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Neurobehavioural defects in adult mice neonatally exposed to nicotine: changes in nicotine-induced behaviour and maze learning performance
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Evolutionary Biology, Environmental Toxicology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Evolutionary Biology, Environmental Toxicology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Evolutionary Biology, Environmental Toxicology.
2001 (English)In: Behavioural Brain Research, ISSN 0166-4328, E-ISSN 1872-7549, Vol. 123, no 2, 185-192 p.Article in journal (Refereed) Published
Abstract [en]

Neonatal exposure to low doses of nicotine has been shown to disturb the development of low-affinity nicotinic binding sites in the cerebral cortex and to elicit a deviant behavioural response to nicotine in adult mice. In this study, 10-day-old male NMRI mice were exposed to one of three different doses of nicotine (3.3, 33, or 66 μg nicotine-base/kg body wt.) s.c. twice daily on 5 consecutive days to study dose–response effects of nicotine on adult spontaneous and nicotine-induced motor behaviour. The nicotine-induced behaviour test revealed a hypoactive response to nicotine in 4-month-old mice neonatally exposed to 33 or 66 μg nicotine-base, whereas the response to nicotine in control animals and mice exposed to 3.3 μg nicotine-base was an increased activity. Learning and memory functions were also investigated in adult animals neonatally exposed to 66 μg nicotine-base/kg body wt. in the same manner, in the Morris water maze and in the Radial arm maze. In the swim maze and the Radial arm maze tests, no significant differences were observed between nicotine-treated and control animals at the age of 4 months. At 7 months, however, a significant difference in performance was evident, indicating a time-response/time-dependent effect. Furthermore, it was shown that in mice exposed neonatally to a nicotine dose known to inhibit the development of the nicotinic low affinity-binding site (LA), the response to nicotine could not cause any increase in spontaneous motor activity as seen in controls.

Place, publisher, year, edition, pages
2001. Vol. 123, no 2, 185-192 p.
Keyword [en]
nicotine, neonatal, development, spontaneous behaviour, adult, maze
National Category
Natural Sciences
Identifiers
URN: urn:nbn:se:uu:diva-91051DOI: 10.1016/S0166-4328(01)00207-8OAI: oai:DiVA.org:uu-91051DiVA: diva2:163633
Available from: 2003-11-11 Created: 2003-11-11 Last updated: 2013-05-21Bibliographically approved
In thesis
1. Neurotoxic Effects of Nicotine During Neonatal Brain Development: Critical Period and Adult Susceptibility
Open this publication in new window or tab >>Neurotoxic Effects of Nicotine During Neonatal Brain Development: Critical Period and Adult Susceptibility
2003 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

This thesis examined neurotoxic effects of nicotine exposure during a defined critical period of neonatal brain development in mice.

In our environment there are numerous hazardous contaminants that an individual can be exposed to during its entire lifetime. In many mammalian species the neonatal period is characterised by a rapid development of the brain. The present studies have identified a defined critical period during the neonatal brain development in mice, where exposure to low doses of nicotine causes permanent disturbances in the cholinergic nicotinic receptors and altered behaviour response to nicotine at adult age. This adult reaction to nicotine, a hypoactive response, was the opposite of that observed in control animals and animals exposed to nicotine before or after this period. Animals showing a hypoactive response to nicotine lacked nicotinic low affinity binding sites in the cerebral cortex. Furthermore, neonatal exposure to nicotine affected learning and memory in adult animals, an effect that was time-dependent. This thesis also showed that neonatal exposure to nicotine increased adult susceptibility to a repeated exposure of nicotine, manifested as an even more pronounced effect in spontaneous behaviour after challenging doses of nicotine. In these animals the nicotinic receptors in the cerebral cortex, assayed by a-bungarotoxin, was decreased.

Neonatal exposure to nicotine was also shown to increase adult susceptibility to the organophosphate paraoxon, a known cholinergic agent, and to the brominated flame retardant 2,2´,4,4´,5-pentabromodiphenyl ether, a novel environmental agent, at adult age. This was seen at doses that did not affect behaviour in control animals, and was manifested as deranged spontaneous behaviour and reduced habituation, aberrations that also worsened with age.

The results indicate that differences in adult susceptibility to environmental pollutants are not necessarily an inherited condition. Rather they may well be acquired by low dose exposure to toxic agents during early life.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2003. 48 p.
Series
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Science and Technology, ISSN 1104-232X ; 907
Keyword
Biology, nicotine, neonatal development, behaviour, nicotinic receptors, susceptibility, cholinergic system, paraoxon, PBDE, Biologi
National Category
Biological Sciences
Identifiers
urn:nbn:se:uu:diva-3770 (URN)91-554-5800-9 (ISBN)
Public defence
2003-12-05, Lindahlsalen, EBC, Norbyv. 18A, Uppsala, 09:00
Opponent
Supervisors
Available from: 2003-11-11 Created: 2003-11-11Bibliographically approved

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Fredriksson, AndersEriksson, Per

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