In:
European Journal of Neuroscience, Wiley, Vol. 16, No. 9 ( 2002-11), p. 1633-1646
Abstract:
It is well established that exposure of experimental animals to nicotine results in upregulation of the α4β2‐subtype of neuronal nicotinic acetylcholine receptors (nAChRs). The aim of this study was to determine the effect of nicotine on the levels of α7‐nAChRs in rat brain, for which only partial information is available. Rats were infused with nicotine (3 mg/kg/day) or saline for 2 weeks and their brains processed for receptor autoradiography with [ 3 H]methyllycaconitine (MLA), a radioligand with nanomolar affinity for α7‐nAChRs. In control rats binding was high in hippocampus, intermediate in cerebral cortex and hypothalamus, and low in striatum, thalamus and cerebellum. There was high correlation between the distribution of [ 3 H]MLA binding sites and α7 subunit mRNA ( r = 0.816). With respect to saline‐treated controls, nicotine‐treated rats presented higher [ 3 H]nicotine binding in 11 out of 15 brain regions analysed (average increase 46 ± 6%). In contrast, only four regions showed greater [ 3 H]MLA binding, among which the ventral tegmental area (VTA) and cingulate cortex (mean increase 32 ± 3%). No changes in α7 mRNA levels were observed after nicotine treatment. Similarly, there was no variation of α6 subunit transcript in the VTA, a region which may contain MLA‐sensitive (non‐α7)‐α6*‐nAChRs ( Klink et al ., 2001 ). In conclusion, nicotine increased [ 3 H]MLA binding, although to a smaller extent and in a more restricted regional pattern than [ 3 H]nicotine. The enhancement of binding was not paralleled by a significant change of α7 and α6 subunit transcription. Finally, the present results provide the first anatomical description of the distribution of [ 3 H]MLA binding sites in rat brain.
Type of Medium:
Online Resource
ISSN:
0953-816X
,
1460-9568
DOI:
10.1046/j.1460-9568.2002.02220.x
Language:
English
Publisher:
Wiley
Publication Date:
2002
detail.hit.zdb_id:
2005178-5
SSG:
12
