scholarly journals Global Cerebral Ischemia Associated with Cardiac Arrest in the Rat: I. Dynamics of Early Neuronal Changes

1992 ◽  
Vol 12 (2) ◽  
pp. 238-249 ◽  
Author(s):  
Kensuke Kawai ◽  
Liliana Nitecka ◽  
Christl A. Ruetzler ◽  
Goro Nagashima ◽  
Ferenc Joó ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Pyramidal Neurons ◽  
Peripheral Zone ◽  
Gabaergic Neurons ◽  
Stratum Radiatum ◽  
Global Cerebral Ischemia ◽  
Cresyl Violet ◽  
Cytoplasmic Vacuoles ◽  
Nucleus Reticularis ◽  
Nissl Substance

Light microscopic neuronal changes were studied in rats subjected to 10 min of global ischemia produced by compression of the major cardiac vessels. Observations of cresyl violet-stained sections revealed early changes involving predominantly GABAergic neurons in various locations. In rats killed 15 min after recirculation, the changes were characterized by the appearance of a clear peripheral zone with condensation of the remaining neuronal cytoplasm. After 1 h, these zones appeared to be compartmentalized into individual pearl-like vacuoles, especially prominent in the nucleus reticularis thalami. After 3 h, the cytoplasmic vacuoles disappeared and the neuronal changes, particularly in the cerebral cortex, striatum, hippocampus, and pars reticulata of the substantia nigra, consisted mainly of hyperchromasia or loss of Nissl substance. After 2 days, the cerebral cortex and thalamus contained occasional neurons with conspicuously large nucleoli. After 7 days, the hippocampus revealed an approximately 50% loss of CA1 pyramidal neurons, associated with intense microglial reactivity in the stratum radiatum, whereas the neuronal destruction was more complete in the nucleus reticularis thalami. Our observations suggest a possibility that early changes in GABAergic neurons may provide a period of neuronal disinhibition and thus contribute to an excitatory ischemic damage in regions connected by GABAergic circuitry.

scholarly journals Pre- and Post-Treatment with Novel Antiepileptic Drug Oxcarbazepine Exerts Neuroprotective Effect in the Hippocampus in a Gerbil Model of Transient Global Cerebral Ischemia

2019 ◽  
Vol 9 (10) ◽  
pp. 279 ◽  
Author(s):  
Ji Hyeon Ahn ◽  
Bich Na Shin ◽  
Joon Ha Park ◽  
Tae-Kyeong Lee ◽  
Young Eun Park ◽  
...  
Keyword(s):  
Antiepileptic Drug ◽  
Calcium Binding ◽  
Pyramidal Neurons ◽  
Neuroprotective Effect ◽  
Post Treatment ◽  
Global Cerebral Ischemia ◽  
Cresyl Violet ◽  
Transient Ischemia ◽  
Fluoro Jade B ◽  
Cornu Ammonis

Oxcarbazepine, an antiepileptic drug, has been reported to modulate voltage-dependent sodium channels, and it is commonly used in epilepsy treatment. In this study, we investigated the neuroprotective effect of oxcarbazepine in the hippocampus after transient ischemia in gerbils. Gerbils randomly received oxcarbazepine 100 or 200 mg/kg before and after transient ischemia. We examined its neuroprotective effect in the cornu ammonis 1 subfield of the gerbil hippocampus at 5 days after transient ischemia by using cresyl violet staining, neuronal nuclei immunohistochemistry and Fluoro-Jade B histofluorescence staining for neuroprotection, and by using glial fibrillary protein and ionized calcium-binding adapter molecule 1 immunohistochemistry for reaction of astrocytes and microglia, respectively. Pre- and post-treatment with 200 mg/kg of oxcarbazepine, but not 100 mg/kg of oxcarbazepine, protected pyramidal neurons of the cornu ammonis 1 subfield from transient ischemic damage. In addition, pre- and post-treatment with oxcarbazepine (200 mg/kg) significantly ameliorated astrocytes and microglia activation in the ischemic cornu ammonis 1 subfield. In brief, our current results indicate that post-treatment as well as pre-treatment with 200 mg/kg of oxcarbazepine can protect neurons from ischemic insults via attenuation of the glia reaction.

