Economical test methods for developmental neurobehavioral toxicity.

Bignami, Giorgio

doi:10.1289/ehp.96104s2285

Cited by 53 publications

(41 citation statements)

References 82 publications

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“…This test exploits the strong tendency of the immature pup to maintain body contact with the dam and the siblings, which requires adequate sensory, olfactory, motor and ultrasonic communication capabilities as well as adequate associative and discriminative capabilities that allow the pup to become imprinted by the mother's odour, to remember it, and to recognize it among others (Bignami 1996). The lack of changes in this simple form of learning is in agreement with recent findings (Tattoli et al 2001) showing that perinatal exposure to low doses of alcohol did not affect the acquisition of an active avoidance task and hippocampal Long-Term Potentiation (a cellular and molecular model for learning (Shepherd et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Genetic Factors Involved in the Effects of Developmental Low-Level Alcohol Induced Behavioral Alterations in Rats

Cagiano

Cassano

Coluccia

et al. 2002

Neuropsychopharmacology

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and neurochemical effects of perinatal alcohol exposure (3% v/v solution from Day 15 of gestation to Day 7 after parturition) have been investigated in Sardinian alcohol-preferring (sP) and alcohol-nonpreferring (sNP) Previous data suggest that genetic factors could contribute to differences in susceptibility to alcohol-related neurodevelopmental disorders (ARNDs) (Gilliam et al. 1987;Gilliam and Irtenkauf 1990;Govoni et al. 1994;Hannigan 1996;Riley and Lochry 1982;Riley et al. 1993). A recent study in the present series has shown that offspring of Sardinian alcohol-preferring (sP) and Sardinian alcohol-nonpreferring (sNP) rats, selectively bred (from Wistar rats) for opposite alcohol preference and consumption, exhibited a different behavioral profile in response to perinatal exposure to this drug of

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Section: Discussionmentioning

confidence: 99%

Genetic Factors Involved in the Effects of Developmental Low-Level Alcohol Induced Behavioral Alterations in Rats

Cagiano

Cassano

Coluccia

et al. 2002

Neuropsychopharmacology

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“…At the start of testing, individual animals were placed in the middle of the open field box and video recorded for 5 min. Video recordings were scored for vertical activity (number of rears), over-all activity (total number of squares crossed), fields entered in both the center and outside squares, and % time spent in the center and outside squares [44].…”

Section: Open Fieldmentioning

confidence: 99%

Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil–DNA glycosylase impair learning in a mouse model of vascular cognitive impairment

Jadavji

Farr

Lips

et al. 2015

Behavioural Brain Research

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(2015) Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil-DNA glycosylase impair learning in a mouse model of vascular cognitive impairment. Behavioural Brain Research, 283 . pp. 215-226. ISSN 1872-7549 Access from the University of Nottingham repository: http://eprints.nottingham.ac.uk/32983/9/UNG_FADD_20140826_manuscript_final.pdf Copyright and reuse:The Nottingham ePrints service makes this work by researchers of the University of Nottingham available open access under the following conditions. This article is made available under the Creative Commons Attribution Non-commercial No Derivatives licence and may be reused according to the conditions of the licence. For more details see: http://creativecommons.org/licenses/by-nc-nd/2.5/ A note on versions:The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription.For more information, please contact eprints@nottingham.ac.uk Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil-DNA glycosylase impair learning in a mouse model of vascular cognitive impairment. ABSTRACTDietary deficiencies in folic acid result in elevated levels of plasma homocysteine, which has been associated with the development of dementia and other neurodegenerative disorders.Previously, we have shown that elevated levels of plasma homocysteine in mice deficient for a DNA repair enzyme, uracil-DNA glycosylase (UNG), result in neurodegeneration. The goal of this study was to evaluate how deficiencies in folic acid and UNG along with elevated levels of homocysteine affect vascular cognitive impairment, via chronic hypoperfusion in an animal model. Ung+/+ and Ung−/− mice were placed on either control (CD) or folic acid deficient (FADD) diets. Six weeks later, the mice either underwent implantation of microcoils around both common carotid arteries. Post-operatively, behavioral tests began at 3-weeks, angiography was measured after 5-weeks using MRI to assess vasculature and at completion of study plasma and brain tissue was collected for analysis. Learning impairments in the Morris water maze (MWM) were observed only in hypoperfused Ung−/− FADD mice and these mice had significantly higher plasma homocysteine concentrations. Interestingly, Ung+/+ FADD produced significant remodeling of the basilar artery and arterial vasculature. Increased expression of GFAP was observed in the dentate gyrus of Ung−/− hypoperfused and FADD sham mice. Chronic hypoperfusion resulted in increased cortical MMP-9 protein levels of FADD hypoperfused mice regardless of genotypes. These results suggest that elevated levels of homocysteine only, as a result of dietary folic acid deficiency, don't lead to memory impairments and neurobiochemical changes. Rather a combination of either chronic hypoperfusion o...

