Calcium and olfactory transduction

Current recording from sensory cilia of olfactory receptor cells in situ. II. Role of mucosal Na+, K+, and Ca2+ ions.

“…Our results match the findings of Nakamura and Gold (1987), who demonstrated that mucosal Ca 2+ blocks the nucleotide-activated conductance, and those of Kurahashi (1989) and Kurahashi and Shibuya (1990), who found a 4.5-fold increase of odorant-induced inward current in newt ORCs when extracellular Ca 2+ was removed. Our results are, however, at variance with several EOG studies which suggested that Ca 2÷ is the charge carrier of the receptor current (Suzuki, 1978;Winegar et al, 1988;Leveteau et al, 1989). In these studies it was usually observed that EOG responses to odorants were greatly diminished when mucosal Ca 2+ was removed.…”

Current recording from sensory cilia of olfactory receptor cells in situ. II. Role of mucosal Na+, K+, and Ca2+ ions.

“…Our results match the findings of Nakamura and Gold (1987), who demonstrated that mucosal Ca 2+ blocks the nucleotide-activated conductance, and those of Kurahashi (1989) and Kurahashi and Shibuya (1990), who found a 4.5-fold increase of odorant-induced inward current in newt ORCs when extracellular Ca 2+ was removed. Our results are, however, at variance with several EOG studies which suggested that Ca 2÷ is the charge carrier of the receptor current (Suzuki, 1978;Winegar et al, 1988;Leveteau et al, 1989). In these studies it was usually observed that EOG responses to odorants were greatly diminished when mucosal Ca 2+ was removed.…”

Olfactory transduction: cross-talk between second-messenger systems

“…Previous models of olfactory transduction have focused on activation of adenylate cyclase by odorants without considering a role for calcium (Lancet & Pace, 1987; Gold . Our demonstration that calcium at physiological concentrations activates this enzyme through calmodulin via a GTP-dependent and a GTP-independent mechanism suggests a role for calcium in regulation of the olfactory adenylate Trotier Winegar et al, 1988;Schild, 1989), possibly through odorant-gated cation channels (Labarca et al, 1988) or as a result of other transduction processes such as phosphatidylinositol hydrolysis. Subsequent formation of a calcium/calmodulin complex (shown as a circle containing four stars; c designates calmodulin) is followed by activation of the olfactory adenylate cyclase.…”

“…However, the specificity of this inhibition is difficult to assess, since calmidazolium inhibited forskolinactivated enzyme activity in a similar manner (data not shown). Inhibition of the electroolfactogram by the calmodulin antagonists trifluoperazine, chlorpromazine, and N-(6aminohexyl)-5-chloro-1 -naphthalenesulfonamide (W-7) has been observed, but these effects were hard to interpret, since in these experiments the inhibitory potencies of these compounds did not correlate with their potencies as calmodulin antagonists, possibly due to nonspecific membrane effects (Winegar et al, 1988).…”

“…cyclase and underscores the importance of cross-talk between second-messenger systems in olfactory transduction. We suggest that odorants at physiological concentrations may cause mobilization of calcium (Trotier, 1986;Winegar et al, 1988) which then leads to a rise in intracellular cyclic AMP levels via the formation of a calcium/calmodulin complex (Figure 4). Only at high micromolar concentrations of odorants would the calcium pathway be bypassed by direct activation of the olfactory adenylate cyclase (Figure 4; Pace et al, 1985;Sklar et al, 1986;Shirley et al, 1986).…”

Calcium‐dependent behavioural responses to acute copper exposure in Oncorhynchus mykiss

“…High Cu concentrations are suggested to impair the function of the olfactory organ, e.g. by blocking or interfering with Ca-binding sites, which may be important for the initiation of the EOG response (Suzuki, 1978;Winegar et al, 1988;Restrepo et al, 1990). Increasing the surrounding Ca concentration, however, could potentially decrease Cu-induced olfactory impairment (Bjerselius et al, 1993), but whether such an effect exists is unclear (Bjerselius et al, 1993;McIntyre et al, 2008a, b;Green et al, 2010;Meyer & Adams, 2010).…”

Current recording from sensory cilia of olfactory receptor cells in situ. II. Role of mucosal Na+, K+, and Ca2+ ions.

“…Our results match the findings of Nakamura and Gold (1987), who demonstrated that mucosal Ca 2+ blocks the nucleotide-activated conductance, and those of Kurahashi (1989) and Kurahashi and Shibuya (1990), who found a 4.5-fold increase of odorant-induced inward current in newt ORCs when extracellular Ca 2+ was removed. Our results are, however, at variance with several EOG studies which suggested that Ca 2÷ is the charge carrier of the receptor current (Suzuki, 1978;Winegar et al, 1988;Leveteau et al, 1989). In these studies it was usually observed that EOG responses to odorants were greatly diminished when mucosal Ca 2+ was removed.…”

Olfactory transduction: cross-talk between second-messenger systems

“…Previous models of olfactory transduction have focused on activation of adenylate cyclase by odorants without considering a role for calcium (Lancet & Pace, 1987; Gold . Our demonstration that calcium at physiological concentrations activates this enzyme through calmodulin via a GTP-dependent and a GTP-independent mechanism suggests a role for calcium in regulation of the olfactory adenylate Trotier Winegar et al, 1988;Schild, 1989), possibly through odorant-gated cation channels (Labarca et al, 1988) or as a result of other transduction processes such as phosphatidylinositol hydrolysis. Subsequent formation of a calcium/calmodulin complex (shown as a circle containing four stars; c designates calmodulin) is followed by activation of the olfactory adenylate cyclase.…”

