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The reducing agent dithiothreitol (DTT) does not abolish the inhibitory nicotinic response recorded from rat dorsolateral septal neuronsPrevious intracellular recordings have demonstrated that dorsolateral septal nucleus (DLSN) neurons express a novel nicotinic receptor which produces a direct membrane hyperpolarization when activated by nicotinic agonists. Activation of the classical excitatory nicotinic receptors has been shown to require a disulfide bond involving the cysteines at positions 192 and 193 of the alpha subunits of the receptor. Reduction of this cystine bond with dithiothreitol (DTT) abolishes agonist activation of excitatory nicotinic receptors. We have now examined whether DTT treatment of the inhibitory nicotinic receptor on DLSN neurons also abolishes the inhibitory nicotinic response. We find that the inhibitory response persists after treatment of the neurons with 1 mM DTT, even if the reduction is followed by alkylation of the receptor with bromoacetylcholine to prevent possible reformation of disulfide bonds. This result suggests that the agonist binding site on the inhibitory nicotinic receptor does not require an intact disulfide bond, similar to the bond on the alpha subunit of the excitatory nicotinic receptor, for agonist activation of the receptor. Some of these results have been previously reported in abstract form.
Document ID
20050000487
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Sorenson, E. M.
(University of Texas Medical Branch Galveston 77555-1031)
Gallagher, J. P.
Date Acquired
August 22, 2013
Publication Date
April 2, 1993
Publication Information
Publication: Neuroscience letters
Volume: 152
Issue: 1-2
ISSN: 0304-3940
Subject Category
Aerospace Medicine
Distribution Limits
Public
Copyright
Other
Keywords
NASA Discipline Number 16-10
Non-NASA Center
NASA Discipline Neuroscience
NASA Program Space Physiology and Countermeasures

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