scholarly journals High levels of 27-hydroxycholesterol results in synaptic plasticity alterations in the hippocampus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Raul Loera-Valencia ◽  
Erika Vazquez-Juarez ◽  
Alberto Muñoz ◽  
Gorka Gerenu ◽  
Marta Gómez-Galán ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Memory Function ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Cholesterol Homeostasis ◽  
Stratum Radiatum ◽  
Actin Binding ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Term Potentiation

AbstractAlterations in brain cholesterol homeostasis in midlife are correlated with a higher risk of developing Alzheimer’s disease (AD). However, global cholesterol-lowering therapies have yielded mixed results when it comes to slowing down or preventing cognitive decline in AD. We used the transgenic mouse model Cyp27Tg, with systemically high levels of 27-hydroxycholesterol (27-OH) to examine long-term potentiation (LTP) in the hippocampal CA1 region, combined with dendritic spine reconstruction of CA1 pyramidal neurons to detect morphological and functional synaptic alterations induced by 27-OH high levels. Our results show that elevated 27-OH levels lead to enhanced LTP in the Schaffer collateral-CA1 synapses. This increase is correlated with abnormally large dendritic spines in the stratum radiatum. Using immunohistochemistry for synaptopodin (actin-binding protein involved in the recruitment of the spine apparatus), we found a significantly higher density of synaptopodin-positive puncta in CA1 in Cyp27Tg mice. We hypothesize that high 27-OH levels alter synaptic potentiation and could lead to dysfunction of fine-tuned processing of information in hippocampal circuits resulting in cognitive impairment. We suggest that these alterations could be detrimental for synaptic function and cognition later in life, representing a potential mechanism by which hypercholesterolemia could lead to alterations in memory function in neurodegenerative diseases.

scholarly journals Integration, coincidence detection and resonance in networks of spiking neurons expressing Gamma oscillations and asynchronous states

2021 ◽  
Vol 17 (9) ◽  
pp. e1009416
Author(s):  
Eduarda Susin ◽  
Alain Destexhe
Keyword(s):  
Cerebral Cortex ◽  
Pyramidal Neurons ◽  
Network Models ◽  
Cell Types ◽  
Gamma Oscillations ◽  
Coincidence Detection ◽  
Biophysical Models ◽  
Firing Mode ◽  
Different Cell Types ◽  
External Stimuli

Gamma oscillations are widely seen in the awake and sleeping cerebral cortex, but the exact role of these oscillations is still debated. Here, we used biophysical models to examine how Gamma oscillations may participate to the processing of afferent stimuli. We constructed conductance-based network models of Gamma oscillations, based on different cell types found in cerebral cortex. The models were adjusted to extracellular unit recordings in humans, where Gamma oscillations always coexist with the asynchronous firing mode. We considered three different mechanisms to generate Gamma, first a mechanism based on the interaction between pyramidal neurons and interneurons (PING), second a mechanism in which Gamma is generated by interneuron networks (ING) and third, a mechanism which relies on Gamma oscillations generated by pacemaker chattering neurons (CHING). We find that all three mechanisms generate features consistent with human recordings, but that the ING mechanism is most consistent with the firing rate change inside Gamma bursts seen in the human data. We next evaluated the responsiveness and resonant properties of these networks, contrasting Gamma oscillations with the asynchronous mode. We find that for both slowly-varying stimuli and precisely-timed stimuli, the responsiveness is generally lower during Gamma compared to asynchronous states, while resonant properties are similar around the Gamma band. We could not find conditions where Gamma oscillations were more responsive. We therefore predict that asynchronous states provide the highest responsiveness to external stimuli, while Gamma oscillations tend to overall diminish responsiveness.

Threshold Conditions for Synaptically Evoking Ca2+Waves in Hippocampal Pyramidal Neurons

2002 ◽  
Vol 87 (4) ◽  
pp. 1799-1804 ◽  
Author(s):  
Suya Zhou ◽  
William N. Ross
Keyword(s):  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Threshold Current ◽  
Lateral Position ◽  
Stratum Radiatum ◽  
Tetanic Stimulation ◽  
Hippocampal Pyramidal Neurons ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Stimulus Current

