In vitro hippocampal dentate frequency potentiation induction as model to detect electrophysiological correlates of some cognitive impairments in striatallt-lesioned rats

1996 ◽  
Vol 20 (6) ◽  
pp. 999-1010
Author(s):  
Maria Rosaria Domenici ◽  
Stefano Sagratella ◽  
Patrizia Popoli
Keyword(s):  
Cognitive Impairments ◽  
Frequency Potentiation

Effects of extracellular calcium on low frequency induced potentiation and habituation in the in vitro hippocampal slice preparation

1982 ◽  
Vol 60 (3) ◽  
pp. 266-275 ◽  
Author(s):  
R. W. Turner ◽  
J. J. Miller
Keyword(s):  
Evoked Potentials ◽  
Hippocampal Slice ◽  
Low Frequency ◽  
Extracellular Calcium ◽  
Population Spike ◽  
Slice Preparation ◽  
Short Term ◽  
High Calcium ◽  
Frequency Potentiation

The electrophysiological characteristics of frequency potentiation and habituation were investigated in two afferent systems of the in vitro hippocampal slice preparation. Low frequency stimulation (1 Hz) of the Schaffer collateral – commissural (Sch–comm) fibers results in a short-term potentiation of the amplitude and rate of rise of the EPSP and population spike responses recorded in the CA1 region. In contrast, 1-Hz stimulation of the perforant path (PP) evokes a short-term, habituation-like depression of the dentate granule cell EPSP and population spike. An inverse relationship was observed between stimulus intensity and the magnitude of frequency potentiation or habituation. Changes in afferent fiber volleys or general excitability of postsynaptic membranes did not contribute significantly to the development of either of these forms of short-term plasticity. Perfusion with a medium containing a high calcium – low magnesium concentration (4 mM Ca+2 and 1 mM Mg+2) produced a differential effect on CA1 and dentate evoked potentials. Following a 20-min exposure to this medium, the amplitude of CA1 potentials was increased while dentate responses were decreased. Frequency potentiation of CA1 responses and habituation of dentate responses were depressed or eliminated by the high calcium medium.The opposing influence of extracellular calcium on CA1 and dentate evoked potentials indicates a fundamental difference in the process of transmitter release in these systems, a characteristic that may contribute to the production of frequency potentiation and habituation.

Endoplasmic reticulum stress/autophagy pathway is involved in diabetes-induced neuronal apoptosis and cognitive decline in mice

2018 ◽  
Vol 132 (1) ◽  
pp. 111-125 ◽  
Author(s):  
Fei-Juan Kong ◽  
Lei-Lei Ma ◽  
Jun-Jie Guo ◽  
Lin-Hao Xu ◽  
Yun Li ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cognitive Decline ◽  
Er Stress ◽  
Hippocampal Neurons ◽  
Neuronal Apoptosis ◽  
Molecular Mechanisms ◽  
Cognitive Impairments ◽  
Public Health Problem ◽  
Diabetic Mice

Diabetes mellitus is a significant global public health problem depicting a rising prevalence worldwide. As a serious complication of diabetes, diabetes-associated cognitive decline is attracting increasing attention. However, the underlying mechanisms are yet to be fully determined. Both endoplasmic reticulum (ER) stress and autophagy have been reported to modulate neuronal survival and death and be associated with several neurodegenerative diseases. Here, a streptozotocin-induced diabetic mouse model and primary cultured mouse hippocampal neurons were employed to investigate the possible role of ER stress and autophagy in diabetes-induced neuronal apoptosis and cognitive impairments, and further explore the potential molecular mechanisms. ER stress markers GRP78 and CHOP were both enhanced in diabetic mice, as was phosphorylation of PERK, IRE1α, and JNK. In addition, the results indicated an elevated level of autophagy in diabetic mice, as demonstrated by up-regulated expressions of autophagy markers LC3-II, beclin 1 and down-regulated level of p62, and increased formation of autophagic vacuoles and LC3-II aggregates. Meanwhile, we found that these effects could be abolished by ER stress inhibitor 4-phenylbutyrate or JNK inhibitor SP600125 in vitro. Furthermore, neuronal apoptosis of diabetic mice was attenuated by pretreatment with 4-phenylbutyrate, while aggravated by application of inhibitor of autophagy bafilomycin A1 in vitro. These results suggest that ER stress pathway may be involved in diabetes-mediated neurotoxicity and promote the following cognitive impairments. More important, autophagy was induced by diabetes possibly through ER stress-mediated JNK pathway, which may protect neurons against ER stress-associated cell damages.

