Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the 02-subunit of the nicotinic acetylcholine receptor (beta2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta2-/- mice a 43% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.

Alteration of hippocampal cell proliferation in mice lacking the beta(2) subunit of the neuronal nicotinic acetylcholine receptor / A., Harrist; R. D., Beech; S. L., King; Zanardi, Alessio; M. A., Cleary; B. J., Caldarone; A., Eisch; Zoli, Michele; M. R., Picciotto. - In: SYNAPSE. - ISSN 0887-4476. - STAMPA. - 54:(2004), pp. 200-206.

Alteration of hippocampal cell proliferation in mice lacking the beta(2) subunit of the neuronal nicotinic acetylcholine receptor

ZANARDI, Alessio;ZOLI, Michele;
2004

Abstract

Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the 02-subunit of the nicotinic acetylcholine receptor (beta2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta2-/- mice a 43% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.
54
200
206
Alteration of hippocampal cell proliferation in mice lacking the beta(2) subunit of the neuronal nicotinic acetylcholine receptor / A., Harrist; R. D., Beech; S. L., King; Zanardi, Alessio; M. A., Cleary; B. J., Caldarone; A., Eisch; Zoli, Michele; M. R., Picciotto. - In: SYNAPSE. - ISSN 0887-4476. - STAMPA. - 54:(2004), pp. 200-206.
A., Harrist; R. D., Beech; S. L., King; Zanardi, Alessio; M. A., Cleary; B. J., Caldarone; A., Eisch; Zoli, Michele; M. R., Picciotto
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

Caricamento pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11380/303395
Citazioni
  • ???jsp.display-item.citation.pmc??? 24
  • Scopus 72
  • ???jsp.display-item.citation.isi??? 63
social impact