scholarly journals Estradiol after Cardiac Arrest and Cardiopulmonary Resuscitation is Neuroprotective and Mediated through Estrogen Receptor-β

2008 ◽  
Vol 29 (2) ◽  
pp. 277-286 ◽  
Author(s):  
Ruediger R Noppens ◽  
Julia Kofler ◽  
Marjorie R Grafe ◽  
Patricia D Hurn ◽  
Richard J Traystman
Keyword(s):  
Estrogen Receptor ◽  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Neuronal Injury ◽  
Loading Dose ◽  
Neuroprotective Effects ◽  
Hippocampal Ca1 ◽  
Term Administration ◽  
Hippocampal Ca1 Field

We evaluated long-term administration of estrogen after cardiac arrest and cardiopulmonary resuscitation (CA/CPR) on neurohistopathological and behavioral outcome. We also examined the effect of estrogen receptor (ER) stimulation using ER-α agonist propyl pyrazole triol (PPT) and ER-θ agonist diarylpropionitrile (DPN) on neuronal survival after CA/CPR to determine whether possible neuroprotective effects of estrogen are ER-mediated. Male C57Bl/6 mice underwent 10 mins of CA/CPR and 3-day survival. In protocol 1, intravenous injection of vehicle (NaCl 0.9%) and 0.5 or 2.5 µg 17β-estradiol (E2 loading dose) was performed followed by subcutaneous implants containing vehicle (oil) or E2 (12.6 µg), according to a treatment group. In experimental protocol 2, mice were injected (intravenously) with the ER-α agonist PPT or ER-θ agonist DPN followed by Alzet pump implants (subcutaneously) containing PPT (200 µg) or DPN (800 µg). Long-term E2 administration reduced neuronal injury in the striatum after administration of either loading dose (41%±19%, 35%±26% of injured neurons), as compared with vehicle (68%±7%, P< 0.01), with no effect in the hippocampal CA1 field. In protocol 2, treatment with ER-θ agonist DPN reduced neuronal injury in the striatum (51%±13% injured neurons) as compared with ER-α agonist PPT (68%±10%) and vehicle (69%±11%; P < 0.01). Estrogen receptor-θ agonist DPN reduced neuronal injury in the hippocampal CA1 field (29%±22% injured neurons) as compared with ER-α agonist PPT treatment (62%±33%; P < 0.05). Injury was not different in hippocampal CA1 between vehicle and ER-α agonist-treated animals. We conclude that long-term E2 administration after CA/CPR is neuroprotective and that this effect is most likely mediated via ER-β.

Time Course of Expression of “Early” Genes during Long-Term Posttetanic Potentiation in Rat Hippocampal CA1 Field

2009 ◽  
Vol 148 (3) ◽  
pp. 416-418 ◽  
Author(s):  
O. O. Sokolova ◽  
M. B. Shtark ◽  
P. D. Lisachev ◽  
V. O. Pustyl’nyak ◽  
I. V. Pan
Keyword(s):  
Time Course ◽  
Posttetanic Potentiation ◽  
Early Genes ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Field

scholarly journals Probiotics Alleviate the Progressive Deterioration of Motor Functions in a Mouse Model of Parkinson's Disease

2020 ◽  
Vol 10 (4) ◽  
pp. 206 ◽  
Author(s):  
Tsung-Hsun Hsieh ◽  
Chi-Wei Kuo ◽  
Kai-Hsuan Hsieh ◽  
Meng-Jyh Shieh ◽  
Chih-Wei Peng ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Coordination ◽  
Dopamine Neurons ◽  
Motor Symptoms ◽  
Neuroprotective Effects ◽  
Motor Functions ◽  
Term Administration ◽  
Nigrostriatal Dopamine Neurons

