment was still observed in dentate granule cells and CA3 neurons, it disappeared in dead CA1 neurons. While astrocytes did not show in any immunoreactivity throughout the experiment, those in the CA1 sector showed moderate immunoreactivity 7 days after the ischemia. The APP fragment has a cytotoxic effect on cultured neurons. These results suggest that the accumulation of the cytotoxic APP fragment in CA1 neurons may play a role in the development of delayed neuronal death after the ischemic insult.

scholarly journals Hyperglycemia and Hypercapnia Suppress BDNF Gene Expression in Vulnerable Regions after Transient Forebrain Ischemia in the Rat

1997 ◽  
Vol 17 (12) ◽  
pp. 1303-1308 ◽  
Author(s):  
H. Uchino ◽  
O. Lindvall ◽  
B. K. Siesjö ◽  
Z. Kokaia
Keyword(s):  
Pyramidal Neurons ◽  
Granule Cells ◽  
Hippocampal Formation ◽  
Cingulate Cortex ◽  
Mrna Levels ◽  
Forebrain Ischemia ◽  
Bdnf Gene ◽  
Bdnf Mrna ◽  
Transient Forebrain Ischemia

Preischemic hyperglycemia or superimposed hypercapnia exaggerates brain damage caused by transient forebrain ischemia. Because high regional levels of brain-derived neurotrophic factor (BDNF) protein correlate with resistance to ischemic damage, we studied the expression of BDNF mRNA using in situ hybridization in rats subjected to 10 minutes of forebrain ischemia under normoglycemic, hyperglycemic, or hypercapnic conditions. Compared with normoglycemic animals, the increase of BDNF mRNA in dentate granule cells was attenuated and that in CA3 pyramidal neurons completely prevented in hyperglycemic rats. No ischemia-induced increases of BDNF mRNA levels in the hippocampal formation were detected in hypercapnic animals. Hyperglycemic and hypercapnic rats showed transiently decreased expression of BDNF mRNA levels in the cingulate cortex, which was not observed in normoglycemic animals. The results suggest that suppression of the BDNF gene might contribute to the increased vulnerability of the CA3 region and cingulate cortex in hyperglycemic and hypercapnic animals.

Ultrasturcture of cerebellar cells and neuropil in rats subjected to partial global cerebral ischemia

1986 ◽  
Vol 44 ◽  
pp. 126-127
Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros
Keyword(s):  
Purkinje Cells ◽  
Glial Cells ◽  
Granule Cells ◽  
Molecular Layer ◽  
Cell Types ◽  
Primary Objective ◽  
Global Cerebral Ischemia ◽  
Forebrain Ischemia ◽  
Substantial Evidence ◽  
Cerebellar Cells

Although a previous study in this laboratory determined that Purkinje cells of the rat cerebellum did not appear to be damaged following 30 min of forebrain ischemia followed by 30 min of reperfusion, it was suggested that an increase in rough endoplasmic reticulum (RER) and/or polysomes had occurred in these cells. The primary objective of the present study was to morphometrically determine whether or not this increase had occurred. In addition, since there is substantial evidence that glial cells may be affected by ischemia earlier than other cell types, glial cells also were examined. To ascertain possible effects on other cerebellar components, granule cells and neuropil near Purkinje cells as well as neuropil in the molecular layer also were evaluated in this investigation.

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