Assessment of Spatial Memory

Wenk, Gary L.

doi:10.1002/0471140856.tx1103s00

Cited by 4 publications

(2 citation statements)

References 53 publications

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“…Learning and memory were tested in mice from Neurobehavioral Testing Group B using the Morris water maze (Morris, 1984; Voikar et al, 2001; Wenk, 1999), which began on PND 70 and was completed on PND 98. The maze consisted of a 165-gallon, circular galvanized stock tank, 122-cm in diameter and 61-cm tall, filled with room temperature water.…”

Section: Methodsmentioning

confidence: 99%

Neurobehavioral assessment of mice following repeated postnatal exposure to chlorpyrifos-oxon

Cole¹,

Fisher²,

Burbacher³

et al. 2012

Neurotoxicology and Teratology

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Chlorpyrifos (CPF), one of the most widely-used organophosphorus (OP) insecticides in agriculture, is degraded in the field to its oxon form, chlorpyrifos-oxon (CPO), which can represent a significant contaminant in exposures to adults and children. CPO is also responsible for the acetylcholinesterase (AChE) inhibition associated with CPF exposures; CPF is converted by liver CYP450 enzymes to CPO, which binds to and inhibits AChE and other serine active-site esterases, lipases and proteases. Young children represent a particularly susceptible population for exposure to CPF and CPO, in part because levels of the plasma enzyme, paraoxonase (PON1), which hydrolyzes CPO, are very low during early development. While a number of studies have demonstrated developmental neurotoxicity associated with CPF exposure, including effects at or below the threshold levels for AChE inhibition, it is unclear whether these effects were due directly to CPF or to its active metabolite, CPO. PON1 knockout (PON1−/−) mice, which lack PON1, represent a highly sensitive mouse model for toxicity associated with exposure to CPF or CPO. To examine the neurobehavioral consequences of CPO exposure during postnatal development, PON1−/− mice were exposed daily from PND 4 to PND 21 to CPO at 0.15, 0.18, or 0.25 mg/kg/d. A neurobehavioral test battery did not reveal significant effects of CPO on early reflex development, motor coordination, pre-pulse inhibition of startle, startle amplitude, open field behavior, or learning and memory in the contextual fear conditioning, Morris water maze, or water radial-arm maze tests. However, body weight gain and startle latency were significantly affected by exposure to 0.25 mg/kg/d CPO. Additionally, from PNDs 15–20 the mice exposed repeatedly to CPO at all three doses exhibited a dose-related transient hyperkinesis in the 20-min period following CPO administration, suggesting possible effects on catecholaminergic neurotransmission. Our previous study demonstrated wide-ranging effects of neonatal CPO exposure on gene expression in the brain and on brain AChE inhibition, and modulation of both of these effects by the PON1Q192R polymorphism. The current study indicates that the neurobehavioral consequences of these effects are more elusive, and suggests that alternative neurobehavioral tests might be warranted, such as tests of social interactions, age-dependent effects on learning and memory, or tests designed specifically to assess dopaminergic or noradrenergic function.

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Section: Methodsmentioning

confidence: 99%

Neurobehavioral assessment of mice following repeated postnatal exposure to chlorpyrifos-oxon

Cole¹,

Fisher²,

Burbacher³

et al. 2012

Neurotoxicology and Teratology

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show abstract

“…Other popular tasks for spatial learning, such as the T-or Y-maze, are more structured, forcing the animals to make only a binary decision, moving towards the right or left arm of the maze [31][32][33]. In our hands, poor activity of muscarinic ligands in the T-maze was observed [23].…”

Section: Discussionmentioning

confidence: 60%

Activation of Metabotropic Glutamate Receptor (mGlu2) and Muscarinic Receptors (M1, M4, and M5), Alone or in Combination, and Its Impact on the Acquisition and Retention of Learning in the Morris Water Maze, NMDA Expression and cGMP Synthesis

et al. 2023

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The Morris water maze (MWM) is regarded as one of the most popular tests for detecting spatial memory in rodents. Long-term potentiation and cGMP synthesis seem to be among the crucial factors involved in this type of learning. Muscarinic (M1, M4, and M5 receptors) and metabotropic glutamate (mGlu) receptors are important targets in the search for antipsychotic drugs with the potency to treat cognitive disabilities associated with the disorder. Here, we show that muscarinic receptor activators (VU0357017, VU0152100, and VU0238429) and an mGlu2 receptor activator, LY487379, dose-dependently prevented the development of cognitive disorders as a result of MK-801 administration in the MWM. The dose-ranges of the compounds were as follows: VU0357017, 0.25, 0.5, and 1 mg/kg; VU0152100, 0.05, 0.25, and 1 mg/kg; VU0238429, 1, 5, and 20 mg/kg; and LY487379, 0.5, 3, and 5 mg/kg. The co-administration of LY487379 with each of the individual muscarinic receptor ligands showed no synergistic effect, which contradicts the results obtained earlier in the novel object recognition (NOR) test. MWM learning resulted in increased cGMP synthesis, both in the cortex and hippocampi, when compared to that in intact animals, which was prevented by MK-801 administration. The investigated compounds at the highest doses reversed this MK-801-induced effect. Neither the procedure nor the treatment resulted in changes in GRIN2B GluN2B-NMDA expression.

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Biochemical deficits and cognitive decline in brain aging: Intervention by dietary supplements

Poddar

Pradhan

Ganguly

et al. 2019

Journal of Chemical Neuroanatomy

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Assessment of Spatial Memory

Cited by 4 publications

References 53 publications

Neurobehavioral assessment of mice following repeated postnatal exposure to chlorpyrifos-oxon

Neurobehavioral assessment of mice following repeated postnatal exposure to chlorpyrifos-oxon

Activation of Metabotropic Glutamate Receptor (mGlu2) and Muscarinic Receptors (M1, M4, and M5), Alone or in Combination, and Its Impact on the Acquisition and Retention of Learning in the Morris Water Maze, NMDA Expression and cGMP Synthesis

Biochemical deficits and cognitive decline in brain aging: Intervention by dietary supplements

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