scholarly journals Selective hippocampal cell damage and mossy fiber sprouting induced by chronic intracerebral injections of 2-deoxy-D-glucose

2020 ◽  
Vol 39 (01) ◽  
pp. 99-106
Author(s):  
Evgeniia Samokhina ◽  
Anton Malkov ◽  
Alexander Samokhin ◽  
Irina Popova
Epilepsia ◽  
1999 ◽  
Vol 40 (10) ◽  
pp. 1393-1401 ◽  
Author(s):  
Bouchaib El Bahh ◽  
Veronique Lespinet ◽  
Dominique Lurton ◽  
Monique Coussemacq ◽  
Gildas Le Gal La Salle ◽  
...  

2019 ◽  
Vol 16 (1) ◽  
pp. 3-11
Author(s):  
Luisa Halbe ◽  
Abdelhaq Rami

Introduction: Endoplasmic reticulum (ER) stress induced the mobilization of two protein breakdown routes, the proteasomal- and autophagy-associated degradation. During ERassociated degradation, unfolded ER proteins are translocated to the cytosol where they are cleaved by the proteasome. When the accumulation of misfolded or unfolded proteins excels the ER capacity, autophagy can be activated in order to undertake the degradative machinery and to attenuate the ER stress. Autophagy is a mechanism by which macromolecules and defective organelles are included in autophagosomes and delivered to lysosomes for degradation and recycling of bioenergetics substrate. Materials and Methods: Autophagy upon ER stress serves initially as a protective mechanism, however when the stress is more pronounced the autophagic response will trigger cell death. Because autophagy could function as a double edged sword in cell viability, we examined the effects autophagy modulation on ER stress-induced cell death in HT22 murine hippocampal neuronal cells. We investigated the effects of both autophagy-inhibition by 3-methyladenine (3-MA) and autophagy-activation by trehalose on ER-stress induced damage in hippocampal HT22 neurons. We evaluated the expression of ER stress- and autophagy-sensors as well as the neuronal viability. Results and Conclusion: Based on our findings, we conclude that under ER-stress conditions, inhibition of autophagy exacerbates cell damage and induction of autophagy by trehalose failed to be neuroprotective.


Neuroreport ◽  
1997 ◽  
Vol 8 (9) ◽  
pp. 2299-2303 ◽  
Author(s):  
Darren K. Hannesson ◽  
Lisa L. Armitage ◽  
Paul Mohapel ◽  
Michael E. Corcoran

Neuroreport ◽  
2000 ◽  
Vol 11 (13) ◽  
pp. 2897-2901 ◽  
Author(s):  
Paul Mohapel ◽  
Lisa L. Armitage ◽  
Trevor H. Gilbert ◽  
Darren K. Hannesson ◽  
G Campbell Teskey ◽  
...  

2010 ◽  
Vol 103 (3) ◽  
pp. 1490-1500 ◽  
Author(s):  
Robert F. Hunt ◽  
Stephen W. Scheff ◽  
Bret N. Smith

Posttraumatic epilepsy is a frequent consequence of brain trauma, but relatively little is known about how neuronal circuits are chronically altered after closed head injury. We examined whether local recurrent excitatory synaptic connections form between dentate granule cells in mice 8–12 wk after cortical contusion injury. Mice were monitored for behavioral seizures shortly after brain injury and ≤10 wk postinjury. Injury-induced seizures were observed in 15% of mice, and spontaneous seizures were observed weeks later in 40% of mice. Timm's staining revealed mossy fiber sprouting into the inner molecular layer of the dorsal dentate gyrus ipsilateral to the injury in 95% of mice but not contralateral to the injury or in uninjured controls. Whole cell patch-clamp recordings were made from granule cells in isolated hippocampal brain slices. Cells in slices with posttraumatic mossy fiber sprouting had an increased excitatory postsynaptic current (EPSC) frequency compared with cells in slices without sprouting from injured and control animals ( P < 0.001). When perfused with Mg2+-free artificial cerebrospinal fluid containing 100 μM picrotoxin, these cells had spontaneous bursts of EPSCs and action potentials. Focal glutamate photostimulation of the granule cell layer evoked a burst of EPSCs and action potentials indicative of recurrent excitatory connections in granule cells of slices with mossy fiber sprouting. In granule cells of slices without sprouting from injured animals and controls, spontaneous or photostimulation-evoked epileptiform activity was never observed. These results suggest that a new regionally localized excitatory network forms between dentate granule cells near the injury site within weeks after cortical contusion head injury.


Neuroreport ◽  
1996 ◽  
Vol 7 (5) ◽  
pp. 1029-1035 ◽  
Author(s):  
Gary W. Mathern ◽  
Joao P. Leite ◽  
Thomas L. Babb ◽  
James K. Pretorius ◽  
Paula A. Kuhlman ◽  
...  

Neuroscience ◽  
1999 ◽  
Vol 92 (1) ◽  
pp. 73-82 ◽  
Author(s):  
A.E Anderson ◽  
R.A Hrachovy ◽  
B.A Antalffy ◽  
D.L Armstrong ◽  
J.W Swann

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