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1 Department of Anatomy and Cell Biology, College of Physicians and Surgeons, Columbia University and 2 Department of Neuroscience, New York State Psychiatric Institute, New York, New York 10032; and 3 Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20892
The actions of
enteric 5-HT are terminated by 5-HT transporter (SERT)-mediated uptake,
and gastrointestinal motility is abnormal in SERT 
/ mice. We tested
the hypothesis that adaptive changes in enteric 5-HT3
receptors help SERT / mice survive despite inefficient 5-HT
inactivation. Expression of mRNA encoding enteric 5-HT3A
subunits was similar in SERT +/+ and / mice, but that of
5-HT3B subunits was fourfold less in SERT / mice.
5-HT3B mRNA was found, by in situ hybridization, in
epithelial cells and enteric neurons. 5-HT evoked a fast inward current
in myenteric neurons that was pharmacologically identified as
5-HT3 mediated. The EC50 of the 5-HT response
was lower in SERT +/+ (18 µM) than in SERT / (36 µM) mice and
desensitized rapidly in a greater proportion of SERT / neurons;
however, peak amplitudes, steady-state current, and decay time
constants were not different. Adaptive changes thus occur in the
subunit composition of enteric 5-HT3 receptors of SERT
/ mice that are reflected in 5-HT3 receptor affinity
and desensitization.
serotonin receptors; small intestine; enteric nervous system; electrophysiology
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