Aquaporin 9 changes in pyramidal cells before and is expressed in astrocytes after delayed neuronal death in the ischemic hippocampal CA1 region of the gerbil

2007 ◽  
Vol 85 (11) ◽  
pp. 2470-2479 ◽  
Author(s):  
In Koo Hwang ◽  
Ki-Yeon Yoo ◽  
Hua Li ◽  
Bong-Hee Lee ◽  
Hong-Won Suh ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Pyramidal Cells ◽  
Delayed Neuronal Death ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Aquaporin 9 ◽  
Hippocampal Ca1

Evidence for a Role of Second Pathophysiological Stress in Prevention of Delayed Neuronal Death in the Hippocampal CA1 Region

2005 ◽  
Vol 30 (11) ◽  
pp. 1397-1405 ◽  
Author(s):  
Jozef Burda ◽  
Milina Matiašová ◽  
Miroslav Gottlieb ◽  
Viera Danielisová ◽  
Miroslava Némethová ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Delayed Neuronal Death ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1

scholarly journals Selective Proteasomal Dysfunction in the Hippocampal CA1 Region after Transient Forebrain Ischemia

2002 ◽  
Vol 22 (6) ◽  
pp. 705-710 ◽  
Author(s):  
Akio Asai ◽  
Nobuyuki Tanahashi ◽  
Jian-hua Qiu ◽  
Nobuhito Saito ◽  
Shunji Chi ◽  
...  
Keyword(s):  
Frontal Cortex ◽  
Neuronal Death ◽  
Proteasome Activity ◽  
26S Proteasome ◽  
Delayed Neuronal Death ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1

Delayed neuronal death in the hippocampal CA1 region after transient forebrain ischemia may share its underlying mechanism with neurodegeneration and other modes of neuronal death. The precise mechanism, however, remains unknown. In the postischemic hippocampus, conjugated ubiquitin accumulates and free ubiquitin is depleted, suggesting impaired proteasome function. The authors measured regional proteasome activity after transient forebrain ischemia in male Mongolian gerbils. At 30 minutes after ischemia, proteasome activity was 40% of normal in the frontal cortex and hippocampus. After 2 hours of reperfusion, it had returned to normal levels in the frontal cortex, CA3 region, and dentate gyrus, but remained low for up to 48 hours in the CA1 region. Thus, the 26S proteasome was globally impaired in the forebrain during transient ischemia and failed to recover only in the CA1 region after reperfusion. The authors also measured 20S and 26S proteasome activities directly after decapitation ischemia (at 5 and 20 minutes) by fractionating the extracts with glycerol gradient centrifugation. Without adenosine triphosphate (ATP), only 20S proteasome activity was detected in extracts from both the hippocampus and frontal cortex. When the extracts were incubated with ATP in an ATP-regenerating system, 26S proteasome activity recovered almost fully in the frontal cortex but only partially in the hippocampus. Thus, after transient forebrain ischemia, ATP-dependent reassociation of the 20S catalytic and PA700 regulatory subunits to form the active 26S proteasome is severely and specifically impaired in the hippocampus. The irreversible loss of proteasome function underlies the delayed neuronal death induced by transient forebrain ischemia in the hippocampal CA1 region.

PARP-1 activation causes neuronal death in the hippocampal CA1 region by increasing the expression of Ca2+-permeable AMPA receptors

2014 ◽  
Vol 70 ◽  
pp. 43-52 ◽  
Author(s):  
E. Gerace ◽  
A. Masi ◽  
F. Resta ◽  
R. Felici ◽  
E. Landucci ◽  
...  
Keyword(s):  
Ampa Receptors ◽  
Neuronal Death ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
Parp 1

scholarly journals Stratum Lacunosum-moleculare Interneurons of the Hippocampus Coordinate Memory Encoding and Retrieval

2021 ◽  
Author(s):  
Jun Guo ◽  
Heankel Cantu Oliveros ◽  
So Jung Oh ◽  
Bo Liang ◽  
Ying Li ◽  
...  
Keyword(s):  
Pyramidal Cells ◽  
Brain Regions ◽  
Cellular Level ◽  
Memory Encoding ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
Stratum Lacunosum Moleculare ◽  
Encoding And Retrieval

Encoding and retrieval of memory are two processes serving distinct biological purposes but operating in highly overlapping brain circuits. It is unclear how the two processes are coordinated in the same brain regions, especially in the hippocampal CA1 region where the two processes converge at the cellular level. Here we find that the neuron-derived neurotrophic factor (NDNF)-positive interneurons at stratum lacunosum-moleculare (SLM) in CA1 play opposite roles in memory encoding and retrieval. These interneurons show high activities in learning and low activities in recall. Increasing their activity facilitates learning but impairs recall. They inhibit the entorhinal- but dis-inhibit the CA3- inputs to CA1 pyramidal cells and thereby either suppress or elevate CA1 pyramidal cells′ activity depending on animal′s behavioral states. Thus, by coordinating entorhinal- and CA3- dual inputs to CA1, these SLM interneurons are key to switching the hippocampus between encoding and retrieval modes.

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