Regenerative Ca2+ release from inositol 1,4,5-trisphosphate (IP3)-sensitive intracellular stores in the form of Ca2+ waves leads to large-amplitude [Ca2+]iincreases in the apical dendrites of hippocampal CA1 pyramidal neurons. Release is generated following synaptic activation of group I metabotropic glutamate (mGlu) receptors. We systematically examined the conditions for evoking these waves in transverse slices from 2- to 3-wk-old rats. Using a sharpened asymmetrical bipolar tungsten stimulating electrode placed in the stratum radiatum, we varied the lateral position of the electrode, the number of stimulating pulses, the train frequency, and stimulus current. Several trends were clear. Increasing the frequency of stimulation from 20 to 100 Hz, keeping the total number of pulses constant, lowered the required stimulus current. Stimulation at frequencies below 20 Hz made it difficult to evoke release. Increasing the number of stimulation pulses, keeping the frequency constant, lowered the threshold current. A minimum of five pulses at 100 Hz was required to evoke release reliably, but several examples of success with three pulses were recorded. Theta-burst stimulation was as effective as tetanic stimulation. Placing the point of the stimulation electrode closer to the pyramidal neuron made it easier to evoke release, although stimulation at a lateral distance of 500 μm with unsharpened electrodes was sometimes successful. The simplest explanation for these results is that a bolus of IP3 must be produced quickly in a restricted region of the dendrites to generate Ca2+ waves. The conditions necessary for evoking regenerative Ca2+ release have many parallels (and some differences) with the conditions required to evoke long-term potentiation in these cells following tetanic stimulation.

scholarly journals Astrocyte-Selective Volume Increase in Elevated Extracellular Potassium Conditions Is Mediated by the Na+/K+ ATPase and Occurs Independently of Aquaporin 4

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142096715
Author(s):  
Erin Walch ◽  
Thomas R. Murphy ◽  
Nicholas Cuvelier ◽  
Murad Aldoghmi ◽  
Cristine Morozova ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Water Movement ◽  
Barium Chloride ◽  
Neuronal Firing ◽  
Aquaporin 4 ◽  
Stratum Radiatum ◽  
Cell Swelling ◽  
Extracellular Potassium ◽  
Atpase Inhibitor ◽  
Extracellular Potassium Concentration

Astrocytes and neurons have been shown to swell across a variety of different conditions, including increases in extracellular potassium concentration (^[K+]o). The mechanisms involved in the coupling of K+ influx to water movement into cells leading to cell swelling are not well understood and remain controversial. Here, we set out to determine the effects of ^[K+]o on rapid volume responses of hippocampal CA1 pyramidal neurons and stratum radiatum astrocytes using real-time confocal volume imaging. First, we found that elevating [K+]o within a physiological range (to 6.5 mM and 10.5 mM from a baseline of 2.5 mM), and even up to pathological levels (26 mM), produced dose-dependent increases in astrocyte volume, with absolutely no effect on neuronal volume. In the absence of compensating for addition of KCl by removal of an equal amount of NaCl, neurons actually shrank in ^[K+]o, while astrocytes continued to exhibit rapid volume increases. Astrocyte swelling in ^[K+]o was not dependent on neuronal firing, aquaporin 4, the inwardly rectifying potassium channel Kir 4.1, the sodium bicarbonate cotransporter NBCe1, , or the electroneutral cotransporter, sodium-potassium-chloride cotransporter type 1 (NKCC1), but was significantly attenuated in 1 mM barium chloride (BaCl2) and by the Na+/K+ ATPase inhibitor ouabain. Effects of 1 mM BaCl2 and ouabain applied together were not additive and, together with reports that BaCl2 can inhibit the NKA at high concentrations, suggests a prominent role for the astrocyte NKA in rapid astrocyte volume increases occurring in ^[K+]o. These findings carry important implications for understanding mechanisms of cellular edema, regulation of the brain extracellular space, and brain tissue excitability.

Erratum to ‘Effects of Short-Term Random Noise Electrical Stimulation on Dissociated Pyramidal Neurons from the Cerebral Cortex’ [Neuroscience 404C (2019) 371–386]

Neuroscience ◽  
2019 ◽  
Vol 417 ◽  
pp. 107-108
Author(s):  
Leonardo Remedios ◽  
Pedro Mabil ◽  
Jorge Flores-Hernández ◽  
Oswaldo Torres-Ramírez ◽  
Nayeli Huidobro ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Electrical Stimulation ◽  
Pyramidal Neurons ◽  
Random Noise ◽  
Short Term
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