Photoreceptor excitation and adaptation by inositol 1,4,5-trisphosphate

Fein, Alan M.; Payne, Richard; Dw, Corson; Mj, Berridge; Rf, Irvine

doi:10.1038/311157a0

Cited by 325 publications

(201 citation statements)

References 22 publications

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“…GTP-␥-S was obtained from Sigma, dissolved into a 1 mM stock solution, and kept at Ϫ70°C. For excitation by InsP 3 , 10 or 100 M InsP 3 in carrier solution was pulse pressure injected into the light-sensitive rhabdomeral lobe of the photoreceptor as described by Fein et al (1984). For activation of G-proteins, 100 M GTP-␥-S in carrier solution was pressure injected into the cell.…”

Section: Methodsmentioning

confidence: 99%

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Protein Kinase C Activators Inhibit the Visual Cascade inLimulusVentral Photoreceptors at an Early Stage

Dabdoub

Payne

1999

J. Neurosci.

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The phosphoinositide cascade mediates visual transduction in invertebrate photoreceptors. Phospholipase C (PLC) catalyzes the hydrolysis of phosphatidylinositol bisphosphate, producing inositol trisphosphate (InsP 3 ) and diacylglycerol (DAG). Protein kinase C (PKC) is a major target of DAG in many cell types. We have used PKC activators to investigate the function of the kinase in the phototransduction cascade in Limulus polyphemus ventral photoreceptors. Extracellular application of (Ϫ)-indolactam V (0.03-30 M) or phorbol-12,13-dibutyrate (10 M) reversibly reduced the sensitivity of the electrical response of the photoreceptors to light by up to 1000-fold. The inert stereoisomer (ϩ)-indolactam V and 4␣-phorbol had no effect. The effect of (Ϫ)-indolactam V was antagonized by the PKC inhibitors bisindolylmaleimide I and Gö 6976. Coapplication of bisindolylmaleimide V, used as a negative control compound for PKC inhibition, did not reduce the effectiveness of (Ϫ)-indolactam V. These findings are consistent with (Ϫ)-indolactam V activating PKC and desensitizing the light response. Furthermore, our pharmacological results indicate that PKC activation does not appear to play a role in light adaptation. We localized the position of the target of PKC in the visual cascade. We chemically excited the cascade at various stages to determine the kinase's target. PKC activation by (Ϫ)-indolactam V decreased the light-induced elevation of intracellular calcium but had no effect on the photoreceptor's excitatory response to intracellular injection of InsP 3 . However, the PKC activator greatly reduced the excitation caused by GTP-␥-S injection. We propose that PKC inhibits the visual transduction cascade at the G-protein and/or PLC stage.

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Section: Methodsmentioning

confidence: 99%

“…Dabdoub and R. Payne, unpublished observations). Second, light adaptation desensitizes the cell's response to InsP 3 (Fein et al, 1984), whereas (Ϫ)-indolactam V does not (Fig. 6 B).…”

Section: Pkc Activators Do Not Mimic Light Adaptation Nor Do Pkc Inhmentioning

confidence: 99%

Protein Kinase C Activators Inhibit the Visual Cascade inLimulusVentral Photoreceptors at an Early Stage

Dabdoub

Payne

1999

J. Neurosci.

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“…Inositol 1,4,5 trisphosphate (InsP3) is thought to mediate the release of Ca from intracellular stores that occurs when Limulus photoreceptors are illuminated (Brown, Rubin, Ghalayini, Tarver, Irvine, Berridge, and Anderson, 1984;Fein, Payne, Corson, Berridge, and Irvine, 1984). Because of their large size, InsP3 can be directly injected into Limulus photoreceptors.…”

Section: Introductionmentioning

confidence: 99%

A lingering elevation of Cai accompanies inhibition of inositol 1,4,5 trisphosphate-induced Ca release in Limulus ventral photoreceptors.

