Motor dysfunction and alterations in glutathione concentration, cholinesterase activity, and BDNF expression in substantia nigra pars compacta in rats with pedunculopontine lesion

Blanco-Lezcano, Lisette; Jimenez-Martin, Javier; Díaz-Hung, Mei-Li; Alberti‐Amador, Esteban; Wong-Guerra, Maylin; González-Fraguela, Ma. Elena; Estupiñán-Díaz, Bárbara; Sánchez, Teresa Serrano; Turner, Liliana Francis; Delgado-Ocaña, Susana; Nuñez-Figueredo, Yanier; Vega-Hurtado, Yamilé; Fernández-Jiménez, Isabel

doi:10.1016/j.neuroscience.2017.02.008

Cited by 10 publications

(21 citation statements)

References 71 publications

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“…Our group has demonstrated that 48 h after the PPN lesion, changes occur in the cellular and molecular nigral scenario, characterized by a transient increase in the gluthatione (GSH) content and the brain-derived neurotrophic factor (BDNF) mRNA expression [ 18 ]. GSH protects cells against exogenous and endogenous toxins including ROS [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

“…The surgical procedure was carried out according to that published [ 17 , 18 ]. Briefly: the rats received an anesthesia injection [chloral hydrate (420 mg/kg weight), intraperitoneal (i.p.)].…”

Section: Methodsmentioning

confidence: 99%

“…Sample collection: the animals were sacrificed by decapitation, after being anesthetized with a lethal dose of chloral hydrate (480 mg/kg i.p.). The procedure for obtaining the nigral and striatal tissue have been previously described [ 17 , 18 ]. Taking into account that, in rats, the pontine–nigral projections are fundamentally ipsilateral [ 35 ], the molecular studies were performed on the right nigrostriatal tissue, ipsilateral to the PPN lesion.…”

Section: Methodsmentioning

confidence: 99%

“…Previous studies have pointed out that considerable PPN lesions induce a Parkinsonian syndrome in monkeys [ 12 , 13 , 14 ]. Excitotoxic lesion of the PPN was documented to induce nigral neuronal death in rats [ 15 , 16 ], while unilateral PPN lesion induced oxidative stress events in both the SNpc and striatum [ 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

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Tyrosine Hydroxylase, Vesicular Monoamine Transporter and Dopamine Transporter mRNA Expression in Nigrostriatal Tissue of Rats with Pedunculopontine Neurotoxic Lesion

Blanco-Lezcano

Alberti‐Amador

Díaz-Hung

et al. 2018

Behavioral Sciences

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Background: The degeneration of the pedunculopontine nucleus (PPN) precedes the degeneration of the nigral cells in the pre-symptomatic stages of Parkinson’s disease (PD). Although the literature recognizes that a lesion of the PPN increases the vulnerability of dopaminergic cells, it is unknown if this risk is associated with the loss of capability of handling the dopaminergic function. Methods: In this paper, the effects of a unilateral neurotoxic lesion of the PPN in tyrosine hydroxylase (TH), vesicular monoamine transporter 2 (VMAT2) and dopamine transporter (DAT) mRNA expression in nigrostriatal tissue were evaluated. Three experimental groups were organized: non-treated rats, NMDA-lesioned rats and Sham-operated rats. Results: Seven days after the PPN lesion, in nigral tissue, TH mRNA expression was higher in comparison with control groups (p < 0.05); in contrast, VMAT2 mRNA expression showed a significant decrease (p < 0.01). DAT mRNA expression showed a significant decrease (p < 0.001) in the striatal tissue. Comparing nigral neuronal density of injured and control rats revealed no significant difference seven days post-PPN injury. Conclusions: Findings suggest that the PPN lesion modifies the mRNA expression of the proteins associated with dopaminergic homeostasis at nigrostriatal level. It could represent vulnerability signals for nigral dopaminergic cells and further increase the risk of degeneration of these cells.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Tyrosine Hydroxylase, Vesicular Monoamine Transporter and Dopamine Transporter mRNA Expression in Nigrostriatal Tissue of Rats with Pedunculopontine Neurotoxic Lesion