Parkinson’s disease (PD) is one of the common long-term degenerative disorders that primarily affect motor systems. Gastrointestinal (GI) symptoms are common in individuals with PD and often present before motor symptoms. It has been found that gut dysbiosis to PD pathology is related to the severity of motor and non-motor symptoms in PD. Probiotics have been reported to have the ability to improve the symptoms related to constipation in PD patients. However, the evidence from preclinical or clinical research to verify the beneficial effects of probiotics for the motor functions in PD is still limited. An experimental PD animal model could be helpful in exploring the potential therapeutic strategy using probiotics. In the current study, we examined whether daily and long-term administration of probiotics has neuroprotective effects on nigrostriatal dopamine neurons and whether it can further alleviate the motor dysfunctions in PD mice. Transgenic MitoPark PD mice were chosen for this study and the effects of daily probiotic treatment on gait, beam balance, motor coordination, and the degeneration levels of dopaminergic neurons were identified. From the results, compared with the sham treatment group, we found that the daily administration of probiotics significantly reduced the motor impairments in gait pattern, balance function, and motor coordination. Immunohistochemically, a tyrosine hydroxylase (TH)-positive cell in the substantia nigra was significantly preserved in the probiotic-treated PD mice. These results showed that long-term administration of probiotics has neuroprotective effects on dopamine neurons and further attenuates the deterioration of motor dysfunctions in MitoPark PD mice. Our data further highlighted the promising possibility of the potential use of probiotics, which could be the relevant approach for further application on human PD subjects.

Characterization of stress-induced suppression of long-term potentiation in the hippocampal CA1 field of freely moving rats

2008 ◽  
Vol 1226 ◽  
pp. 27-32 ◽  
Author(s):  
Riki Hirata ◽  
Hiroko Togashi ◽  
Machiko Matsumoto ◽  
Taku Yamaguchi ◽  
Takeshi Izumi ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Freely Moving Rats ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Field ◽  
Freely Moving

scholarly journals Long-term depression in Purkinje neurons is persistently impaired following cardiac arrest and cardiopulmonary resuscitation in mice

2016 ◽  
Vol 37 (8) ◽  
pp. 3053-3064 ◽  
Author(s):  
Nidia Quillinan ◽  
Guiying Deng ◽  
Kaori Shimizu ◽  
Ivelisse Cruz-Torres ◽  
Christian Schroeder ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Motor Coordination ◽  
Purkinje Neurons ◽  
Long Term Depression ◽  
Initial Injury ◽  
Cerebellar Purkinje Neurons ◽  
Whole Cell Recordings ◽  
Time Point

Cardiac arrest and cardiopulmonary resuscitation (CA/CPR) produce brain ischemia that results in cognitive and motor coordination impairments subsequent to injury of vulnerable populations of neurons, including cerebellar Purkinje neurons. To determine the effects of CA/CPR on plasticity in the cerebellum, we used whole cell recordings from Purkinje neurons to examine long-term depression (LTD) at parallel fiber (PF) synapses. Acute slices were prepared from adult male mice subjected to 8 min cardiac arrest at 1, 7, and 30 days after resuscitation. Concurrent stimulation of PF and climbing fibers (CFs) resulted in robust LTD of PF-evoked excitatory postsynaptic currents (EPSCs) in controls. LTD was absent in recordings obtained from mice subjected to CA/CPR, with no change in EPSC amplitude from baseline at any time point tested. AMPA and mGluR-mediated responses at the PF were not altered by CA/CPR. In contrast, CF-evoked NMDA currents were reduced following CA/CPR, which could account for the loss of LTD observed. A loss of GluN1 protein was observed following CA/CPR that was surprisingly not associated with changes in mRNA expression. These data demonstrate sustained impairments in synaptic plasticity in Purkinje neurons that survive the initial injury and which likely contribute to motor coordination impairments observed after CA/CPR.

scholarly journals Hydroxychloroquine-Induced Creatine Kinase Elevation

2020 ◽  
Vol 25 (4) ◽  
pp. 599-602
Author(s):  
Sinem Bayrakçı ◽  
Nursel Sürmelioğlu ◽  
Ezgi Özyılmaz
Keyword(s):  
Risk Factors ◽  
Intensive Care Unit ◽  
Creatine Kinase ◽  
Intensive Care ◽  
General Condition ◽  
Creatine Kinase Level ◽  
Loading Dose ◽  
Term Administration ◽  
Drug Cessation

Long-term administration of hydroxychloroquine and chloroquine leads to deposition in the tissues including muscles, nerves and retina. Here, we report a case of hydroxychloroquine induced creatine kinase elevation after loading dose. An 80-year-old man with comorbidities, presented with a dry cough, high fever, diarrhea and general condition disorder ongoing for the last 3 days. The patient was admitted to the intensive care unit. The treatment was commenced with hydroxychloroquine. On the first day of treatment, the loading dose of hydroxychloroquine was started as 400 mg q12h, and treatment was continued as 200 mg q12h from the 3rd dose. After the hydroxychloroquine loading dose, the patient’s creatine kinase level increased, and after drug cessation, the level decreased. Hydroxychloroquine-induced creatine kinase elevated may be on not only long-term use but also acute period. Clinicians should have a high suspicion for hydroxychloroquine toxicity in patients with risk factors.

