Spontaneous, transient adenosine release is not enhanced in the CA1 region of hippocampus during severe ischemia models

Ganesana, Mallikarjunarao; Venton, B. Jill

doi:10.1111/jnc.15496

Cited by 7 publications

(9 citation statements)

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“…The recovery ability of VD rats is mainly associated to the operation method and the postoperative rest time. 4VO is a modeling method that has a greater effect on rat trauma and death, and the recovery difficulty of this method should be greater than that of 2VO, EO, and MCAO (Ganesana and Venton, 2021 ). Tuo et al ( 2021 ) found that 8-week to 3-month resting after modeling, cerebral blood flow in rats could restore to normal.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of acupuncture in animal models of vascular dementia: A systematic review and network meta-analysis

Shi

Zhang

et al. 2022

Front. Aging Neurosci.

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Background and purposeAcupuncture is widely used in clinical practice for the treatment of vascular diseases. However, the protocol, efficacy, and mechanism of acupuncture in animal models of vascular dementia are still controversial. Based on the above problems, we initiated this comprehensive study.MethodsTo analyze the literatures included in this study, 4 databases were searched and the SYRCLE's Risk of bias tool was employed. To perform the subgroup analysis of different acupuncture methods and the Review Manager 5.3 was applied. Meanwhile, the pairwise and network meta-analysis were conducted using Addis 1.16.8. The outcomes included escape latency, number of crossings, time spent in the target quadrant, and swimming speed.ResultsForty-two studies with a total of 1,486 animals were included in this meta-analysis. According to the results from subgroup analysis, GV20 + ST36 (Baihui + bilateral Zusanli) combined with 14-day manual acupuncture can obtain best improvement of the rats cognitive function among all acupuncture regimens (MD: −23.41; 95%CI: −26.66, −20.15; I2 = 0%; P < 0.001). The heterogeneity of other acupuncture treatments was significantly higher than that of GV20 + ST36, because the treatment courses were not uniform. Pair-wise and network comparisons are highly consistent. The major results of the network meta-analysis were as follows, In comparison to the impaired group, the acupuncture group showed significantly reduced escape latency (MD: −25.87; 95%CI: −30.75, −21.12), increased number of original platform crossings (MD: 2.63; 95%CI: 1.94, 3.34) and time spent in the target quadrant (MD: 7.88; 95%CI: 4.25, 11.44). The overall results of the network meta-analysis are as follows: the normal and sham-operated groups performed the best, followed by medicine and acupuncture, while no effect was found in the impaired group treated with non-acupoint and palliative.ConclusionsAcupuncture significantly improves cognitive function in rats with vascular dementia. Compared to other acupuncture plans, (GV20 + ST36, MA) and 14 -day manual acupuncture can be used to obtain better results. The main mechanism of acupuncture in the treatment of vascular dementia is reduced oxidative stress, neuronal inflammation, and apoptosis, as well as the increased synaptic plasticity and neurotransmitters.Systematic review registrationhttps://inplasy.com/inplasy-2021-11-0036/, identifier: INPLASY2021110036.

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Section: Discussionmentioning

confidence: 99%

Efficacy of acupuncture in animal models of vascular dementia: A systematic review and network meta-analysis

Shi

Zhang

et al. 2022

Front. Aging Neurosci.

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“…In this issue of Journal of Neurochemistry, Ganesana and Venton (2021) report on spontaneous adenosine release as a potential mechanism of brain tissue defense in ischemic conditions. Adenosine, an endogenous neuromodulator and a homeostatic modulator controlling many brain functions, exerts its effects through its multiple receptors.…”

Section: Adenos Ine Rele a S E A S A P Otentially Neuroprotec Tive Me...mentioning

confidence: 99%

“…In their study, Ganesana and Venton (2021) selected the CA1 area of the hippocampus, an area most susceptible to ischemia, to explore rapid changes in spontaneous, transient adenosine. To associate changes in adenosine release with ischemia severity, they performed a comparative study of transient adenosine event frequency and adenosine concentration in three stroke models with different ischemia intensity.…”

Section: B R Ain Ischemia Fail S To Induce Adenos Ine Rele a S E In H...mentioning

confidence: 99%

“…However, the role of potential failure of neuroprotective mechanisms as a likely critical cause for selective hippocampal vulnerability generally remains obscure. In this study by Ganesana and Venton (2021), the most vulnerable hippocampal area, the CA1 subfield, was selected to identify whether adenosine‐mediated neuroprotective mechanisms were activated by ischemia, as occurs in some other brain regions (Ganesana & Venton, 2018). This is one of the first convincing studies to clearly show that upon ischemia, the hippocampal CA1 region fails to switch on an adenosine‐mediated neuroprotective mechanism thus being unable to combat detrimental consequences of insufficient blood flow.…”

Section: Failure Of Ischemia‐induced Adenosine Release May Beinvolved...mentioning

confidence: 99%

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Does the inability of CA1 area to respond to ischemia with early rapid adenosine release contribute to hippocampal vulnerability?

