This work is in memory of John Browning.
Mouse strain-specific nicotinic acetylcholine receptor expression by inhibitory interneurons and astrocytes in the dorsal hippocampus†
Article first published online: 4 DEC 2003
Copyright © 2003 Wiley-Liss, Inc.
Journal of Comparative Neurology
Volume 468, Issue 3, pages 334–346, 12 January 2004
How to Cite
Gahring, L. C., Persiyanov, K., Dunn, D., Weiss, R., Meyer, E. L. and Rogers, S. W. (2004), Mouse strain-specific nicotinic acetylcholine receptor expression by inhibitory interneurons and astrocytes in the dorsal hippocampus. J. Comp. Neurol., 468: 334–346. doi: 10.1002/cne.10943
- Issue published online: 4 DEC 2003
- Article first published online: 4 DEC 2003
- Manuscript Accepted: 21 AUG 2003
- Manuscript Revised: 2 JUL 2003
- Manuscript Received: 1 MAY 2003
- National Institute on Drug Abuse (NIDA). Grant Number: DA015148
- National Institute on Aging. Grant Number: AG17517
- NIDA/ National Heart, Blood, and Lung Institute. Grant Number: PO1 HL72903
- Val A. Browning Foundation
- mouse strains;
- nicotinic receptors;
The response by individuals to nicotine is likely to reflect the interaction of this compound with target nAChRs. However, resolving how different genetic backgrounds contribute to unique mouse strain-specific responses to this compound remains an important and unresolved issue. To examine this question in detail, expression of the nicotine acetylcholine receptor (nAChR) subunits α3, α4, α5, α7, β2, and β4 was measured in the dorsal hippocampus using immunohistochemistry in mouse strains or lines BALB/c, C3H/J, C57BL/6, CBA/J, DBA/2, Long Sleep (LS), Short Sleep (SS), and CF1. The nAChRs in all mice colocalized with glutamic acid decarboxylase (GAD)-positive interneurons that were subclassified into at least four groups based on nAChR subunit heterogeneity. A notable difference between mouse strains was the expression of nAChRs by astrocyte subpopulations in CA1 subregions whose numbers vary inversely with nAChR-immunostained neurons. This novel relationship also correlated with published parameters of strain sensitivity to nicotine. Attempts to identify the origin of this significant difference in nAChR expression among strains included comparison of the entire nAChRα4 gene sequence. Although multiple polymorphisms were identified, including two that changed nAChRα4 amino acid coding, none of these clearly correlate with strain-related differences in cell type-specific nAChR expression. These findings suggest that mouse strain-specific behavioral and physiological responses to nicotine are likely to be a reflection of a complex interplay between genetic factors that shape differences in expression and cellular architecture of this modulatory neurotransmitter system in the mammalian nervous system. J. Comp. Neurol. 468:334–346, 2004. © 2003 Wiley-Liss, Inc.