The Role of Hippocampal Neurogenesis in ANT-DBS for LiCl-Pilocarpine-Induced Epileptic Rats

Tang, Weiting; He, Xinghui; Feng, Li; Liu, Dingyang; Yang, Zhiyong; Zhang, Junmei; Xiao, Bo; Yang, Zhiquan

doi:10.1159/000509314

Cited by 5 publications

(5 citation statements)

References 45 publications

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“…Moreover, allosteric modulators of GABA A receptor such as benzodiazepines could progressively lose their potency as synaptic GABA A receptors internalize. Such therapeutic limitations highlight the need for improved antiseizure medications to treat pharmaco-resistant seizure [ 23 – 25 ].…”

Section: Discussionmentioning

confidence: 99%

“…A rat model of SE was induced by injecting LiCl-pilocarpine and was evaluated as described previously [ 15 , 16 , 25 ]. Briefly, rats were randomized into six groups (18 per group) as follows: naïve control (BLK), SE seizure (SE+saline), 50 mg/kg propofol (SE+PPF), 10 mg/kg diazepam (SE+DZP), 10 mg/kg scopolamine (SE+SCOP), and 2 mg/kg of the nonspecific NMDA receptor antagonist dizocilpine (SE+MK801).…”

Section: Methodsmentioning

confidence: 99%

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Propofol mitigates brain injury and oxidative stress, and enhances GABAA receptor ?1 subunit expression in a rat model of lithium chloride-pilocarpine induced status epilepticus

Li,

Liu,

et al. 2023

Turkish Journal of Medical Sciences

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Background/aim Propofol is a positive allosteric modulator of GABAA receptor (GABAAR) and has potent antioxidant activity. The aim of this study was to investigate the effect of propofol on damage to the cerebral cortex and hippocampus in a lithium chloride (LiCl)-pilocarpine animal model of status epilepticus (SE). Materials and methods Adult male Sprague Dawley rats were injected with LiCl-pilocarpine to induce SE. They were then randomized and injected 30 min later with vehicle saline (SE+saline), propofol (SE+PPF, 50 mg/kg), Diazepam (SE+DZP, 10 mg/kg), Scopolamine (SE+SCOP, 10 mg/kg), or MK-801 (SE+MK-801, 2 mg/kg). Another group of rats received saline only and served as the naïve control (BLK). The levels of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) in the serum, cortex and hippocampus were analyzed 2 and 24 h posttreatment. The degree of tissue damage in the cortex and hippocampus of individual rats was assessed 24 h posttreatment, together with expression of the GABAAR α1 subunit. Results The propofol group showed reduced levels of tissue damage in the cerebral cortex and hippocampus, decreased levels of MDA, and increased levels of GSH compared to the SE+saline group. No changes in SOD level were observed in serum and tissue samples from the cortex and hippocampus of SE+saline rats. Immunohistochemistry and Western blot assays showed that propofol treatment significantly increased the expression of GABA A R α1 subunit in the cortical and hippocampal tissues of SE rats. Conclusion Propofol treatment protected against SE-induced tissue injury in the cortex and hippocampus of rats. This was due at least in part to its antioxidant activity and to its induction of GABAAR α1 subunit expression in the brain.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Propofol mitigates brain injury and oxidative stress, and enhances GABAA receptor ?1 subunit expression in a rat model of lithium chloride-pilocarpine induced status epilepticus

Li,

Liu,

et al. 2023

Turkish Journal of Medical Sciences

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“…Several factors, including statistical methods and interesting brain regions in the analysis, might have contributed to this discrepancy. In addition, the application of a single modal MRI or histopathological approach in the previous studies (Christiaen et al, 2019; Gill et al, 2017; Tang et al, 2021; Zhu et al, 2018) could not identify multi‐scale hippocampal alterations induced by ANT‐DBS in the TLE model. Therefore, a longitudinal study combining multimodal MRI with histopathology is necessary to investigate the macro‐ and micro‐effects of long‐term ANT‐DBS in a TLE model.…”

Section: Introductionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Long‐term ANT‐DBS effects in pilocarpine‐induced epileptic rats: A combined 9.4T MRI and histological study

Xie

Deng

et al. 2023

J of Neuroscience Research

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Deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) appears to be effective against seizures in animals and humans however, its therapeutic mechanisms remain elusive. This study aimed to combine 9.4T multimodal magnetic resonance imaging (MRI) with histology to investigate the longitudinal effects of long-term ANT-DBS in pilocarpine-induced epileptic rats. Status epilepsy (SE) was induced by

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“…It is divided into two distinct areas, core (NAcc) and shell (NAcSh) [7,8]. In addition to the extended amygdala, lateral hypothalamic area, and ventral tegmental area(VTA), the NAc projects to other related regions [9,10]. TLE has recently been shown to be mediated by the NAc, particularly the NAcSh [6,11].…”

Section: Introductionmentioning

confidence: 99%

Nucleus accumbens shell lesions alleviate symptoms in kainic acid-induced epileptic rats

Xue

2023

Preprint

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Epilepsy is a recurrent neurological disease caused by hypersynchronous firing of neurons in the brain. Neuronal apoptosis, microgliosis, or astrogliosis in hippocampus are considered to be important features of temporal lobe epilepsy. As an important part of the ventral striatum, the nucleus accumbens is closely connected to the hippocampus. As the findings of the reviewed articles indicated, the nuleus accumbens is divided into the shell and the core. The nucleus accumbens shell is a relevant brain region to process reward-related and motivated behaviours, emotional process and social information. Nucleus accumbens shell has a good application effect in the field of drug addiction and mania. Our previous studies have shown that the nucleus accumbens shows abnormal excitation after seizures. In our previous experiments, the number of seizures decreased when this excitation was disrupted. However, the mechanisms of action of Nucleus accumbens shell lesions remain unclear. In this paper, we explored the hippocampal changes inhibited by nucleus accumbens lesions on the basis of the kainic acid animal model of epilepsy. We explored the anti-epileptic effect and mechanism of action of electrical lesions in nucleus accumbens, and found that the mechanism may be to reduce the toxic effects caused by the proliferation of astrocytes and microglia in the hippocampus. It can also inhibit the reduction of neurons and thus play a role in controlling seizures. These results suggest that the nucleus accumbens plays an important role in inhibiting seizures.

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The Role of Hippocampal Neurogenesis in ANT-DBS for LiCl-Pilocarpine-Induced Epileptic Rats

Cited by 5 publications

References 45 publications

Propofol mitigates brain injury and oxidative stress, and enhances GABAA receptor ?1 subunit expression in a rat model of lithium chloride-pilocarpine induced status epilepticus

Propofol mitigates brain injury and oxidative stress, and enhances GABAA receptor ?1 subunit expression in a rat model of lithium chloride-pilocarpine induced status epilepticus

Long‐term ANT‐DBS effects in pilocarpine‐induced epileptic rats: A combined 9.4T MRI and histological study

Nucleus accumbens shell lesions alleviate symptoms in kainic acid-induced epileptic rats

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