Characterization of Forskolin-Induced Ca2+ Signals in Rat Olfactory Receptor Neurons

Forskolin-induced Ca2+ signals were examined in isolated rat olfactory receptor neurons (ORNs) using a Ca2+ indicator, fura-2. In the soma of the ORNs, forskolin caused an increase in the intracellular Ca2+ concentration ([Ca2+]i) that was enhanced by a phosphodiesterase (PDE) 1 inhibitor, 8-methoxy...

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Main Authors: Ken-ichi Otsuguro, Shree Hari Gautam, Shigeo Ito, Yoshiaki Habara, Toshiyuki Saito
Format: Article
Language:English
Published: Elsevier 2005-01-01
Series:Journal of Pharmacological Sciences
Online Access:http://www.sciencedirect.com/science/article/pii/S1347861319322339
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author Ken-ichi Otsuguro
Shree Hari Gautam
Shigeo Ito
Yoshiaki Habara
Toshiyuki Saito
author_facet Ken-ichi Otsuguro
Shree Hari Gautam
Shigeo Ito
Yoshiaki Habara
Toshiyuki Saito
author_sort Ken-ichi Otsuguro
collection DOAJ
description Forskolin-induced Ca2+ signals were examined in isolated rat olfactory receptor neurons (ORNs) using a Ca2+ indicator, fura-2. In the soma of the ORNs, forskolin caused an increase in the intracellular Ca2+ concentration ([Ca2+]i) that was enhanced by a phosphodiesterase (PDE) 1 inhibitor, 8-methoxymethyl-3-isobutyl-1-methyl-xanthine, but not a PDE4 inhibitor, rolipram. Forskolin-induced Ca2+ signals were abolished with the removal of extracellular Ca2+ and un-affected by treatment with thapsigargin or caffeine plus ryanodine. Niflumic acid, a Ca2+-activated Cl- channel inhibitor, or nifedipine, an L-type Ca2+ channel inhibitor, slowed the initial rate of the increase in [Ca2+]i in response to forskolin. Nifedipine did not affect the increase in [Ca2+]i that was slowed by niflumic acid. In Ca2+ measurements with a confocal microscope and a calcium indicator, Fluo-4, the onset of the response to forskolin in the knob region occurred simultaneously or earlier, but not later, than that in the soma. It is suggested that the forskolin-induced Ca2+ signals are due to Ca2+ influx, but not the release of Ca2+ from Ca2+ stores, and that the initial rapid increase in [Ca2+]i is associated with the activation of the voltage-dependent Ca2+ channels in rat ORNs. Keywords:: olfactory receptor neuron, forskolin, Ca2+ signal, phosphodiesterase, Ca2+ channel
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spelling doaj.art-f418a07c6d2c459f9e1d1af58f3e834e2022-12-22T00:58:23ZengElsevierJournal of Pharmacological Sciences1347-86132005-01-01974510518Characterization of Forskolin-Induced Ca2+ Signals in Rat Olfactory Receptor NeuronsKen-ichi Otsuguro0Shree Hari Gautam1Shigeo Ito2Yoshiaki Habara3Toshiyuki Saito4Laboratory of Pharmacology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan; Corresponding author. FAX: +81-11-706-5220 E-mail: otsuguro@vetmed.hokudai.ac.jpLaboratory of Physiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, JapanLaboratory of Pharmacology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, JapanLaboratory of Physiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, JapanAnimal Neurophysiology Laboratory, National Institute of Agrobiological Sciences, Tsukuba 305-0901, JapanForskolin-induced Ca2+ signals were examined in isolated rat olfactory receptor neurons (ORNs) using a Ca2+ indicator, fura-2. In the soma of the ORNs, forskolin caused an increase in the intracellular Ca2+ concentration ([Ca2+]i) that was enhanced by a phosphodiesterase (PDE) 1 inhibitor, 8-methoxymethyl-3-isobutyl-1-methyl-xanthine, but not a PDE4 inhibitor, rolipram. Forskolin-induced Ca2+ signals were abolished with the removal of extracellular Ca2+ and un-affected by treatment with thapsigargin or caffeine plus ryanodine. Niflumic acid, a Ca2+-activated Cl- channel inhibitor, or nifedipine, an L-type Ca2+ channel inhibitor, slowed the initial rate of the increase in [Ca2+]i in response to forskolin. Nifedipine did not affect the increase in [Ca2+]i that was slowed by niflumic acid. In Ca2+ measurements with a confocal microscope and a calcium indicator, Fluo-4, the onset of the response to forskolin in the knob region occurred simultaneously or earlier, but not later, than that in the soma. It is suggested that the forskolin-induced Ca2+ signals are due to Ca2+ influx, but not the release of Ca2+ from Ca2+ stores, and that the initial rapid increase in [Ca2+]i is associated with the activation of the voltage-dependent Ca2+ channels in rat ORNs. Keywords:: olfactory receptor neuron, forskolin, Ca2+ signal, phosphodiesterase, Ca2+ channelhttp://www.sciencedirect.com/science/article/pii/S1347861319322339
spellingShingle Ken-ichi Otsuguro
Shree Hari Gautam
Shigeo Ito
Yoshiaki Habara
Toshiyuki Saito
Characterization of Forskolin-Induced Ca2+ Signals in Rat Olfactory Receptor Neurons
Journal of Pharmacological Sciences
title Characterization of Forskolin-Induced Ca2+ Signals in Rat Olfactory Receptor Neurons
title_full Characterization of Forskolin-Induced Ca2+ Signals in Rat Olfactory Receptor Neurons
title_fullStr Characterization of Forskolin-Induced Ca2+ Signals in Rat Olfactory Receptor Neurons
title_full_unstemmed Characterization of Forskolin-Induced Ca2+ Signals in Rat Olfactory Receptor Neurons
title_short Characterization of Forskolin-Induced Ca2+ Signals in Rat Olfactory Receptor Neurons
title_sort characterization of forskolin induced ca2 signals in rat olfactory receptor neurons
url http://www.sciencedirect.com/science/article/pii/S1347861319322339
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