Electrophysiology of cerebral ischemia and reperfusion: First evidence for the role of synapse in ischemic tolerance

Haghani, Masoud; Keshavarz, Somaye; Nazari, Maryam; Rafati, Ali

doi:10.1002/syn.21910

Cited by 14 publications

(7 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effects of PRP administration on short-term plasticity in bile duct ligated rats Short-term synaptic plasticity was evaluated by the paired-pulse ratio pre-and post-HFS (Haghani et al, 2016). The sample traces of the paired-pulse ratio at ISI of 25 ms are shown in Figure 5a.…”

Section: 32mentioning

confidence: 99%

Effects of platelet‐rich plasma on the memory impairment, apoptosis, and hippocampal synaptic plasticity in a rat model of hepatic encephalopathy

et al. 2021

Self Cite

View full text Add to dashboard Cite

Objectives:In the present study, we aimed to determine whether intraperitoneal injection of platelet-rich plasma (PRP) could have a neuroprotective effect on learning, memory, and synaptic plasticity impairment as well as hippocampal apoptosis in rats with hepatic encephalopathy induced by bile duct ligated (BDL). Methods:The rats were divided into four groups: the control, sham, BDL+ V (vehicle), and BDL+ PRP. The BDL rats were treated with PRP immediately after the surgery, and the injection was done every 3 days for 30 days. The passive avoidance and Morris water maze tests were used for the evaluation of learning and memory. The long-term potentiation (LTP), basal-synaptic transmission, and paired-pulse ratio, as an index for measurement of neurotransmitter release probability, were evaluated by fieldpotential recording. After taking a blood sample for assessment of the liver enzymes, the animals were sacrificed and their hippocampus was removed for evaluation of cleaved caspase-3 by Western blot.Results: Serological assessment of the liver function showed that BDL severely impaired the liver function. Also, PRP treatment could partially improve the liver dysfunction along with recovery in fear memory and spatial learning memory performance, LTP, basal-synaptic transmission, and neurotransmitter release probability.PRP-treated rats also showed a significant reduction in neuronal apoptosis in the CA1 area. Conclusions:The results of this study suggest that PRP improves cognitive performance and synaptic plasticity in BDL rats via direct neuroprotective property and/or indirectly by improvement of hepatic dysfunction.

show abstract

Section: 32mentioning

confidence: 99%

Effects of platelet‐rich plasma on the memory impairment, apoptosis, and hippocampal synaptic plasticity in a rat model of hepatic encephalopathy

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…In addition to hypoxia‐induced depolarization, hypoxia induces pathologic potentiation of excitatory synaptic transmission. When cells fall into short‐term hypoxia and then oxygen is given again, the EPSPs become larger than normal and may cause reperfusion injury (Gajendiran, Ling, Pang, & Xu, ; Gao, Pulsinelli, & Xu, ; Haghani, Keshavarz, Nazari, & Rafati, ). We investigated the effect of sevoflurane pretreatment on the oxygen and glucose deprivation‐induced EPSP potentiation.…”

Section: Resultsmentioning

confidence: 99%

Volatile anesthetic sevoflurane pretreatment alleviates hypoxia‐induced potentiation of excitatory inputs to striatal medium spiny neurons of mice

Fukuda

Ando

Sugasawa

et al. 2019

Eur J of Neuroscience

View full text Add to dashboard Cite

Sevoflurane, a commonly used anesthetic in surgery, has drawn attention because of its preconditioning effects in hypoxic conditions. To investigate the preconditioning effects in the striatum, a common site for ischemic stroke, we collected whole‐cell current‐clamp recordings from striatal medium spiny neurons. In our in vitro brain slice experiments, deprivation of oxygen and glucose depolarized the striatal neurons to subthreshold potentials, and the pre‐administration of sevoflurane (4%, 15 min) prolonged the time to depolarization. Furthermore, transient hypoxia induced the potentiation of excitatory postsynaptic potentials, which play a part in post‐ischemic excitotoxicity. Glibenclamide, a KATP channel inhibitor, reversed the prolonged time to depolarization and the prevention of the pathological potentiation of excitatory responses, indicating that the short exposure to sevoflurane likely participates in neuroprotection against hypoxia via activation of KATP channels. A monocarboxylate transporter blocker, 4‐CIN, also depolarized striatal neurons. Interestingly, the blockade of monocarboxylate transporters that supply lactate to neurons caused the pathological potentiation, even in the presence of enough oxygen and glucose. In this case, sevoflurane could not prevent the pathological potentiation, suggesting the involvement of monocarboxylate transporters in the sevoflurane‐mediated effects. These results indicate that sevoflurane protects striatal neurons from hypoxic damage and alleviates the pathological potentiation. Under these conditions, sevoflurane may become an effective intervention for patients undergoing surgery.

