Decreased synaptic plasticity in the medial prefrontal cortex underlies short-term memory deficits in 6-OHDA-lesioned rats

Matheus, Filipe C.; Rial, Daniel; Real, Joana I.; Lemos, Cristina; Ben, Juliana; Guaita, Gisele Oliveira; Pita, Inês; Sequeira, Ana; Pereira, Frederico C.; Walz, Roger; Takahashi, Reinaldo Ν.; Bertoglio, Leandro J.; Cunha, Cláudio Da; Cunha, Rodrigo A.; Prediger, Rui Daniel

doi:10.1016/j.bbr.2015.12.011

Cited by 28 publications

(30 citation statements)

References 67 publications

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“…All tests were observed through a video camera (Samsung ST93 Digital Camera, Suwon, South Korea). The equipment were cleaned by 70% ethanol to avoid odor cues for animals [34].…”

Section: Behavioral Testsmentioning

confidence: 99%

“…A wooden arena (100 × 100 × 60 height, brown wall, and floor) was divided into 25 squares (20 cm per square). Rat was put in the center of the arena for 15 min and freely allowed to explore it [34]. Latency to move from the center was observed, and the total distance moved by meter (m) was assessed by calculating the numbers of crossed squares.…”

Section: Assessment Of Motor Functionmentioning

confidence: 99%

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Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory, Gliosis, and Oxidative Stress

et al. 2020

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This study evaluated the neuroprotective potential of Allium sativum against monosodium glutamate (MSG)-induced neurotoxicity with respect to its impact on short-term memory in rats. Forty male Wistar albino rats were assigned into four groups. The control group received distilled water. The second group was administered Allium sativum powder (200 mg/kg of body weight) orally for 7 successive days, then was left without treatment until the 30th day. The third group was injected intraperitoneally with MSG (4 g/kg of body weight) for 7 successive days, then left without treatment until the 30th day. The fourth group was injected with MSG in the same manner as the third group and was treated with Allium sativum powder in the same manner as the second group, simultaneously. Phytochemical analysis of Allium sativum powder identified the presence of diallyl disulphide, carvone, diallyl trisulfide, and allyl tetrasulfide. MSG-induced excitotoxicity and cognitive deficit were represented by decreased distance moved and taking a long time to start moving from the center in the open field, as well as lack of curiosity in investigating the novel object and novel arm. Moreover, MSG altered hippocampus structure and increased MDA concentration and protein expression of glial fibrillary acidic protein (GFAP), calretinin, and caspase-3, whereas it decreased superoxide dismutase (SOD) activity and protein expression of Ki-67 in brain tissue. However, Allium sativum powder prevented MSG-induced neurotoxicity and improved short-term memory through enhancing antioxidant activity and reducing lipid peroxidation. In addition, it decreased protein expression of GFAP, calretinin, and caspase-3 and increased protein expression of Ki-67 in brain tissues and retained brain tissue architecture. This study indicated that Allium sativum powder ameliorated MSG-induced neurotoxicity through preventing oxidative stress-induced gliosis and apoptosis of brain tissue in rats.

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“…All tests were observed through a video camera (Samsung ST93 Digital Camera, Suwon, South Korea). The equipment were cleaned by 70% ethanol to avoid odor cues for animals [34].…”

Section: Behavioral Testsmentioning

confidence: 99%

Section: Assessment Of Motor Functionmentioning

confidence: 99%

Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory, Gliosis, and Oxidative Stress

et al. 2020

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“…These results are supported by numerous previous studies. Bilateral administration of 20 μg of 6-OHDA in the dorsolateral striatum of rats promotes significant deficits in locomotor activity addressed in the open field test, 21 days after 6-OHDA administration (Matheus et al, 2016). Similarly, motor impairments were observed with unilateral administration of 10 μg of 6-OHDA in the striatum, which included a decrease in locomotion and exploratory behavior of male Wistar rats, observed 3 weeks after treatment with the 6-OHDA neurotoxin (Hegazy et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Glucose Homeostasis Is Not Affected in a Murine Model of Parkinson’s Disease Induced by 6-OHDA

