scholarly journals Neurogliaform cells in the molecular layer of the dentate gyrus as feed-forward γ-aminobutyric acidergic modulators of entorhinal-hippocampal interplay

2011 ◽  
Vol 519 (8) ◽  
pp. 1476-1491 ◽  
Author(s):  
Caren Armstrong ◽  
János Szabadics ◽  
Gábor Tamás ◽  
Ivan Soltesz
Keyword(s):  
Dentate Gyrus ◽  
Molecular Layer ◽  
Feed Forward

scholarly journals Molecular layer perforant path-associated cells contribute to feed-forward inhibition in the adult dentate gyrus

2013 ◽  
Vol 110 (22) ◽  
pp. 9106-9111 ◽  
Author(s):  
Y. Li ◽  
F. J. Stam ◽  
J. B. Aimone ◽  
M. Goulding ◽  
E. M. Callaway ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Molecular Layer ◽  
Perforant Path ◽  
Feed Forward ◽  
Feed Forward Inhibition

Quantitation of astrocytes in the molecular layer of the dentate gyrus in schizophrenic patients

1989 ◽  
Vol 25 (7) ◽  
pp. A58 ◽  
Author(s):  
Manuel F. Casanova ◽  
Richard Saunders ◽  
Jan Stevens ◽  
Joel E. Kleinman
Keyword(s):  
Dentate Gyrus ◽  
Molecular Layer ◽  
Schizophrenic Patients

Author response for "Long‐term environmental enrichment reduces microglia morphological diversity of the molecular layer of dentate gyrus"

2020 ◽  
Author(s):  
Thaís Cristina Galdino de Oliveira ◽  
Dario Carvalho‐Paulo ◽  
Camila Mendes de Lima ◽  
Roseane Borner de Oliveira ◽  
Carlos Santos Filho ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Environmental Enrichment ◽  
Molecular Layer ◽  
Morphological Diversity ◽  
Author Response

scholarly journals The Proteome of the Dentate Terminal Zone of the Perforant Path Indicates Presynaptic Impairment in Alzheimer Disease

2019 ◽  
Vol 19 (1) ◽  
pp. 128-141 ◽  
Author(s):  
Hazal Haytural ◽  
Georgios Mermelekas ◽  
Ceren Emre ◽  
Saket Milind Nigam ◽  
Steven L. Carroll ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Dentate Gyrus ◽  
Molecular Mechanisms ◽  
Molecular Layer ◽  
Synaptic Proteins ◽  
Perforant Path ◽  
Synaptic Dysfunction ◽  
Complexin 2 ◽  
Terminal Zone ◽  
Vesicle Cycle

Synaptic dysfunction is an early pathogenic event in Alzheimer disease (AD) that contributes to network disturbances and cognitive decline. Some synapses are more vulnerable than others, including the synapses of the perforant path, which provides the main excitatory input to the hippocampus. To elucidate the molecular mechanisms underlying the dysfunction of these synapses, we performed an explorative proteomic study of the dentate terminal zone of the perforant path. The outer two-thirds of the molecular layer of the dentate gyrus, where the perforant path synapses are located, was microdissected from five subjects with AD and five controls. The microdissected tissues were dissolved and digested by trypsin. Peptides from each sample were labeled with different isobaric tags, pooled together and pre-fractionated into 72 fractions by high-resolution isoelectric focusing. Each fraction was then analyzed by liquid chromatography-mass spectrometry. We quantified the relative expression levels of 7322 proteins, whereof 724 showed significantly altered levels in AD. Our comprehensive data analysis using enrichment and pathway analyses strongly indicated that presynaptic signaling, such as exocytosis and synaptic vesicle cycle processes, is severely disturbed in this area in AD, whereas postsynaptic proteins remained unchanged. Among the significantly altered proteins, we selected three of the most downregulated synaptic proteins; complexin-1, complexin-2 and synaptogyrin-1, for further validation, using a new cohort consisting of six AD and eight control cases. Semi-quantitative analysis of immunohistochemical staining confirmed decreased levels of complexin-1, complexin-2 and synaptogyrin-1 in the outer two-thirds of the molecular layer of the dentate gyrus in AD. Our in-depth proteomic analysis provides extensive knowledge on the potential molecular mechanism underlying synaptic dysfunction related to AD and supports that presynaptic alterations are more important than postsynaptic changes in early stages of the disease. The specific synaptic proteins identified could potentially be targeted to halt synaptic dysfunction in AD.

Optical Recording Study of Granule Cell Activities in the Hippocampal Dentate Gyrus of Kainate-Treated Rats

2000 ◽  
Vol 83 (4) ◽  
pp. 2421-2430 ◽  
Author(s):  
Yo Otsu ◽  
Eiichi Maru ◽  
Hisayuki Ohata ◽  
Ichiro Takashima ◽  
Riichi Kajiwara ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Granule Cell ◽  
Granule Cells ◽  
Mossy Fiber ◽  
Molecular Layer ◽  
Mossy Fibers ◽  
Optical Recording ◽  
Granule Cell Layer ◽  
Gabaergic Inhibition ◽  
Mossy Fiber Sprouting

In the epileptic hippocampus, newly sprouted mossy fibers are considered to form recurrent excitatory connections to granule cells in the dentate gyrus and thereby increase seizure susceptibility. To study the effects of mossy fiber sprouting on neural activity in individual lamellae of the dentate gyrus, we used high-speed optical recording to record signals from voltage-sensitive dye in hippocampal slices prepared from kainate-treated epileptic rats (KA rats). In 14 of 24 slices from KA rats, hilar stimulation evoked a large depolarization in almost the entire molecular layer in which granule cell apical dendrites are located. The signals were identified as postsynaptic responses because of their dependence on extracellular Ca2+. The depolarization amplitude was largest in the inner molecular layer (the target area of sprouted mossy fibers) and declined with increasing distance from the granule cell layer. In the inner molecular layer, a good correlation was obtained between depolarization size and the density of mossy fiber terminals detected by Timm staining methods. Blockade of GABAergic inhibition by bicuculline enlarged the depolarization in granule cell dendrites. Our data indicate that mossy fiber sprouting results in a large and prolonged synaptic depolarization in an extensive dendritic area and that the enhanced GABAergic inhibition partly masks the synaptic depolarization. However, despite the large dendritic excitation induced by the sprouted mossy fibers, seizurelike activity of granule cells was never observed, even when GABAergic inhibition was blocked. Therefore, mossy fiber sprouting may not play a critical role in epileptogenesis.

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