Levy

Payne

1993

The Journal of General Physiology

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Injection of inositol 1,4,5 trisphosphate (ImPs) into Limulus ventral photoreceptors causes an elevation of intracellular free Ca concentration (Cai) and depolarizes the photoreceptors. When measured with the photoprotein aequorin, the InsPs-induced Cai increase follows the time course of depolarization and declines within 1-2 s. However, sensitivity to further injections of InsP3 remains suppressed for several tens of seconds. The possibility that the suppression of Ca release (feedback inhibition) is due to a small lingering elevation of Cai, below the existing detection limit of aequorin, was investigated by measuring Cai with Ca-sensitive electrodes. Double-barreled, Ca-selective microelectrodes were used to pressure inject InsPs and measure Cai at the same point. Light or InsPs injections into the light-sensitive compartment depolarized the photoreceptors and induced an elevation of Cai that persisted for tens of seconds. Injections of InsP3 during the decay of Cai showed that sensitivity to InsP3 recovered as resting Cai approached the prestimulus level. The relationship between elevated Cai and feedback inhibition was very steep. An elevation of Cai of 1 o.M or more was associated with inhibitions of 79 +-12.4% (SEM; n = 7) for the InsP~-induced Cai increase and of 76 ± 8% for depolarizations. With a residual Cai elevation of 0.01 o.M or less, the mean inhibition was 10 ± 7.4% for InsPs-induced Cai increase and 6.6 ± 4% for InsPz-induced depolarization. Injections of InsP3 into a light-insensitive compartment within the cell induced elevations of Cai with no associated depolarizations or feedback inhibition. To verify that a sustained elevation of Ca i is necessary for inhibition of InsPz-induced Cai increase and depolarization, we injected ethyleneglycol-bis-(13-aminoethylether)-N,N'-tetraacetic acid (EGTA) between two injections of InsP3. Injection of 1 mM EGTA or the related Ca chelator BAPTA, delivered 750 ms after the first injection of InsPs, restored the peak depolarization caused by the second injection of InsP3 to > 80 ± 3% of control, compared with 13 ± 8% without an intervening injection of EGTA. Measurement of Cai with aequorin showed that an intervening injection of EGTA partially restored the InsP3-induced Ca i increase.

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“…In many cell systems, it seems likely that these two messenger substances synergistically activate cells by the mobilization of intracellular Ca*+ and the activation of protein kinase C, which are mediated by inositol trisphosphate and diacylglycerol, respectively [ 10,191. Furthermore, inositol trisphosphate has been reported to provoke electrophysiological responses in ventral photoreceptors of Limulus [20,21] and in Xenopus oocytes [22] and to enhance protein phosphorylation in a variety of cells [23,24]. It thus appears that the Ca*+-independent phosphodiesteratic hydrolysis of PI-4,5-P* is the initial event which links bradykinin-receptor interaction to the neuronal activities in NG108-15 cells.…”

Section: Resultsmentioning

confidence: 99%

Evidence for a Ca²⁺‐independent hydrolysis of phosphatidylinositol 4,5‐bisphosphate in neuron‐like cell line NG108‐15 cells

1985

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The addition of bradykinin to 32P-labeled neuroblastoma x glioma hybrid NGlOS-15 cells caused a sub-, stantial loss of radioactivity from phosphatidylinositol 4,5-bisphosphate (PI-4,5-P,). The bradykinin-induced hydrolysis of PI-4,5-P, was almost equally observed even when extracellular Ca2+ was depleted with EGTA (1OOpM). On the other hand, high K+ depolarization of the cells, which allows Caz+ influx through voltage-dependent CaZ+ channels, failed to induce any significant decrease in the radioactivity of PI-4,5-P,. These data indicate that the bradykinin-stimulated PI-4,5-P, hydrolysis in NGlO&15 cells is independent of extracellular Ca2+ and also that PI-4,5-P, hydrolysis is not stimulated by an elevation of intracellular Ca2+ concentration. Neuroblastoma x glioma BradykininPotassium depolarization Phosphoinositide Calcium

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Photoreceptor excitation and adaptation by inositol 1,4,5-trisphosphate

Cited by 325 publications

References 22 publications

Protein Kinase C Activators Inhibit the Visual Cascade inLimulusVentral Photoreceptors at an Early Stage

Protein Kinase C Activators Inhibit the Visual Cascade inLimulusVentral Photoreceptors at an Early Stage

A lingering elevation of Cai accompanies inhibition of inositol 1,4,5 trisphosphate-induced Ca release in Limulus ventral photoreceptors.

Evidence for a Ca²⁺‐independent hydrolysis of phosphatidylinositol 4,5‐bisphosphate in neuron‐like cell line NG108‐15 cells

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Photoreceptor excitation and adaptation by inositol 1,4,5-trisphosphate

Cited by 325 publications

References 22 publications

Protein Kinase C Activators Inhibit the Visual Cascade inLimulusVentral Photoreceptors at an Early Stage

Protein Kinase C Activators Inhibit the Visual Cascade inLimulusVentral Photoreceptors at an Early Stage

A lingering elevation of Cai accompanies inhibition of inositol 1,4,5 trisphosphate-induced Ca release in Limulus ventral photoreceptors.

Evidence for a Ca2+‐independent hydrolysis of phosphatidylinositol 4,5‐bisphosphate in neuron‐like cell line NG108‐15 cells

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Evidence for a Ca²⁺‐independent hydrolysis of phosphatidylinositol 4,5‐bisphosphate in neuron‐like cell line NG108‐15 cells