Orexinergic theta rhythm in the rat hippocampal formation: In vitro and in vivo findings

Hippocampus ◽  
2015 ◽  
Vol 25 (11) ◽  
pp. 1393-1406 ◽  
Author(s):  
Renata Bocian ◽  
Paulina Kazmierska ◽  
Paulina Kłos-Wojtczak ◽  
Tomasz Kowalczyk ◽  
Jan Konopacki
2009 ◽  
Vol 78 (6) ◽  
pp. 290-298 ◽  
Author(s):  
Renata Bocian ◽  
Anna Posłuszny ◽  
Tomasz Kowalczyk ◽  
Henryk Gołębiewski ◽  
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.


1997 ◽  
Vol 78 (5) ◽  
pp. 2631-2640 ◽  
Author(s):  
John H. Williams ◽  
Julie A. Kauer

Williams, John H. and Julie A. Kauer. Properties of carbachol-induced oscillatory activity in rat hippocampus. J. Neurophysiol. 78: 2631–2640, 1997. The recent resurgence of interest in carbachol oscillations as an in vitro model of theta rhythm in the hippocampus prompted us to evaluate the circuit mechanisms involved. In extracellular recordings, a regularly spaced bursting pattern of field potentials was observed in both CA3 and CA1 subfields in the presence of carbachol. Removal of the CA3 region abolished oscillatory activity observed in CA1, suggesting that the oscillatory generator is located in CA3. An α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX), blocked carbachol oscillations, indicating that AMPA receptor-mediated synaptic currents are necessary for the population oscillation. Moreover, the spread of oscillatory activity into CA1 required intact N-methyl-d-aspartate receptors. These data are more consistent with epileptiform bursting than with theta rhythm described in vivo. In the presence of carbachol, individual CA3 pyramidal cells exhibited a slow, rhythmic intrinsic oscillation that was not blocked by DNQX and that was enhanced by membrane hyperpolarization. We hypothesize that this slower oscillation is the fundamental oscillator that participates in triggering the population oscillation by exciting multiple synaptically connected CA3 neurons. γ-aminobutyric acid-A (GABAA) receptors are not necessary for carbachol to elicit synchronous CA3 field events but are essential to the bursting pattern observed. Neither GABABnor metabotropic glutamate receptors appear to be necessary for carbachol oscillations. However, both nicotinic and M1 and M3 muscarinic cholinergic receptors contribute to the generation of this activity. These results establish the local circuit elements and neurotransmitter receptors that contribute to carbachol-induced oscillations and indicate that carbachol-induced oscillations are fundamentally distinct from theta rhythm in vivo.


Hippocampus ◽  
2012 ◽  
Vol 23 (1) ◽  
pp. 30-39 ◽  
Author(s):  
Tomasz Kowalczyk ◽  
Jan Konopacki ◽  
Renata Bocian ◽  
Bartosz Caban

2013 ◽  
Vol 67 ◽  
pp. 617-630 ◽  
Author(s):  
Tomasz Kowalczyk ◽  
Bartosz Caban ◽  
Renata Bocian

2020 ◽  
Author(s):  
Teresa Cramer ◽  
Raminder Gill ◽  
Zahra S Thirouin ◽  
Markus Vaas ◽  
Suchita Sampath ◽  
...  

AbstractMicroglia interact with neurons to facilitate synapse plasticity; however, signal transducers between microglia and neuron remain unknown. Here, using in vitro organotypic hippocampal slice cultures and transient MCAO in genetically-engineered mice in vivo, we report that at 24 h post-ischemia microglia release BDNF to downregulate glutamatergic and GABAergic synapses within the peri-infarct area. Analysis of the CA1 hippocampal formation in vitro shows that proBDNF and mBDNF downregulate glutamatergic dendritic spines and gephyrin scaffold stability through p75NTR and TrkB receptors respectively. Post-MCAO, we report that in the peri- infarct area and in the corresponding contralateral hemisphere similar neuroplasticity occur through microglia activation and gephyrin phosphorylation at Ser268, Ser270 in vivo. Targeted deletion of the Bdnf gene in microglia or GphnS268A/S270A (phospho-null) point-mutations protect against ischemic brain damage, neuroinflamation and synapse downregulation normally seen post-MCAO. Collectively, we report that gephyrin phosphorylation and microglia derived BDNF faciliate synapse plasticity after transient ischemia.


2002 ◽  
Vol 87 (3) ◽  
pp. 1196-1205 ◽  
Author(s):  
Bradley J. Molyneaux ◽  
Michael E. Hasselmo

Cyclical activity of GABAergic interneurons during theta rhythm could mediate phasic changes in strength of glutamatergic synaptic transmission in the hippocampal formation if presynaptic inhibition from activation of GABAB receptors is sufficiently rapid to change within a theta cycle. The experiments described here analyzed the time course of GABABmodulation using a heterosynaptic depression paradigm in anesthetized rats at physiological temperatures. Heterosynaptic depression of the slope of evoked potentials decayed with a time constant that would allow significant changes in transmission across different phases of the theta cycle. This heterosynaptic depression was significantly reduced by local infusion of the GABAB receptor antagonist CGP55845A.


Hippocampus ◽  
2013 ◽  
Vol 24 (1) ◽  
pp. 7-20 ◽  
Author(s):  
Tomasz Kowalczyk ◽  
Renata Bocian ◽  
Bartosz Caban ◽  
Jan Konopacki

2002 ◽  
Vol 87 (2) ◽  
pp. 1165-1168 ◽  
Author(s):  
Stephen K. Towers ◽  
Fiona E. N. LeBeau ◽  
Tengis Gloveli ◽  
Roger D. Traub ◽  
Miles A. Whittington ◽  
...  

The dentate gyrus is a prominent source of gamma frequency activity in the hippocampal formation in vivo. Here we show that transient epochs of gamma frequency network activity (67 ± 12 Hz) can be generated in the dentate gyrus of rat hippocampal slices, following brief pressure ejections of a high-molarity potassium solution onto the molecular layer. Oscillatory activity remains synchronized over distances >300 μm and is accompanied by a modest rise in [K+]o. Gamma frequency oscillations were abolished by a GABAA receptor antagonist demonstrating their dependence on rhythmic inhibition. However, in many cases, higher frequency oscillations (>80 Hz) remained in the absence of synaptic transmission, thus demonstrating that nonsynaptic factors may underlie fast oscillatory activity.


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