scholarly journals Theta rhythm recorded in the hippocampal formation in vitro

2013 ◽  
Vol 67 ◽  
pp. 617-630 ◽  
Author(s):  
Tomasz Kowalczyk ◽  
Bartosz Caban ◽  
Renata Bocian
2009 ◽  
Vol 78 (6) ◽  
pp. 290-298 ◽  
Author(s):  
Renata Bocian ◽  
Anna Posłuszny ◽  
Tomasz Kowalczyk ◽  
Henryk Gołębiewski ◽  
Jan Konopacki

Hippocampus ◽  
2015 ◽  
Vol 25 (11) ◽  
pp. 1393-1406 ◽  
Author(s):  
Renata Bocian ◽  
Paulina Kazmierska ◽  
Paulina Kłos-Wojtczak ◽  
Tomasz Kowalczyk ◽  
Jan Konopacki

2019 ◽  
Vol 20 (12) ◽  
pp. 3030 ◽  
Author(s):  
Soo Jung Shin ◽  
Seong Gak Jeon ◽  
Jin-il Kim ◽  
Yu-on Jeong ◽  
Sujin Kim ◽  
...  

Alzheimer’s disease (AD) is the most common neurodegenerative disease and is characterized by neurodegeneration and cognitive deficits. Amyloid beta (Aβ) peptide is known to be a major cause of AD pathogenesis. However, recent studies have clarified that mitochondrial deficiency is also a mediator or trigger for AD development. Interestingly, red ginseng (RG) has been demonstrated to have beneficial effects on AD pathology. However, there is no evidence showing whether RG extract (RGE) can inhibit the mitochondrial deficit-mediated pathology in the experimental models of AD. The effects of RGE on Aβ-mediated mitochondrial deficiency were investigated in both HT22 mouse hippocampal neuronal cells and the brains of 5XFAD Aβ-overexpressing transgenic mice. To examine whether RGE can affect mitochondria-related pathology, we used immunohistostaining to study the effects of RGE on Aβ accumulation, neuroinflammation, neurodegeneration, and impaired adult hippocampal neurogenesis in hippocampal formation of 5XFAD mice. In vitro and in vivo findings indicated that RGE significantly improves Aβ-induced mitochondrial pathology. In addition, RGE significantly ameliorated AD-related pathology, such as Aβ deposition, gliosis, and neuronal loss, and deficits in adult hippocampal neurogenesis in brains with AD. Our results suggest that RGE may be a mitochondria-targeting agent for the treatment of AD.


2018 ◽  
Author(s):  
Jean Simonnet ◽  
Michael Brecht

AbstractThe subiculum is the major output structure of the hippocampal formation and is involved in learning and memory as well as in spatial navigation. Little is known about how the cellular diversity of subicular neurons is related to function. Primed by in vitro studies, which identified distinct bursting patterns in subicular cells, we asked how subicular burst firing is related to spatial coding in vivo. Using high-resolution juxtacellular recordings in freely moving rats, we analyzed the firing patterns of 51 subicular principal neurons and distinguished two populations based on their bursting behavior, i.e. sparsely bursting (∼80%) and dominantly bursting neurons (∼20%). Dominantly bursting neurons had significantly higher firing rates than sparsely bursting neurons. Furthermore, the two clusters had distinct spatial properties, sparsely bursting cells showing strong positional tuning and dominantly bursting cells being only weakly tuned. Additionally, the occurrence of bursts in sparsely bursting neurons defined well-defined spatial fields. In contrast, isolated spikes contained less spatial information. We conclude that burst firing distinguishes subicular principal cell types and constitutes a distinct unit encoding spatial information in sparsely bursting spatial cells. Overall, our results demonstrate that burst firing is highly relevant to subicular space coding.


1996 ◽  
Vol 76 (3) ◽  
pp. 1657-1666 ◽  
Author(s):  
J. R. Greene ◽  
A. Mason

1. We used intracellular current-clamp techniques to record from 33 ventral subicular neurons in slices or rat hippocampal formation. Presumed pyramidal neurons were characterized by their responses to depolarizing current pulses as either intrinsically burst firing (IB) or regular spiking (RS). Within the subiculum, IB cells were encountered most frequently in the deep cell layer, whereas RS cells were encountered most frequently in the superficial cell layer. IB cells had more depolarized resting potentials, lower input resistances, and more sag in their voltage responses to hyperpolarizing current pulses. 2. Somatostatin (5 microM) applied in the bathing medium caused a hyperpolarization and reduction in input resistance. These effects were of greater magnitude in IB cells. Somatostatin had no effect on sag in either cell type. These effects of somatostatin were unchanged in the presence of gamma-aminobutyric acid (GABA) receptor antagonists. 3. In a series of experiments conducted in RS cells only, somatostatin reduced the amplitude of the late but not the early component of evoked biphasic inhibitory postsynaptic potentials (IPSPs). 4. A second series of experiments was conducted in RS and IB cells. Somatostatin reduced the amplitude of pharmacologically isolated GABAA IPSPS in both cell types. In IB cells but not RS cells there was a correlation between this effect and the somatostatin-induced hyperpolarization. Somatostatin also reduced the amplitude of isolated GABAB IPSPS in both cell types, but more so in IB cells. 5. Somatostatin had no effect on the reversal potential of either IPSP in either cell type and no effect on the GABAA-mediated conductance in either cell type. In contrast, the GABAB-mediated conductance was reduced, especially in IB cells. 6. The effects of somatostatin on GABAA IPSPS are principally a result of membrane shunting and reductions in ionic driving force, but these mechanisms do not account for the reduction in GABAB IPSPS. 7. We suggest that the combined effects of somatostatin are likely to alter the balance between fast and slow inhibition and to do so more in IB cells than in RS cells.


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