scholarly journals d-Serine Intervention In The Medial Entorhinal Area Alters TLE-Related Pathology In CA1 Hippocampus Via The Temporoammonic Pathway

Neuroscience ◽  
2021 ◽  
Vol 453 ◽  
pp. 168-186
Author(s):  
Stephen Beesley ◽  
Thomas Sullenberger ◽  
Roshan Ailani ◽  
Cameron D'Orio ◽  
Mathew S. Crockett ◽  
...  
Keyword(s):  
Epilepsia ◽  
2005 ◽  
Vol 46 (s5) ◽  
pp. 72-81 ◽  
Author(s):  
Else A. Tolner ◽  
Fabian Kloosterman ◽  
Stiliyan N. Kalitzin ◽  
Fernando H. Lopes da Silva ◽  
Jan A. Gorter

2013 ◽  
Vol 57 (3) ◽  
pp. 387-391
Author(s):  
Radosław Szalak ◽  
Jadwiga Jaworska-Adamu ◽  
Karol Rycerz ◽  
Paweł Kulik ◽  
Marcin Bartłomiej Arciszewski

Abstract Ten adult male chinchillas were used. The localisation of calbindin D28k (CB) was examined with the use of two types of reactions: immunocytochemical peroxidase-antiperoxidase and immunofluorescence staining with a specific monoclonal antibody against CB. Immunocytochemical examination demonstrated the presence of CB-positive neurons in the following layers of all parts the parahippocampal gyrus (PG): marginal, external cellular, middle cellular, and internal cellular, i.e. in entorhinal area, parasubiculum, and presubiculum. Immunofluorescence staining revealed the presence of CB in both Hu C/Dimmunoreactive (IR) neurons and nervous fibers of the PG. CB-IR neuronal cell bodies were moderately numerous (ca. 10% of Hu C/D-IR neurons) and clearly distinguished from the background. Each layer of the brain area consisted of two types of neurons: pyramidal and multiform. Among the second type of neurons, four kinds of morphologically different neuronal subclasses were observed: multipolar, bipolar, round, and Cajal-Retzius cells. It is concluded that the expression of CB in the PG of the chinchilla is species specific and limited to several subclasses of neurons


2008 ◽  
pp. 1126-1129
Author(s):  
Menno P. Witter
Keyword(s):  

1979 ◽  
Vol 57 (12) ◽  
pp. 1462-1466 ◽  
Author(s):  
Y. Ben-Ari ◽  
K. Krnjević ◽  
W. Reinhardt

The powerful inhibition of CA3 pyramidal neurons evoked in rats (under urethane) by stimulating the fimbria or the perforant path from the entorhinal area is associated with a large increase in input conductance. Microiontophoretic applications of GABA produce a very similar large conductance increase, which is characterized by rapid fading, and causes a marked depression of the inhibitory postsynaptic potential (IPSP) conductance change. During repetitive stimulation at frequencies as low as 3–5/s, the IPSP conductance change can be much reduced, and it vanishes when electrical seizures begin. Since the effect of GABA is also reduced or abolished, a loss of efficacy of GABA (caused by desensitization or some other process) may be responsible for the failure of inhibition observed during tetanic stimulation, as well as for the subsequent seizures.


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