This work is in memory of John Browning.
Neuronal and astrocyte expression of nicotinic receptor subunit β4 in the adult mouse brain†
Article first published online: 4 DEC 2003
Copyright © 2003 Wiley-Liss, Inc.
Journal of Comparative Neurology
Volume 468, Issue 3, pages 322–333, 12 January 2004
How to Cite
Gahring, L. C., Persiyanov, K. and Rogers, S. W. (2004), Neuronal and astrocyte expression of nicotinic receptor subunit β4 in the adult mouse brain. J. Comp. Neurol., 468: 322–333. doi: 10.1002/cne.10942
- Issue published online: 4 DEC 2003
- Article first published online: 4 DEC 2003
- Manuscript Accepted: 21 AUG 2003
- Manuscript Revised: 19 AUG 2003
- Manuscript Received: 1 MAY 2003
- National Institute of 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
- nicotinic receptors;
- mouse strains
Neuronal nicotinic acetylcholine receptor (nAChR) expression and function are customized in different brain regions through assembling receptors from closely related but genetically distinct subunits. Immunohistochemical analysis of one of these subunits, nAChRβ4, in the mouse brain suggests an extensive and potentially diverse role for this subunit in both excitatory and inhibitory neurotransmission. Prominent immunostaining included: 1) the medial habenula, efferents composing the fasciculus retroflexus, and the interpeduncular nucleus; 2) nuclei and ascending tracts of the auditory system inclusive of the medial geniculate; 3) the sensory cortex barrel field and cell bodies of the ventral thalamic nucleus; 4) olfactory-associated structures and the piriform cortex; and 5) sensory and motor trigeminal nuclei. In the hippocampus, nAChRβ4 staining was limited to dendrites and soma of a subset of glutamic acid dehydrogenase-positive neurons. In C57BL/6 mice, but to a lesser extent in C3H/J, CBA/J, or CF1 mice, a subpopulation of astrocytes in the hippocampal CA1 region prominently expressed nAChRβ4 (and nAChRα4). Collectively, these results suggest that the unique functional and pharmacological properties exerted by nAChRβ4 on nAChR function could modify and specialize the development of strain-specific sensory and hippocampal-related characteristics of nicotine sensitivity including the development of tolerance. J. Comp. Neurol. 468:322–333, 2004. © 2003 Wiley-Liss, Inc.