Parenteral domoic acid impairs spatial learning in mice

Petrie, Bruce F.; Pinsky, Carl M.; Standish, N.M.; Bose, Ratna; Glavin, Gary B.

doi:10.1016/0091-3057(92)90084-s

Cited by 41 publications

(22 citation statements)

References 20 publications

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“…These animals also failed to select the appropriate problem-solving strategies in their attempt to search for the underwater platform (longer escape latencies than controls) (Petrie et al, 1992). This impairment of acquisition and retention of this spatial navigation task by DomA, was associated with neuronal damage not only in the hippocampus, but also in limbic brain regions (Petrie et al, 1992). Similar results were obtained in a different study that also utilised the Morris water maze but in rats (Kuhlmann and Guilarte, 1997).…”

Section: Weight Of Evidencesupporting

confidence: 74%

“…It is worth mentioning that similar findings have been found in human subjects, where by combining behavioural and electrophysiological data from patients with temporal lobe epilepsy exposed to ketamine, the involvement of NMDA receptors in human memory processes was demonstrated (Grunwald et al, 1999). Domoic Acid (DomA) Mice exposed to DomA (2.0 mg/kg) showed impairment of the acquisition of the place task in the Morris water maze (Petrie et al, 1992). These animals also failed to select the appropriate problem-solving strategies in their attempt to search for the underwater platform (longer escape latencies than controls) (Petrie et al, 1992).…”

Section: Weight Of Evidencementioning

confidence: 61%

“…Domoic Acid (DomA) Mice exposed to DomA (2.0 mg/kg) showed impairment of the acquisition of the place task in the Morris water maze (Petrie et al, 1992). These animals also failed to select the appropriate problem-solving strategies in their attempt to search for the underwater platform (longer escape latencies than controls) (Petrie et al, 1992). This impairment of acquisition and retention of this spatial navigation task by DomA, was associated with neuronal damage not only in the hippocampus, but also in limbic brain regions (Petrie et al, 1992).…”

Section: Weight Of Evidencementioning

confidence: 99%

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Adverse Outcome Pathway on binding of agonists to ionotropic glutamate receptors in adult brain leading to excitotoxicity that mediates neuronal cell death, contributing to learning and memory impairment

Sachana

Munn

Bal‐Price

2016

OECD Series on Adverse Outcome Pathways

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Section: Weight Of Evidencesupporting

confidence: 74%

Section: Weight Of Evidencementioning

confidence: 61%

Section: Weight Of Evidencementioning

confidence: 99%

See 1 more Smart Citation

Adverse Outcome Pathway on binding of agonists to ionotropic glutamate receptors in adult brain leading to excitotoxicity that mediates neuronal cell death, contributing to learning and memory impairment

Sachana

Munn

Bal‐Price

2016

OECD Series on Adverse Outcome Pathways

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“…The models of neurodegeneration used display behavioral deficits that can be quantified through task-oriented tests. Spatial memory in hippocampal-lesioned mice can be evaluated with the water maze test (Petrie et al, 1992). We followed procedures described in detail previously using a water tank at 22°C with intramaze and extramaze orientation cues (Frisch et al, 2000).…”

Section: Models Of Neurodegenerationmentioning

confidence: 99%

Circulating Insulin-Like Growth Factor I Mediates the Protective Effects of Physical Exercise against Brain Insults of Different Etiology and Anatomy

et al. 2001

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Physical exercise ameliorates age-related neuronal loss and is currently recommended as a therapeutical aid in several neurodegenerative diseases. However, evidence is still lacking to firmly establish whether exercise constitutes a practical neuroprotective strategy. We now show that exercise provides a remarkable protection against brain insults of different etiology and anatomy. Laboratory rodents were submitted to treadmill running (1 km/d) either before or after neurotoxin insult of the hippocampus (domoic acid) or the brainstem (3-acetylpyridine) or along progression of inherited neurodegeneration affecting the cerebellum (Purkinje cell degeneration). In all cases, animals show recovery of behavioral performance compared with sedentary ones, i.e., intact spatial memory in hippocampal-injured mice, and normal or near to normal motor coordination in brainstem-and cerebellum-damaged animals. Furthermore, exercise blocked neuronal impairment or loss in all types of injuries. Because circulating insulin-like growth factor I (IGF-I), a potent neurotrophic hormone, mediates many of the effects of exercise on the brain, we determined whether neuroprotection by exercise is mediated by IGF-I. Indeed, subcutaneous administration of a blocking anti-IGF-I antibody to exercising animals to inhibit exercise-induced brain uptake of IGF-I abrogates the protective effects of exercise in all types of lesions; antibodytreated animals showed sedentary-like brain damage. These results indicate that exercise prevents and protects from brain damage through increased uptake of circulating IGF-I by the brain. The practice of physical exercise is thus strongly recommended as a preventive measure against neuronal demise. These findings also support the use of IGF-I as a therapeutical aid in brain diseases coursing with either acute or progressive neuronal death.

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“…Various researchers have also reported that DA exposure causes prolonged neuroexcitation and extensive degeneration in the hippocampus as well as more rostral areas of the brain, including the septum and olfactory bulb (Peng and Ramsdell 1996; Peng et al 1994; Scallet et al 1993, 2004). DA-induced damage to hippocampal formation has been correlated with both learning (Clayton et al 1999) and memory deficits in humans and experimental animals (Nakajima and Potvin 1992; Petrie et al 1992; Sutherland et al 1990; Teitelbaum et al 1990). …”

mentioning

confidence: 99%

Domoic Acid Transfer to Milk: Evaluation of a Potential Route of Neonatal Exposure

Maucher¹,

Ramsdell²

2005

Environ Health Perspect

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Domoic acid (DA), produced by the diatom genus Pseudo-nitzschia, is a glutamate analog and a neurotoxin in humans. During diatom blooms, DA can contaminate filter-feeding organisms, such as shellfish, and can be transferred by ingestion to higher trophic levels. Several intoxication events involving both humans and various marine mammals have been attributed to DA. Affected organisms show neurological symptoms such as seizures, ataxia, headweaving, and stereotypic scratching, as well as prolonged deficits in memory and learning. Neonatal animals have been shown to be substantially more sensitive to DA than adults. However, it has not been demonstrated whether DA can be transferred to nursing young from DA-exposed mothers. This study demonstrates transfer of DA from spiked milk (0.3 and 1.0 mg/kg) to the plasma of nursing neonatal rats and an overall longer DA retention in milk than in plasma after 8 hr in exposed dams. DA was detectable in milk up to 24 hr after exposure (1.0 mg/kg) of the mothers, although the amount of DA transferred to milk after exposure was not sufficient to cause acute symptoms in neonates.

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Parenteral domoic acid impairs spatial learning in mice

Cited by 41 publications

References 20 publications

Adverse Outcome Pathway on binding of agonists to ionotropic glutamate receptors in adult brain leading to excitotoxicity that mediates neuronal cell death, contributing to learning and memory impairment

Adverse Outcome Pathway on binding of agonists to ionotropic glutamate receptors in adult brain leading to excitotoxicity that mediates neuronal cell death, contributing to learning and memory impairment

Circulating Insulin-Like Growth Factor I Mediates the Protective Effects of Physical Exercise against Brain Insults of Different Etiology and Anatomy

Domoic Acid Transfer to Milk: Evaluation of a Potential Route of Neonatal Exposure

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