Blanco-Lezcano

Alberti‐Amador

Díaz-Hung

et al. 2018

Behavioral Sciences

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“…We found a reduction of more than 70% in the GSH content in cognitive-deficient old rats compared to the young rats. The majority of authors have reported a decreases of tripeptide in brain tissue of around 50% in previous rodent studies [ 27 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

Cellular Redox Imbalance and Neurochemical Effect in Cognitive-Deficient Old Rats

González-Fraguela

Blanco-Lezcano

Fernández

et al. 2018

Behavioral Sciences

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The purpose of the present study is to access the linkage between dysregulation of glutamatergic neurotransmission, oxidative metabolism, and serine signaling in age-related cognitive decline. In this work, we evaluated the effect of natural aging in rats on the cognitive abilities for hippocampal-dependent tasks. Oxidative metabolism indicators are glutathione (GSH), malondialdehyde (MDA) concentrations, and cytosolic phospholipase A2 (PLA2) activity. In addition, neurotransmitter amino acid (L-Glutamic acid, γ-aminobutyric acid (GABA), DL-Serine and DL-Aspartic acid) concentrations were studied in brain areas such as the frontal cortex (FC) and hippocampus (HPC). The spatial long-term memory revealed significant differences among experimental groups: the aged rats showed an increase in escape latency to the platform associated with a reduction of crossings and spent less time on the target quadrant than young rats. Glutathione levels decreased for analyzed brain areas linked with a significant increase in MDA concentrations and PLA2 activity in cognitive-deficient old rats. We found glutamate levels only increased in the HPC, whereas a reduced level of serine was found in both regions of interest in cognitive-deficient old rats. We demonstrated that age-related changes in redox metabolism contributed with alterations in synaptic signaling and cognitive impairment.

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Study on the Correlation Between NF-κB and Central Fatigue

Yang

Liu

et al. 2021

J Mol Neurosci

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In recent years, the World Health Organization (WHO) has included fatigue as a major risk factor for human life and health. The incidence rate of fatigue is high. In Europe and America, nearly 1/3 of the population is suffering from fatigue. Due to the acceleration of modern people’s life rhythm and the increase of work pressure, more and more attention has been paid to central fatigue. The activation of NF-κB is related to central fatigue, which has been paid little attention by previous studies. At the same time, previous studies have mostly focused on the immune regulation function of NF-κB, while the NF-κB pathway plays an equally important role in regulating nerve function. NF-κB can participate in the occurrence and development of central fatigue by mediating immune inflammatory response, regulating central excitability and inhibitory transmitters, regulating synaptic plasticity and regulating central nervous system (CNS) functional genes. In addition to neuroprotective effects, NF-κB also has nerve damage effects, which is also closely related to the occurrence and development of central fatigue. In this review, we focus on the relationship between NF-κB pathway and central fatigue and further explore the biological mechanism of central fatigue. At the same time, the clinical application and potential of typical NF-κB inhibitors in the treatment of fatigue were analyzed to provide reference for the clinical treatment of central fatigue.

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Motor dysfunction and alterations in glutathione concentration, cholinesterase activity, and BDNF expression in substantia nigra pars compacta in rats with pedunculopontine lesion

Cited by 10 publications

References 71 publications

Tyrosine Hydroxylase, Vesicular Monoamine Transporter and Dopamine Transporter mRNA Expression in Nigrostriatal Tissue of Rats with Pedunculopontine Neurotoxic Lesion

Tyrosine Hydroxylase, Vesicular Monoamine Transporter and Dopamine Transporter mRNA Expression in Nigrostriatal Tissue of Rats with Pedunculopontine Neurotoxic Lesion

Cellular Redox Imbalance and Neurochemical Effect in Cognitive-Deficient Old Rats

Study on the Correlation Between NF-κB and Central Fatigue

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