et al. 2019

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There is a mutual relationship between metabolic and neurodegenerative diseases. However, the causal relationship in this crosstalk is unclear and whether Parkinson’s disease (PD) causes a posterior impact on metabolism remains unknown. Considering that, this study aimed to evaluate the appearance of possible changes in metabolic homeostasis due to 6-hydroxydopamine (6-OHDA) administration, a neurotoxin that damage dopaminergic neurons leading to motor impairments that resemble the ones observed in PD. For this, male Wistar rats received bilateral 6-OHDA administration in the dorsolateral striatum, and the motor and metabolic outcomes were assessed at 7, 21, or 35 days post-surgical procedure. Dexamethasone, a diabetogenic glucocorticoid (GC), was intraperitoneally administered in the last 6 days to challenge the metabolism and reveal possible metabolic vulnerabilities caused by 6-OHDA. Controls received only vehicles. The 6-OHDA-treated rats displayed a significant decrease in locomotor activity, exploratory behavior, and motor coordination 7 and 35 days after neurotoxin administration. These motor impairments paralleled with no significant alteration in body mass, food intake, glucose tolerance, insulin sensitivity, and biochemical parameters (plasma insulin, triacylglycerol, and total cholesterol levels) until the end of the experimental protocol on days 35–38 post-6-OHDA administration. Moreover, hepatic glycogen and fat content, as well as the endocrine pancreas mass, were not altered in rats treated with 6-OHDA at the day of euthanasia (38th day after neurotoxin administration). None of the diabetogenic effects caused by dexamethasone were exacerbated in rats previously treated with 6-OHDA. Thus, we conclude that bilateral 6-OHDA administration in the striatum causes motor deficits in rats with no impact on glucose and lipid homeostasis and does not exacerbate the adverse effects caused by excess GC. These observations indicate that neurodegeneration of dopaminergic circuits in the 6-OHDA rats does not affect the metabolic outcomes.

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“…These additional symptoms should be considered when designing treatment regimens for people with PD. Some studies have characterized short‐term memory deficits and depressive‐like behaviors in rodents with bilateral 6‐OHDA or MPTP lesions (Ferro et al., ; Matheus et al., ; Santiago et al., ). However, no studies published to date have investigated the effects of trophic factors in these bilateral models of nonmotor symptoms of PD.…”

Section: Limitations Of Preclinical Models For Testing Trophic Factormentioning

confidence: 99%

Trophic factors for Parkinson's disease: Where are we and where do we go from here?

Paul

Sullivan

2018

Eur J of Neuroscience

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Perhaps the most important unmet clinical need in Parkinson's disease (PD) is the development of a therapy that can slow or halt disease progression. Extensive preclinical research has provided evidence for the neurorestorative properties of several growth factors, yet only a few have been evaluated in clinical studies. Attempts to achieve neuroprotection by addressing cell-autonomous mechanisms and targeting dopaminergic neurons have been disappointing. Four different trophic factors have so far entered clinical trials in PD: glial cell line-derived growth factor, its close structural and functional analog neurturin, platelet-derived growth factor and cerebral dopaminergic neurotrophic factor. This article reviews the pre-clinical evidence for the neuroprotective and neurorestorative actions of these growth factors and discusses limitations of preclinical models, which may hamper successful translation to the clinic. We summarize the previous and ongoing clinical trials using growth factors in PD and emphasize the caveats in clinical trial design that may prevent the further development and registration of potentially neuroprotective and neurorestorative treatments for individuals suffering from PD.

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Decreased synaptic plasticity in the medial prefrontal cortex underlies short-term memory deficits in 6-OHDA-lesioned rats

Cited by 28 publications

References 67 publications

Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory, Gliosis, and Oxidative Stress

Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory, Gliosis, and Oxidative Stress

Glucose Homeostasis Is Not Affected in a Murine Model of Parkinson’s Disease Induced by 6-OHDA

Trophic factors for Parkinson's disease: Where are we and where do we go from here?

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