Layer I Ectopias and Increased Excitability in Murine Neocortex

2002 ◽  
Vol 87 (5) ◽  
pp. 2471-2479 ◽  
Author(s):  
Lisa A. Gabel ◽  
Joseph J. LoTurco
Keyword(s):  
Animal Models ◽  
Cognitive Impairments ◽  
Epileptiform Activity ◽  
Brain Slices ◽  
Inbred Lines ◽  
Seizure Susceptibility ◽  
Cortical Dysplasias ◽  
Layer I

Cortical dysplasias are associated with both epilepsy and cognitive impairments in humans. Similarly, several animal models of cortical dysplasia show that dysplasia causes increased seizure susceptibility and behavioral deficits in vivo and increased levels of excitability in vitro. As most current animal models involve either global disruptions in cortical architecture or the induction of lesions, it is not yet clear whether small spontaneous neocortical malformations are also associated with increased excitability or seizure susceptibility. Small groups of displaced neurons in layer I of the neocortex, ectopias, have been identified in patients with cognitive impairments, and similar malformations occur sporadically in some inbred lines of mice where they are associated with behavioral and sensory-processing deficits. In a previous study, we characterized the physiology of cells within neocortical ectopias, in one of the inbred lines (NXSM-D/Ei) and showed that the presence of multiple ectopias is associated with the generation of spontaneous epileptiform activity in slices. In this study, we use extracellular recordings from brain slices to show that even single-layer I ectopias are associated with higher excitability. Specifically, slices that contain single ectopias display epileptiform activity at significantly lower concentrations of the GABAA receptor antagonist bicuculline than do slices without ectopias (either from opposite hemispheres or animals without ectopias). Moreover, because removal of ectopias from slices does not restore normal excitability, enhanced excitability is not generated within the ectopia. Finally, we show that in vivo, mice with ectopias are more sensitive to the convulsant pentylenetetrazole than are mice without ectopias. Together these results suggest that alterations in cortical hemispheres containing focal layer I malformations increase cortical excitability and that even moderately small spontaneous cortical dysplasias are associated with increased excitability in vitro and in vivo.

A comparison between frequency potentiation and postextrasystolic potentiation in vitro and in situ

1969 ◽  
Vol 311 (3) ◽  
pp. 226-242 ◽  
Author(s):  
U. Kilz ◽  
W. Niedermayer ◽  
K. J. Nordmann ◽  
J. Schaefer ◽  
H. J. Schwarzkopf ◽  
...  
Keyword(s):  
Postextrasystolic Potentiation ◽  
Frequency Potentiation

scholarly journals Curcumin Protects Against Cognitive Impairments in a Rat Model of Chronic Cerebral Hypoperfusion Combined with Diabetes Mellitus by Suppressing Neuroinflammation, Apoptosis, and Pyroptosis

2020 ◽  
Author(s):  
Yaling Zheng ◽  
Jiawei Zhang ◽  
Yao Zhao ◽  
Yaxuan Zhang ◽  
Xiaojie Zhang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cognitive Impairments ◽  
Neuronal Cell ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Receptor Protein ◽  
Therapeutic Effects ◽  
Protective Effects

Abstract BackgroundChronic cerebral hypoperfusion (CCH) is regarded as a high-risk factor for cognitive decline in vascular dementia (VaD). We have previously shown that diabetes mellitus (DM) synergistically promotes CCH-induced cognitive dysfunction via exacerbating neuroinflammation. Furthermore, curcumin has been shown to exhibit anti-inflammatory and neuroprotective activities. However, the effects of curcumin on CCH-induced cognitive impairments in DM have remained unknown.MethodsRats were fed with a high-fat diet (HFD) and injected with low-dose streptozotocin (STZ), followed by bilateral common carotid artery occlusion (BCCAO), to model DM and CCH in vivo. After BCCAO, curcumin (50 mg/kg) was administered intraperitoneally every two days for eight weeks to evaluate its therapeutic effects. Additionally, mouse BV2 microglial cells were exposed to hypoxia and high glucose to model CCH and DM pathologies in vitro. ResultsCurcumin treatment significantly improved DM/CCH-induced cognitive deficits and attenuated neuronal cell death. Molecular analysis revealed that curcumin exerted protective effects via suppressing neuroinflammation induced by microglial activation, regulating the triggering receptor expressed on myeloid cells 2 (TREM2)/toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) pathway, alleviating apoptosis, and reducing nod-like receptor protein 3 (NLRP3)-dependent pyroptosis.ConclusionsTaken together, our findings suggest that curcumin represents a promising therapy for DM/CCH-induced cognitive impairments.

