Prenatal exposure to ketamine in rats: Implications on animal models of schizophrenia

Coronel-Oliveros, Carlos; Pacheco-Calderón, Renny

doi:10.1002/dev.21586

Cited by 28 publications

(16 citation statements)

References 73 publications

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“…In humans, schizophrenia is characterized by positive symptoms (e.g., hallucination, delusion), negative symptoms (e.g., loss of motivation, social isolation), and cognitive symptoms (e.g., impairments in attention and memory). Coronel-Oliveros and Pacheco-Calderón (2018) observed that the animals prenatally exposed to ketamine exhibited disinhibition and hyperactive behavior in pubertal stage, and cognitive impairments, social withdrawal, anxiety, depression, and aggressive-like behaviors in adulthood. These schizophrenia-like phenotypes in animals with prenatal ketamine challenge strongly supported the deleterious effects of ketamine on neurobehavioral functions throughout life.…”

Section: Neurotoxicity Of Ketamine To the Developing Brainmentioning

confidence: 99%

“…It has been hypothesized that glutamatergic dysfunction may be involved in the etiology of schizophrenia (Moghaddam et al, 1997; Frohlich and Van Horn, 2014), a neuropsychiatric disorder with peak onset periods at late adolescence and early adulthood. In this regard, Coronel-Oliveros and Pacheco-Calderón (2018) has recently proposed an animal model of schizophrenia using rats prenatally exposed to ketamine. In humans, schizophrenia is characterized by positive symptoms (e.g., hallucination, delusion), negative symptoms (e.g., loss of motivation, social isolation), and cognitive symptoms (e.g., impairments in attention and memory).…”

Section: Neurotoxicity Of Ketamine To the Developing Brainmentioning

confidence: 99%

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Effects of Perinatal Exposure to Ketamine on the Developing Brain

Cheung

Yew

2019

Front. Neurosci.

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Initially used as an analgesic and anesthetic, ketamine has unfortunately been abused as a popular recreational party drug due to its psychotropic effects. Over the last decade, ketamine has also emerged as an effective rapid-onset anti-depressant. The increasingly widespread use and misuse of the drug in infants and pregnant women has posed a concern about the neurotoxicity of ketamine to the immature brains of developing fetuses and children. In this review, we summarize recent research findings on major possible mechanisms of perinatal ketamine-induced neurotoxicity. We also briefly summarize the neuroprotective effects of ketamine in the presence of noxious stimuli. Future actions include implementation of more drug abuse education and prevention campaigns to raise the public’s awareness of the harmful effects of ketamine abuse; further investigations to justify the clinical use of ketamine as analgesic, anesthetic and anti-depressant; and further studies to develop alternatives to ketamine or treatments that can alleviate the detrimental effects of ketamine use, especially in infants and pregnant women.

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Section: Neurotoxicity Of Ketamine To the Developing Brainmentioning

confidence: 99%

Section: Neurotoxicity Of Ketamine To the Developing Brainmentioning

confidence: 99%

Effects of Perinatal Exposure to Ketamine on the Developing Brain

Cheung

Yew

2019

Front. Neurosci.

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“…Acute ketamine administration in animals results in cognitive deficits including reduced sensorimotor gating, spatial learning and memory impairments, along with changes in theta and gamma band activity (Verma and Moghaddam, 1996; de Bruin et al, 1999; Ehrlichman et al, 2009; Kittelberger et al, 2012; Szlachta et al, 2017; Coronel-Oliveros and Pacheco-Calderon, 2018). In contrast to cortical hypodopaminergic state observed in schizophrenia, these cognitive deficits are accompanied by increased DA release in the PFC (Verma and Moghaddam, 1996).…”