Gulyaeva

2021

Journal of Neurochemistry

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This Editorial highlights a remarkable study in the current issue of the Journal of Neurochemistry in which Ganesana & Venton (2021) report new data showing that brain ischemia does not elicit transient adenosine release in the CA1 hippocampal area. Using fast‐scan cyclic voltammetry at a carbon‐fiber microelectrode implanted in the CA1 subfield of the hippocampus, it was shown that none of three different ischemia/reperfusion models could increase spontaneous, transient adenosine release, and more severe models even suppressed this presumably neuroprotective release. Since the authors have previously shown that in the caudate putamen, ischemia increased the frequency of spontaneous adenosine release (Ganesana & Venton, 2018), the new data may disclose a mechanism underlying important regional differences in rapid neuroprotective adenosine signaling. The phenomenon of selective susceptibility of the hippocampus to ischemia/hypoxia is well‐documented, and the reported failure of its CA1 area to respond to ischemia by rapid adenosine release may be indicative of an insufficiency of this neuroprotective mechanism contributing to hippocampal vulnerability.

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“…Rapid adenosine acts as a neuromodulator, signaling through receptors to modulate blood flow, the sleep–awake cycle, pain, and memory. − Adenosine receptors are located both presynaptically and postsynaptically and adenosine often has an overall inhibitory effect, acting at A 1 receptors to dampen dopamine, glutamate, and GABA neurotransmission. − The hippocampus CA1 region is an important region for adenosine neuromodulation, as adenosine inhibits excitatory synaptic transmission during ischemia. There is a high frequency and concentration of adenosine transient events in the hippocampus CA1 region, and the CA1 may be susceptible to ischemic damage because adenosine transient events do not increase during ischemia . Exogenous adenosine protects hippocampal neurons from death during cerebral ischemic injury, but the endogenous pool of adenosine is depletable in the CA1 …”

Section: Introductionmentioning

confidence: 99%

Dual-Channel Electrochemical Measurements Reveal Rapid Adenosine is Localized in Brain Slices

Chang

Venton

2022

ACS Chem. Neurosci.

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Rapid adenosine signaling has been detected spontaneously or after mechanical stimulation in the brain, providing rapid neuromodulation in a local area. To measure rapid adenosine signaling, a single carbon-fiber microelectrode has traditionally been used, which limits spatial resolution and an understanding of regional coordination. In this study, we utilized dual-channel fast-scan cyclic voltammetry to measure the spontaneous or mechanically stimulated adenosine release at two electrodes placed at different spacings in hippocampal CA1 mouse brain slices. For mechanically stimulated adenosine release, adenosine can be detected up to 150 μm away from where it was stimulated, although the signal is smaller and delayed. While spontaneous adenosine transients were detected at both electrodes, only 10 percent of the events were detected concurrently, and that number was similar at 50 and 200 μm electrode spacings. Thus, most adenosine transients were not caused by the widespread coordination of release. There was no evidence of diffusion of spontaneous transients to a second electrode 50–200 μm away. This study shows that spontaneous adenosine events are very localized and thus provide only local neuromodulation. Injury, such as mechanical stimulation, allows adenosine to diffuse farther, but the neuroprotective effects are still regional. These results provide a better understanding of the spatial and temporal profiles of adenosine available to act at receptors, which is crucial for future studies that design neuroprotective treatments based on rapid adenosine signaling.

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Spontaneous, transient adenosine release is not enhanced in the CA1 region of hippocampus during severe ischemia models

Cited by 7 publications

References 68 publications

Efficacy of acupuncture in animal models of vascular dementia: A systematic review and network meta-analysis

Efficacy of acupuncture in animal models of vascular dementia: A systematic review and network meta-analysis

Does the inability of CA1 area to respond to ischemia with early rapid adenosine release contribute to hippocampal vulnerability?

Dual-Channel Electrochemical Measurements Reveal Rapid Adenosine is Localized in Brain Slices

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