Cardiopulmonary Resuscitation

2009 ◽  
Vol 20 (4) ◽  
pp. 373-383
Author(s):  
Cindy Goodrich
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Survival Rates ◽  
Sudden Cardiac Arrest ◽  
Heart Association ◽  
New Techniques ◽  
Cardiac Assist ◽  
Mechanical Devices

Dismal survival statistics associated with sudden cardiac arrest have led to the development of new strategies and mechanical devices aimed at improving the quality of cardiopulmonary resuscitation (CPR). The most recent American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care were published in 2005. Major changes included revisions to current practices related to airway and ventilation, circulation, and defibrillation management. Greater emphasis is placed on providing simple, high-quality, effective CPR. New techniques and mechanical devices have been developed to augment CPR, hopefully improving survival rates and long-term outcomes. These include active compression-decompression CPR, Lund University Cardiac Assist System, LifeBelt, AutoPulse, and the impedance threshold device. This article focuses on current strategies aimed at improving survival rates for patients with sudden cardiac arrest. New techniques and mechanical devices developed to augment cardiopulmonary resuscitation will be discussed. These strategies will most likely shape future resuscitation practices.

Fluvoxamine suppresses the long-term potentiation in the hippocampal CA1 field of anesthetized rats: an effect mediated via 5-HT1A receptors

2003 ◽  
Vol 959 (1) ◽  
pp. 165-168 ◽  
Author(s):  
Taku Kojima ◽  
Machiko Matsumoto ◽  
Hiroko Togashi ◽  
Kaori Tachibana ◽  
Osamu Kemmotsu ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Anesthetized Rats ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Field

scholarly journals Long-term effects of aripiprazole exposure on monoaminergic and glutamatergic receptor subtypes: comparison with cariprazine

CNS Spectrums ◽  
2017 ◽  
Vol 22 (6) ◽  
pp. 484-494 ◽  
Author(s):  
Yong Kee Choi ◽  
Nika Adham ◽  
Béla Kiss ◽  
István Gyertyán ◽  
Frank I. Tarazi
Keyword(s):  
Ampa Receptors ◽  
Brain Regions ◽  
Receptor Subtypes ◽  
Long Term Effects ◽  
Caudate Putamen ◽  
Chronic Effects ◽  
Hippocampal Ca1 ◽  
Term Administration ◽  
Clinical Benefits

ObjectiveThis study examined the chronic effects of aripiprazole and cariprazine on serotonin (5-HT1Aand 5-HT2A) and glutamate (NMDA and AMPA) receptor subtypes. In addition, the effects of aripiprazole on D2and D3receptors were tested and compared with previously reported cariprazine data.MethodsRats received vehicle, aripiprazole (2, 5, or 15 mg/kg), or cariprazine (0.06, 0.2, or 0.6 mg/kg) for 28 days. Receptor levels were quantified using autoradiographic assays on brain sections from the medial prefrontal cortex (MPC), dorsolateral frontal cortex (DFC), nucleus accumbens (NAc), caudate-putamen medial (CPu–M), caudate-putamen lateral (CPu–L), hippocampal CA1 (HIPP–CA1) and CA3 (HIPP–CA3) regions, and the entorhinal cortex (EC).ResultsSimilar to previous findings with cariprazine, aripiprazole upregulated D2receptor levels in various regions; D3receptor changes were less than those reported with cariprazine. All aripiprazole doses and higher cariprazine doses increased 5-HT1Areceptors in the MPC and DFC. Higher aripiprazole and all cariprazine doses increased 5-HT1Areceptors in HIPP–CA1 and HIPP–CA3. Aripiprazole decreased 5-HT2Areceptors in the MPC, DFC, HIPP–CA1, and HIPP–CA3 regions. Both compounds decreased NMDA receptors and increased AMPA receptors in select brain regions.ConclusionsLong-term administration of aripiprazole and cariprazine had similar effects on 5-HT1A, NMDA, and AMPA receptors. However, cariprazine more profoundly increased D3receptors while aripiprazole selectively reduced 5-HT2Areceptors. These results suggest that the unique actions of cariprazine on dopamine D3receptors, combined with its effects on serotonin and glutamate receptor subtypes, may confer the clinical benefits, safety, and tolerability of this novel compound in schizophrenia and bipolar mania.

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