scholarly journals Fucoxanthin, a Marine Carotenoid, Reverses Scopolamine-Induced Cognitive Impairments in Mice and Inhibits Acetylcholinesterase in Vitro

Marine Drugs ◽  
2016 ◽  
Vol 14 (4) ◽  
pp. 67 ◽  
Author(s):  
Jiajia Lin ◽  
Ling Huang ◽  
Jie Yu ◽  
Siying Xiang ◽  
Jialing Wang ◽  
...  
Keyword(s):  
Cognitive Impairments

scholarly journals Thrombopoietin receptor agonist eltrombopag alleviates cognitive impairment via NRG1/ErbB4 signaling

2021 ◽  
Author(s):  
jian wang ◽  
leping liu ◽  
xuebao wang ◽  
he yu ◽  
baihui chen ◽  
...  
Keyword(s):  
Protein Expression ◽  
Rat Model ◽  
Receptor Agonist ◽  
Synapse Formation ◽  
Cognitive Impairments ◽  
Sirtuin 1 ◽  
Synaptic Protein ◽  
Thrombopoietin Receptor ◽  
Thrombopoietin Receptor Agonist

Abstract Background Patients with minimal hepatic encephalopathy (MHE) show mild cognitive impairments. Thrombopoietin (TPO) has been shown to be neuroprotective. This study aimed to explore the therapeutic effect of Thrombopoietin receptor agonist eltrombopag (ELT) on MHE and the involvement of NRG1 signaling using primary rat neurons and a MHE rat model. Methods We explored the effects of ELT stimulation on NRG1/ErbB4 signaling and synapse formation in the primary rat neurons. Furthermore, we explored the cerebral TPO expression level and the effect of TPO replacement therapy in an MHE rat model. Results The results showed that ELT stimulation activated NRG1/ErbB4 signaling and enhanced synaptic protein expression in the primary rat neurons via sirtuin 1. An anti-NRG1 antibody, ErbB4 inhibitor, or knockdown of NRG1 or ErbB4 could significantly abolish ELT-induced upregulation of synaptic protein expression in the primary rat neurons. MHE rats had significantly decreased cerebral ELT expression compared with normal rats. ELT activated NRG1/ErbB4 signaling in MHE rat brains. Administration or overexpression of ELT or TPO promoted synapse formation and alleviated cognitive impairments in MHE rats. Conclusions These data suggest that ELT promotes synapse formation in vitro and in vivo via activating NRG1/ErbB4 signaling, serving as a promising therapeutic agent for MHE treatment.

Frequency Potentiation in the Medial Cortex of Young Turtle Brains in vitro

1998 ◽  
Vol 52 (6) ◽  
pp. 263-269 ◽  
Author(s):  
M.D. Muñoz ◽  
C. Magariños-Ascone ◽  
J.M. Gaztelu ◽  
E. García-Austt
Keyword(s):  
Medial Cortex ◽  
Frequency Potentiation

Ultrastructural Investigations of the Contractile Filaments of Amoebae

1974 ◽  
Vol 32 ◽  
pp. 188-189
Author(s):  
P.L. Moore
Keyword(s):  
Cytoplasmic Streaming ◽  
Three Dimensional ◽  
Freeze Fracture ◽  
Amoeboid Movement ◽  
Different Types ◽  
Chemical Conditions ◽  
Complete Interpretation

Previous freeze fracture results on the intact giant, amoeba Chaos carolinensis indicated the presence of a fibrillar arrangement of filaments within the cytoplasm. A complete interpretation of the three dimensional ultrastructure of these structures, and their possible role in amoeboid movement was not possible, since comparable results could not be obtained with conventional fixation of intact amoebae. Progress in interpreting the freeze fracture images of amoebae required a more thorough understanding of the different types of filaments present in amoebae, and of the ways in which they could be organized while remaining functional.The recent development of a calcium sensitive, demembranated, amoeboid model of Chaos carolinensis has made it possible to achieve a better understanding of such functional arrangements of amoeboid filaments. In these models the motility of demembranated cytoplasm can be controlled in vitro, and the chemical conditions necessary for contractility, and cytoplasmic streaming can be investigated. It is clear from these studies that “fibrils” exist in amoeboid models, and that they are capable of contracting along their length under conditions similar to those which cause contraction in vertebrate muscles.

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