Section: Pharmacological Approaches To Induce Nmdar Hypofunctionmentioning

confidence: 99%

“…Other studies also reported that cognitive deficits are associated with increased frontal cortical blood flow (Ingvar and Franzen, 1974; Vollenweider et al, 1997). Moreover, acute ketamine administration induces hyperlocomotor activity and stereotypic behaviors, which might be attributed to increased DA and serotonin turnover in the striatum and cortex (Irifune et al, 1991; Chatterjee et al, 2011, 2012; Coronel-Oliveros and Pacheco-Calderon, 2018). However, there are inconsistent reports as to the effect of acute ketamine administration on negative symptoms-related behaviors based on social interaction tests (Silvestre et al, 1997; Chatterjee et al, 2011; Coronel-Oliveros and Pacheco-Calderon, 2018).…”

Section: Pharmacological Approaches To Induce Nmdar Hypofunctionmentioning

confidence: 99%

NMDAR Hypofunction Animal Models of Schizophrenia

Lee

Zhou

2019

Front. Mol. Neurosci.

111

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The N-methyl-d-aspartate receptor (NMDAR) hypofunction hypothesis has been proposed to help understand the etiology and pathophysiology of schizophrenia. This hypothesis was based on early observations that NMDAR antagonists could induce a full range of symptoms of schizophrenia in normal human subjects. Accumulating evidence in humans and animal studies points to NMDAR hypofunctionality as a convergence point for various symptoms of schizophrenia. Here we review animal models of NMDAR hypofunction generated by pharmacological and genetic approaches, and how they relate to the pathophysiology of schizophrenia. In addition, we discuss the limitations of animal models of NMDAR hypofunction and their potential utility for therapeutic applications.

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“…The average value was calculated for the number of positive cells: 6 rats per group, one slice per rat per region. 24…”

Section: Nissl Stainmentioning

confidence: 99%

<p>Astaxanthin Attenuates Neuroinflammation in Status Epilepticus Rats by Regulating the ATP-P2X7R Signal</p>

Wang

Deng

Xie

et al. 2020

DDDT

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Background: As a life-threatening neurological emergency, status epilepticus (SE) is often refractory to available treatment. Current studies have shown a causal role of neuroinflammation in patients with lower seizure thresholds and driving seizures. The ATP-gated purinergic P2X7 receptor (P2X7R) is mainly expressed on the microglia, which function as gatekeepers of inflammation. Although emerging evidence has demonstrated significant anti-inflammatory effects of astaxanthin (AST) in SE, the associated mechanism remains unclear. Therefore, this study aimed to clarify the effects of AST on P2X7R-related inflammation in SE. Methods: SE was induced in rats using lithium-pilocarpine, and AST was administered 1 h after SE induction. Rat microglia were treated with lipopolysaccharide (LPS), AST, ATP, 2,3-O-4-benzoyl-4-benzoyl-ATP (BzATP) and oxidized ATP (oxATP). The Morris water maze, immunohistochemistry, and Nissl staining were performed in rats. Expressions of P2X7R and inflammatory cytokines (such as cycloxygenase-2 (Cox-2), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α)) were detected using real-time polymerase chain reaction (RT-PCR) and Western blot (WB) both in rats and microglia. ATP concentration in the microglia was evaluated using ELISA. Results: The AST alleviated hippocampal injury and improved cognitive dysfunction induced by SE. AST also effectively inhibited inflammation and downregulated P2X7R expression in both rat brain and microglia. The results also showed that AST reduced the extracellular ATP levels and that P2X7R expression could be increased by extracellular ATP. In addition, BzATP upregulates the expression of P2X7R and inflammatory factors in microglia. Conversely, it downregulates the expression of P2X7R and inflammatory factors. Conclusion: Our study suggests that AST attenuated ATP-P2X7R mediated inflammation in SE.

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Prenatal exposure to ketamine in rats: Implications on animal models of schizophrenia

Cited by 28 publications

References 73 publications

Effects of Perinatal Exposure to Ketamine on the Developing Brain

Effects of Perinatal Exposure to Ketamine on the Developing Brain

NMDAR Hypofunction Animal Models of Schizophrenia

<p>Astaxanthin Attenuates Neuroinflammation in Status Epilepticus Rats by Regulating the ATP-P2X7R Signal</p>

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