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“….] associative and discriminative capabilities that allow the pup to become imprinted by the mother's odor, to remember it, and to recognize it among others' (Bignami, 1996). Thus, impaired homing performance has been associated with the reciprocal interaction deficits observed in autistic patients early in infancy (Rutgers et al, 2004;Laviola et al, 2009).…”

Section: Rl/+ Mice Display Behavioral Alterations Isomorphic To Asdmentioning

confidence: 99%

“…In the light of the extensive connections between the cerebellum and the neocortex (Strick et al, 2009), we also hypothesized the role of altered cerebrocerebellar loops for behavioral and attentional deficits in rl/+ mice. To investigate the functional significance of this hypothesis, here we compared neonatal social capabilities (homing test, Bignami, 1996) and adult attentional set-shifting abilities in rl/+ and +/+ male mice exposed to 17b-E or vehicle on postnatal day 5. Based on these evidences and on the synergistic role played by the amygdala and the prefrontal cortex in regulating purposive behavior (reviewed in Barbas, 2000;Bechara et al, 2000;Birrell and Brown, 2000) we also measured the number of Parvalbumin-positive, GABAergic inhibitory interneurons in the prefrontal cortex and amygdala, and of PCs in the cerebellum.…”

Section: Introductionmentioning

confidence: 99%

Perseverative responding and neuroanatomical alterations in adult heterozygous reeler mice are mitigated by neonatal estrogen administration

Macrı̀

Biamonte

Romano

et al. 2010

Psychoneuroendocrinology

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Summary According to the ''extreme-male brain'' theory, elevated fetal testosterone levels may partly explain the skewed sex ratio found in Autism Spectrum Disorders (ASD). Correcting this testosterone imbalance by increasing estrogen levels may mitigate the abnormal phenotype. Accordingly, while control heterozygous reeler (rl/+) male mice -a putative model of neuroanatomical and behavioral endophenotypes in ASD -show a decreased number of Purkinje cells (PC) compared to control wild-type (+/+) littermates, neonatal estradiol administration has been shown to correct this deficit in the short-term (i.e. on postnatal day 15). Here, we further investigated the neuroanatomical and behavioral abnormalities of rl/+ male mice and the potential compensatory effects of neonatal treatment with estradiol. In a longitudinal study, we observed that: i) infant rl/+ mice showed reduced motivation for social stimuli; ii) adult rl/+ male mice showed reduced cognitive flexibility; iii) the number of amygdalar parvalbuminpositive GABAergic interneurons were remarkably reduced in rl/+ mice; iv) neonatal estradiol administration into the cisterna magna reverted the abnormal profile both at the behavioral and at the neuroanatomical level in the amygdala but did not compensate for the cerebellar abnormalities in adulthood. This study supports the view that an increased excitation-toinhibition ratio in the cerebellum and in the amygdala during a critical window of development could be crucial to the social and cognitive phenotype of male rl/+ mice, and that acute estradiol treatment during this critical window may mitigate symptoms' severity. #

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Economical test methods for developmental neurobehavioral toxicity.

Abstract: 285-298 (1996)

Cited by 53 publications

References 82 publications

Genetic Factors Involved in the Effects of Developmental Low-Level Alcohol Induced Behavioral Alterations in Rats

Genetic Factors Involved in the Effects of Developmental Low-Level Alcohol Induced Behavioral Alterations in Rats

Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil–DNA glycosylase impair learning in a mouse model of vascular cognitive impairment

Perseverative responding and neuroanatomical alterations in adult heterozygous reeler mice are mitigated by neonatal estrogen administration

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