Abstract
A single 17β-oestradiol (E(2)) treatment reduces the loss in cholinergic fibre density in the cortex after NMDA lesion into the nucleus basalis magnocellularis (NBM) of the basal forebrain (BF) in young female mice. In the present study, we examined whether age influences this protective effect of E(2) on cholinergic neurones in male and female mice. Gonad-intact young and aged animals of both sexes were treated with E(2) after unilateral NMDA lesion into the NBM. NMDA lesion elicited ipsilateral cholinergic cell loss in the NBM and ipsilateral fibre loss in the somatosensory cortex to the same extent, irrespective of age or sex. A single E(2) injection performed 1 h post-lesion did not affect the cholinergic cell loss but reduced the loss of fibres in the ipsilateral cortex in young male and female mice. By contrast, E(2) did not have an effect on the NMDA-induced cholinergic cell and fibre loss in aged male or female mice. The oestrous stage of young female mice did not alter the number of cholinergic cells/fibres or the protective effect of E(2) on cholinergic fibres after NMDA injection. Our results show that E(2) has a protective action on BF cholinergic fibres in young males and females, although the treatment potential of E(2) declines with age.
Original language | English |
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Pages (from-to) | 1243-1248 |
Number of pages | 6 |
Journal | Journal of Neuroendocrinology |
Volume | 24 |
Issue number | 9 |
Early online date | 25 Apr 2012 |
DOIs | |
Publication status | Published - 1 Sept 2012 |
Bibliographical note
© 2012 The Authors. Journal of Neuroendocrinology © 2012 British Society for Neuroendocrinology.Keywords
- Aging/drug effects
- Animals
- Basal Nucleus of Meynert/drug effects
- Cell Death/drug effects
- Cholinergic Neurons/drug effects
- Disease Models, Animal
- Estradiol/administration & dosage
- Estrous Cycle/drug effects
- Female
- Male
- Mice
- Mice, Inbred C57BL
- Microinjections
- Molecular Imaging/methods
- N-Methylaspartate
- Nerve Degeneration/chemically induced
- Neural Pathways/drug effects
- Neuroprotective Agents/pharmacology
- Somatosensory Cortex/drug effects