GABA and Dopamine Release from Different Brain Regions in Mice with Chronic Exposure to Organophosphate Methamidophos

Noriega-Ortega, Blanca Rosa; Armienta-Aldana, Ernesto; Cervantes-Pompa, José Ángel; Armienta-Aldana, Eduardo; Hernández-Ruíz, Enrique; Chaparro-Huerta, V.; Bravo-Cuéllar, Alejandro; Beas‐Zárate, Carlos

doi:10.1293/tox.24.163

Cited by 9 publications

(6 citation statements)

References 13 publications

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“…[79], 2.6 mg/kg of methamidophos was administered to male BALB/c mice every three days, until the mice were three, six or nine months old. Exposure to methamidophos was related to a decrease of GABA release in the cerebral cortex after three months, while an increase of GABA release in the same brain area was observed after nine months.…”

Section: Resultsmentioning

confidence: 99%

“…In addition, decreased GABA levels were observed after exposure of adult male Lister hooded rats to a single dose of 250 mg/kg of the organophosphate chlorpyrifos Furthermore, in a study by Noriega-Ortega et al . [79] male BALB/c mice were exposed to 2.6 mg/kg of methamidophos every three days resulting in a decrease of GABA release in the cortex and hippocampus after three and six months. An exposure to 30 mg/kg/day of the phthalate DEHP throughout gestation until weaning (GD1-PND21) also resulted in decreased GABA levels in prepubertal male rats.…”

Section: Resultsmentioning

confidence: 99%

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The Dynamics of Autism Spectrum Disorders: How Neurotoxic Compounds and Neurotransmitters Interact

Quaak¹,

Brouns²,

Bor³

2013

IJERPH

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In recent years concern has risen about the increasing prevalence of Autism Spectrum Disorders (ASD). Accumulating evidence shows that exposure to neurotoxic compounds is related to ASD. Neurotransmitters might play a key role, as research has indicated a connection between neurotoxic compounds, neurotransmitters and ASD. In the current review a literature overview with respect to neurotoxic exposure and the effects on neurotransmitter systems is presented. The aim was to identify mechanisms and related factors which together might result in ASD. The literature reported in the current review supports the hypothesis that exposure to neurotoxic compounds can lead to alterations in the GABAergic, glutamatergic, serotonergic and dopaminergic system which have been related to ASD in previous work. However, in several studies findings were reported that are not supportive of this hypothesis. Other factors also might be related, possibly altering the mechanisms at work, such as time and length of exposure as well as dose of the compound. Future research should focus on identifying the pathway through which these factors interact with exposure to neurotoxic compounds making use of human studies.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

The Dynamics of Autism Spectrum Disorders: How Neurotoxic Compounds and Neurotransmitters Interact

Quaak¹,

Brouns²,

Bor³

2013

IJERPH

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“…They indicated that this widely used OP pesticide is deleterious to brain function. Noriega‐Ortega et al () reported that MT, like other OP, disrupts endocrine pathways and the results indicate changes in gamma aminobutyric acid and dopamine neurotransmission, suggesting a specific neuronal damage. Moreover, MT induced diaphragm muscle necrosis and brain oxidative stress (Kalkan et al, ).…”

Section: Introductionmentioning

confidence: 99%

Toxic effects of methamidophos on paraoxonase 1 activity and on rat kidney and liver and ameliorating effects of alpha‐tocopherol

Araoud

Neffeti

Khaled

et al. 2014

Environmental Toxicology

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The role of alpha-tocopherol on nephrotoxicity and hepatotoxicity induced by methamidophos (MT) was investigated in wistar rats. Animals were given via gavage, for four weeks, a low dose of MT (MT1), a high dose of MT (MT2), vitamin E (200 mg/kg of bw) or both MT2 plus vitamin E (Vit E) and control group was given distillate water. MT treatment resulted in a significant decrease in the body weight of MT2-treated group. Moreover, MT-treated groups had significantly lower butyrylcholinesterase (p < 0.01) and paraoxonase 1 (PON1) activities compared with the control group (p < 0.05). However, MT2-treated group had significantly higher alkaline phosphatase activity compared with untreated rats (p < 0.05). Both MT-treated groups had significantly higher urea (p < 0.01) and uric acid levels (p < 0.05) compared with the control group. However, significant low uric acid level (p < 0.05) was noted in MT2 plus vit E-treated rats compared with MT2-treated group. Histopathological changes in organ tissues were observed in both MT-treated groups and MT2 plus vit E-treated rats. However, the damage was reduced in MT2 plus vit E-treated rats. Therefore, this study deduces that alpha-tocopherol administration may ameliorate the adverse effects of subacute exposure to MT on rat liver and kidney and this antioxidant can protect PON1 from oxidative stress induced by this organophosphorus pesticide. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 842-854, 2016.

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“…Sustková-Fišerová et al (2009) showed that socially isolated non-aggressive mice had almost three times higher levels of GABA in the pre-frontal cortex when compared with aggressive mice. Additionally, chronic exposure to methamidophos was shown to decrease GABA release in cerebral cortex and hippocampal slices (Noriega-Ortega et al 2011). …”

Section: Discussionmentioning

confidence: 99%

Methamidophos, an Organophosphorus Insecticide, Induces Pro-aggressive Behaviour in Mice

Nascimento

Maretto²,

Marques

et al. 2017

Neurotox Res

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Although evidence indicates that exposure to organophosphorus (OP) pesticides induces neurobehavioral disorders, little is known about the effects of OP on aggressive behaviour. Our study investigated the effects of repeated exposure to an OP pesticide, methamidophos, on the isolation-induced aggressive behaviour in mice. Forty seven male mice were individually housed for a month. Socially isolated animals were then confronted with a standard non-isolated opponent for 15 minutes (pre-treatment trial), and the latency and frequency of aggressive and general exploratory behaviours were recorded. Based on the presence of attack behaviour in the pre-treatment trial, mice were classified as isolation-induced aggressive and non-aggressive. All mice were then treated for seven days with methamidophos (3.5 mg/kg/day, n=22, ip) or saline (1 mL/kg/day, control group, n=25, ip) and a second trial performed. Repeated exposure to methamidophos induced attack behaviour in non-aggressive mice. The treatment with methamidophos also decreased plasma butyrylcholinesterase and brain acetylcholinesterase activity. These results suggest that methamidophos has a pro-aggressive effect on socially isolated mice.

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GABA and Dopamine Release from Different Brain Regions in Mice with Chronic Exposure to Organophosphate Methamidophos

Cited by 9 publications

References 13 publications

The Dynamics of Autism Spectrum Disorders: How Neurotoxic Compounds and Neurotransmitters Interact

The Dynamics of Autism Spectrum Disorders: How Neurotoxic Compounds and Neurotransmitters Interact

Toxic effects of methamidophos on paraoxonase 1 activity and on rat kidney and liver and ameliorating effects of alpha‐tocopherol

Methamidophos, an Organophosphorus Insecticide, Induces Pro-aggressive Behaviour in Mice

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