“…However, the specificity of this inhibition is difficult to assess, since calmidazolium inhibited forskolinactivated enzyme activity in a similar manner (data not shown). Inhibition of the electroolfactogram by the calmodulin antagonists trifluoperazine, chlorpromazine, and N-(6aminohexyl)-5-chloro-1 -naphthalenesulfonamide (W-7) has been observed, but these effects were hard to interpret, since in these experiments the inhibitory potencies of these compounds did not correlate with their potencies as calmodulin antagonists, possibly due to nonspecific membrane effects (Winegar et al, 1988).…”

“…cyclase and underscores the importance of cross-talk between second-messenger systems in olfactory transduction. We suggest that odorants at physiological concentrations may cause mobilization of calcium (Trotier, 1986;Winegar et al, 1988) which then leads to a rise in intracellular cyclic AMP levels via the formation of a calcium/calmodulin complex (Figure 4). Only at high micromolar concentrations of odorants would the calcium pathway be bypassed by direct activation of the olfactory adenylate cyclase (Figure 4; Pace et al, 1985;Sklar et al, 1986;Shirley et al, 1986).…”

Calcium‐dependent behavioural responses to acute copper exposure in Oncorhynchus mykiss

“…High Cu concentrations are suggested to impair the function of the olfactory organ, e.g. by blocking or interfering with Ca-binding sites, which may be important for the initiation of the EOG response (Suzuki, 1978;Winegar et al, 1988;Restrepo et al, 1990). Increasing the surrounding Ca concentration, however, could potentially decrease Cu-induced olfactory impairment (Bjerselius et al, 1993), but whether such an effect exists is unclear (Bjerselius et al, 1993;McIntyre et al, 2008a, b;Green et al, 2010;Meyer & Adams, 2010).…”

Current recording from sensory cilia of olfactory receptor cells in situ. II. Role of mucosal Na+, K+, and Ca2+ ions.

“…Our results match the findings of Nakamura and Gold (1987), who demonstrated that mucosal Ca 2+ blocks the nucleotide-activated conductance, and those of Kurahashi (1989) and Kurahashi and Shibuya (1990), who found a 4.5-fold increase of odorant-induced inward current in newt ORCs when extracellular Ca 2+ was removed. Our results are, however, at variance with several EOG studies which suggested that Ca 2÷ is the charge carrier of the receptor current (Suzuki, 1978;Winegar et al, 1988;Leveteau et al, 1989). In these studies it was usually observed that EOG responses to odorants were greatly diminished when mucosal Ca 2+ was removed.…”

Olfactory transduction: cross-talk between second-messenger systems

“…Previous models of olfactory transduction have focused on activation of adenylate cyclase by odorants without considering a role for calcium (Lancet & Pace, 1987; Gold . Our demonstration that calcium at physiological concentrations activates this enzyme through calmodulin via a GTP-dependent and a GTP-independent mechanism suggests a role for calcium in regulation of the olfactory adenylate Trotier Winegar et al, 1988;Schild, 1989), possibly through odorant-gated cation channels (Labarca et al, 1988) or as a result of other transduction processes such as phosphatidylinositol hydrolysis. Subsequent formation of a calcium/calmodulin complex (shown as a circle containing four stars; c designates calmodulin) is followed by activation of the olfactory adenylate cyclase.…”

“…However, the specificity of this inhibition is difficult to assess, since calmidazolium inhibited forskolinactivated enzyme activity in a similar manner (data not shown). Inhibition of the electroolfactogram by the calmodulin antagonists trifluoperazine, chlorpromazine, and N-(6aminohexyl)-5-chloro-1 -naphthalenesulfonamide (W-7) has been observed, but these effects were hard to interpret, since in these experiments the inhibitory potencies of these compounds did not correlate with their potencies as calmodulin antagonists, possibly due to nonspecific membrane effects (Winegar et al, 1988).…”

“…cyclase and underscores the importance of cross-talk between second-messenger systems in olfactory transduction. We suggest that odorants at physiological concentrations may cause mobilization of calcium (Trotier, 1986;Winegar et al, 1988) which then leads to a rise in intracellular cyclic AMP levels via the formation of a calcium/calmodulin complex (Figure 4). Only at high micromolar concentrations of odorants would the calcium pathway be bypassed by direct activation of the olfactory adenylate cyclase (Figure 4; Pace et al, 1985;Sklar et al, 1986;Shirley et al, 1986).…”

Calcium‐dependent behavioural responses to acute copper exposure in Oncorhynchus mykiss

“…High Cu concentrations are suggested to impair the function of the olfactory organ, e.g. by blocking or interfering with Ca-binding sites, which may be important for the initiation of the EOG response (Suzuki, 1978;Winegar et al, 1988;Restrepo et al, 1990). Increasing the surrounding Ca concentration, however, could potentially decrease Cu-induced olfactory impairment (Bjerselius et al, 1993), but whether such an effect exists is unclear (Bjerselius et al, 1993;McIntyre et al, 2008a, b;Green et al, 2010;Meyer & Adams, 2010).…”