Involvement of monocarboxylate transporters in the cross-tolerance between epilepsy and cerebral infarction: A promising choice towards new treatments

Gao, Chen; Li, Zhi-Yun; Bai, Jie; Wang, Ruijuan; Gao, Lingyi

doi:10.1016/j.neulet.2019.134305

Cited by 5 publications

(3 citation statements)

References 28 publications

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“…These PC-treated astrocytes are more efficient, protecting neurons upon OGD possibly due in part to higher lactate release [ 178 ]. In line with this result, cross-tolerance mechanisms like epileptic PC seem to strongly depend on lactate transport into the mitochondria [ 179 ]. Other studies suggest that exosomes released by PC-treated astrocytes, which are then engulfed by neurons, could contain neuroprotective molecules such as miR-92b-3p [ 180 ].…”

Section: Astrocytesmentioning

confidence: 79%

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury

Hernández

Villa-González

Martín

et al. 2021

Cells

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Ischemic stroke is the second cause of mortality and the first cause of long-term disability constituting a serious socioeconomic burden worldwide. Approved treatments include thrombectomy and rtPA intravenous administration, which, despite their efficacy in some cases, are not suitable for a great proportion of patients. Glial cell-related therapies are progressively overcoming inefficient neuron-centered approaches in the preclinical phase. Exploiting the ability of microglia to naturally switch between detrimental and protective phenotypes represents a promising therapeutic treatment, in a similar way to what happens with astrocytes. However, the duality present in many of the roles of these cells upon ischemia poses a notorious difficulty in disentangling the precise pathways to target. Still, promoting M2/A2 microglia/astrocyte protective phenotypes and inhibiting M1/A1 neurotoxic profiles is globally rendering promising results in different in vivo models of stroke. On the other hand, described oligodendrogenesis after brain ischemia seems to be strictly beneficial, although these cells are the less studied players in the stroke paradigm and negative effects could be described for oligodendrocytes in the next years. Here, we review recent advances in understanding the precise role of mentioned glial cell types in the main pathological events of ischemic stroke, including inflammation, blood brain barrier integrity, excitotoxicity, reactive oxygen species management, metabolic support, and neurogenesis, among others, with a special attention to tested therapeutic approaches.

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Section: Astrocytesmentioning

confidence: 79%

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury

Hernández

Villa-González

Martín

et al. 2021

Cells

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“…Metabolic therapies focus on reducing the amount of energy available to neurons typically by inhibiting metabolic pathways 41 , 42 or modulating metabolite transport. 43 This approach might be challenged by the observation that 2-deoxy-D-glucose could facilitates seizure-like activity via an excitatory mechanism dependent on oxidative phosphorylation impairment. 44 The ketogenic diet is the prime example that modifying metabolism is an effective way of epilepsy management.…”

Section: Discussionmentioning

confidence: 99%

The lactate receptor HCAR1: A key modulator of epileptic seizure activity

Alessandri,

Osorio-Forero,

Lüthi

et al. 2024

iScience

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“…Then, the thionine-stained brain tissues were subjected to HG and ND assessments. HG was divided into four grades and assigned as follows 57 , 58 : grade 0, no neuron death; grade I, scattered single neuron death; grade II, massive neuron death; and grade III, almost complete neuron death. ND was determined by counting the number of surviving pyramidal neurons with intact cell membranes, full nuclei, and clear nucleoli within a 250-μm linear length of the hippocampal CA1 subfield.…”

Section: Methodsmentioning

confidence: 99%

A monocarboxylate transporter-dependent mechanism confers resistance to exercise-induced fatigue in a high-altitude hypoxic environment

Gao

Yang

et al. 2023

Sci Rep

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The body is more prone to fatigue in a high-altitude hypoxic environment, in which fatigue occurs in both peripheral muscles and the central nervous system (CNS). The key factor determining the latter is the imbalance in brain energy metabolism. During strenuous exercise, lactate released from astrocytes is taken up by neurons via monocarboxylate transporters (MCTs) as a substrate for energy metabolism. The present study investigated the correlations among the adaptability to exercise-induced fatigue, brain lactate metabolism and neuronal hypoxia injury in a high-altitude hypoxic environment. Rats were subjected to exhaustive incremental load treadmill exercise under either normal pressure and normoxic conditions or simulated high-altitude, low-pressure and hypoxic conditions, with subsequent evaluation of the average exhaustive time as well as the expression of MCT2 and MCT4 in the cerebral motor cortex, the average neuronal density in the hippocampus, and the brain lactate content. The results illustrate that the average exhaustive time, neuronal density, MCT expression and brain lactate content were positively correlated with the altitude acclimatization time. These findings demonstrate that an MCT-dependent mechanism is involved in the adaptability of the body to central fatigue and provide a potential basis for medical intervention for exercise-induced fatigue in a high-altitude hypoxic environment.

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Involvement of monocarboxylate transporters in the cross-tolerance between epilepsy and cerebral infarction: A promising choice towards new treatments

Cited by 5 publications

References 28 publications

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury

The lactate receptor HCAR1: A key modulator of epileptic seizure activity

A monocarboxylate transporter-dependent mechanism confers resistance to exercise-induced fatigue in a high-altitude hypoxic environment

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