show abstract

“…Moreover, the LTP magnitude remained at a relatively low level 4 months after permanent MCAO (57). IPreC can dramatically increase the neurotransmitter content in presynaptic neurons to promote basal synaptic transmission without obvious adverse effects on the LTP induction (205).…”

Section: Electrophysiologymentioning

confidence: 95%

“…For ethical reasons, it is not allowed to repeatedly block the cerebral arteries to mediate neuroprotection through ischemic preconditioning in humans; cross-preconditioning, induced by stressors or stimuli other than ischemia, such as hyperoxia/hypoxia, hypothermia or hyperthermia, chemical/pharmacological pretreatment, cortical spreading depression, electroacupuncture, excise, et al ( 29 , 38 , 58 , 105 , 205 ), has gradually become a new research hot spot hoping to develop a new IPreC strategy in humans. Interestingly, research suggests that many stresses or stimuli seem to mediate protective tolerance through a common signaling pathway ( 105 ).…”

Section: Understanding Cerebral Ischemic Preconditioningmentioning

confidence: 99%

Review Cerebral Ischemic Tolerance and Preconditioning: Methods, Mechanisms, Clinical Applications, and Challenges

et al. 2020

View full text Add to dashboard Cite

Stroke is one of the leading causes of morbidity and mortality worldwide, and it is increasing in prevalence. The limited therapeutic window and potential severe side effects prevent the widespread clinical application of the venous injection of thrombolytic tissue plasminogen activator and thrombectomy, which are regarded as the only approved treatments for acute ischemic stroke. Triggered by various types of mild stressors or stimuli, ischemic preconditioning (IPreC) induces adaptive endogenous tolerance to ischemia/reperfusion (I/R) injury by activating a multitude cascade of biomolecules, for example, proteins, enzymes, receptors, transcription factors, and others, which eventually lead to transcriptional regulation and epigenetic and genomic reprogramming. During the past 30 years, IPreC has been widely studied to confirm its neuroprotection against subsequent I/R injury, mainly including local ischemic preconditioning (LIPreC), remote ischemic preconditioning (RIPreC), and cross preconditioning. Although LIPreC has a strong neuroprotective effect, the clinical application of IPreC for subsequent cerebral ischemia is difficult. There are two main reasons for the above result: Cerebral ischemia is unpredictable, and LIPreC is also capable of inducing unexpected injury with only minor differences to durations or intensity. RIPreC and pharmacological preconditioning, an easy-to-use and non-invasive therapy, can be performed in a variety of clinical settings and appear to be more suitable for the clinical management of ischemic stroke. Hoping to advance our understanding of IPreC, this review mainly focuses on recent advances in IPreC in stroke management, its challenges, and the potential study directions.

show abstract

Electrophysiology of cerebral ischemia and reperfusion: First evidence for the role of synapse in ischemic tolerance

Cited by 14 publications

References 33 publications

Effects of platelet‐rich plasma on the memory impairment, apoptosis, and hippocampal synaptic plasticity in a rat model of hepatic encephalopathy

Effects of platelet‐rich plasma on the memory impairment, apoptosis, and hippocampal synaptic plasticity in a rat model of hepatic encephalopathy

Volatile anesthetic sevoflurane pretreatment alleviates hypoxia‐induced potentiation of excitatory inputs to striatal medium spiny neurons of mice

Review Cerebral Ischemic Tolerance and Preconditioning: Methods, Mechanisms, Clinical Applications, and Challenges

Contact Info

Product

Resources

About