Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 289, Issue 1, Pages H212-H219Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.01210.2004
Keywords
blood-brain barrier; mecamylamine; hexamethonium; nicotine; immunofluorescence microscopy
Funding
- NIDA NIH HHS [DA-11271] Funding Source: Medline
- NINDS NIH HHS [NS-42652, NS-039592] Funding Source: Medline
Ask authors/readers for more resources
Nicotine increases the permeability of the blood-brain barrier in vivo. This implies a possible role for nicotinic acetylcholine receptors in the regulation of cerebral microvascular permeability. Expression of nicotinic acetylcholine receptor subunits in cerebral microvessels was investigated with immunofluorescence microscopy. Positive immunoreactivity was found for receptor subunits alpha(3), alpha(5), alpha(7), and beta(2), but not subunits alpha(4), beta(3), or beta(4). Blood-brain barrier permeability was assessed via in situ brain perfusion with [C-14] sucrose. Nicotine increased the rate of sucrose entry into the brain from 0.3 +/- 0.1 to 1.1 +/- 0.2 mu l.g(-1).min(-1), as previously described. This nicotine-induced increase in blood-brain barrier permeability was significantly attenuated by both the blood-brain barrier-permeant nicotinic antagonist mecamylamine and the blood-brain barrier-impermeant nicotinic antagonist hexamethonium to 0.5 +/- 0.2 and 0.3 +/- 0.2 mu l.g(-1).min(-1), respectively. These data suggest that nicotinic acetylcholine receptors expressed on the cerebral microvascular endothelium mediate nicotine-induced changes in blood-brain barrier permeability.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available