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Tetrahydroaminoacridine (THA) reduces voltage-dependent calcium currents in rat sensory neurons

Authors :
Department of Neurology, University of Michigan Medical Center, Ann Arbor, Michigan 48109, U.S.A.
Department of Physiology, University of Michigan Medical Center, Ann Arbor, Michigan 48109, U.S.A.; Department of Neurology, University of Michigan Medical Center, Ann Arbor, Michigan 48109, U.S.A.
Kelly, Kevin M.
Gross, Robert A.
Macdonald, Robert L.
Department of Neurology, University of Michigan Medical Center, Ann Arbor, Michigan 48109, U.S.A.
Department of Physiology, University of Michigan Medical Center, Ann Arbor, Michigan 48109, U.S.A.; Department of Neurology, University of Michigan Medical Center, Ann Arbor, Michigan 48109, U.S.A.
Kelly, Kevin M.
Gross, Robert A.
Macdonald, Robert L.
Publication Year :
2006

Abstract

Tetrahydroaminoacridine (THA) is a centrally active anticholinesterase that also interacts with neuronal K+ and Na+ channels and cardiac Ca2+ channels. The effects of THA on neuronal voltage-dependent Ca2+ channels are not known. We tested the effects of THA (25 nM-250 [mu]M) on the Ca2+ current components of acutely dissociated rat nodose ganglion and dorsal root ganglion (DRG) neurons using the whole cell patch clamp recording technique. THA reduced the low-threshold (T) and high-threshold (N/L) Ca2+ current components in a concentration-dependent manner (IC50 [congruent with] 125 [mu]M for T; [congruent with] 80 [mu]M for (N/L). Minimal current reduction was seen below ~ 10 [mu]M. Our results show that THA reduces voltage-dependent Ca2+ currents in rodent sensory neurons suggesting another means by which THA may affect Ca2+-dependent physiologic processes.

Details

Database :
OAIster
Notes :
En_US
Publication Type :
Electronic Resource
Accession number :
edsoai.ocn894059293
Document Type :
Electronic Resource