Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

Stella, Salvatore; Bryson, Eric J.; Thoreson, Wallace B.

doi:10.1097/00001756-200104170-00017

Cited by 26 publications

(21 citation statements)

References 23 publications

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“…The amplitude and voltage dependence of photoreceptor I Ca also are affected by a large number of extrinsic neuromodulators, including dopamine , somatostatin (Akopian et al, 2000), cannabinoids (Straiker and Sullivan, 2003;Fan and Yazulla, 2003), adenosine , nitric oxide (Kurenny et al, 1994), insulin (Stella et al, 2001), polyunsaturated fats (Vellani et al, 2000) and various ions. The list of substances that can modulate photoreceptor I Ca is probably not yet complete.…”

Section: Intrinsic Mechanisms That Regulate I Camentioning

confidence: 99%

“…I Ca in rods and cones can be regulated by cAMP-dependent protein kinase . Tyrosine kinase inhibitors also alter rod I Ca , suggesting that tyrosine phosphorylation might regulate channel activity (Stella et al, 2001). The ineffectiveness of cGMP analogs (Kurenny et al, 1994) argues against modulation by a cGMP-dependent protein kinase.…”

Section: Intrinsic Mechanisms That Regulate I Camentioning

confidence: 99%

“…In the rat retina, Johnson et al (2001) found that SRIF reduced Ca 2+ influx into rod bipolar terminals. (Gosbell et al, 1996) and L-type Ca 2+ channels in rod photoreceptors (Stella et al, 2001). The potency of insulin's actions (IC50 = 2 nM) and the effectiveness of an insulin receptor-specific tyrosine kinase inhibitor suggest that receptors for insulin, and not insulin-like growth factor, are responsible for these effects (Stella et al, 2001).…”

Section: Cannabinoids-cannabinoidsmentioning

confidence: 99%

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Synaptic transmission at retinal ribbon synapses

Heidelberger

Thoreson

Witkovsky

2005

Progress in Retinal and Eye Research

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209

231

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The molecular organization of ribbon synapses in photoreceptors and ON bipolar cells is reviewed in relation to the process of neurotransmitter release. The interactions between ribbon synapseassociated proteins, synaptic vesicle fusion machinery and the voltage-gated calcium channels that gate transmitter release at ribbon synapses are discussed in relation to the process of synaptic vesicle exocytosis. We describe structural and mechanistic specializations that permit the ON bipolar cell to release transmitter at a much higher rate than the photoreceptor does, under in vivo conditions. We also consider the modulation of exocytosis at photoreceptor synapses, with an emphasis on the regulation of calcium channels.

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Section: Intrinsic Mechanisms That Regulate I Camentioning

confidence: 99%

Section: Intrinsic Mechanisms That Regulate I Camentioning

confidence: 99%

Section: Cannabinoids-cannabinoidsmentioning

confidence: 99%

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Synaptic transmission at retinal ribbon synapses

Heidelberger

Thoreson

Witkovsky

2005

Progress in Retinal and Eye Research

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209

231

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“…Use-dependent feedback mechanisms include voltage-and calcium-dependent inhibition of I Ca [140][141][142][143], inhibition of cone I Ca by the pre-synaptic actions of glutamate on group III mGluRs [208], inhibition of cone I Ca by vesicular protons [208,209], inhibition of I Ca by vesicular zinc [116,210,211], inhibitory effects of adenosine which can be derived from vesicular ATP [212][213][214], inhibition of rod I Ca due to chloride efflux mediated by pre-synaptic glutamate transporters [215], inhibition of rod I Ca due to chloride efflux through calcium-activated chloride channels [138], and enhancement of rod I Ca due to K+ efflux through calcium-activated potassium channels [19]. Various neurotransmitters and neuromodulators also regulate rod and cone I Ca , including nitric oxide [216,217], dopamine [132], cannabinoids [218][219][220], somatostatin [221], insulin [222], retinoids, and polyunsaturated fats [223]. Feedback from horizontal cells onto cones [224] also modulates I Ca [225].…”

Section: Synaptic Depression and Vesicle Replenishmentmentioning

confidence: 99%

Kinetics of Synaptic Transmission at Ribbon Synapses of Rods and Cones

Thoreson

2007

Mol Neurobiol

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The ribbon synapse is a specialized structure that allows photoreceptors to sustain the continuous release of vesicles for hours upon hours and years upon years but also respond rapidly to momentary changes in illumination. Light responses of cones are faster than those of rods and, mirroring this difference, synaptic transmission from cones is also faster than transmission from rods. This review evaluates the various factors that regulate synaptic kinetics and contribute to kinetic differences between rod and cone synapses. Presynaptically, the release of glutamate-laden synaptic vesicles is regulated by properties of the synaptic proteins involved in exocytosis, influx of calcium through calcium channels, calcium release from intracellular stores, diffusion of calcium to the release site, calcium buffering, and extrusion of calcium from the cytoplasm. The rate of vesicle replenishment also limits the ability of the synapse to follow changes in release. Post-synaptic factors include properties of glutamate receptors, dynamics of glutamate diffusion through the cleft, and glutamate uptake by glutamate transporters. Thus, multiple synaptic mechanisms help to shape the responses of second-order horizontal and bipolar cells. KeywordsPhotoreceptor; Synaptic transmission; Glutamate; Calcium; Vesicles; Retina Vision begins with the transduction of light into membrane potential changes as the result of an enzymatic cascade occurring in the outer segments of rod and cone photoreceptors [1,2]. Light-evoked membrane potential changes are modified by voltage-dependent currents in the inner segment [3] and transmitted to second order bipolar and horizontal cells by changes in release of the neurotransmitter, L-glutamate, from the synaptic terminals of both rods and cones. Because all of the visual information available to downstream retinal neurons must first pass through the photoreceptor synapse, synaptic transmission from photoreceptors has a considerable impact on visual perception. The focus of this review is on mechanisms that shape the kinetics of synaptic transmission at synapses of rods and cones. Additional information on other physiological and anatomical characteristics of photoreceptor ribbon synapses can be found in recent reviews [4][5][6]. Differences in Rod and Cone KineticsRod and cone photoreceptors are tonically depolarized in darkness with membrane potentials of −35 to −45 mV that allow continuous release of the neurotransmitter, L-glutamate. Light onset causes photoreceptors to hyperpolarize by as much as 30 mV, leading to a reduction in

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“…Stella et al (128) have recently shown that insulin also inhibits influx of Ca 2+ into ISs of rods via the insulin receptor-mediated activation of tyrosine kinases.…”

Section: Insulin Both Inner and Outer Segments Of Photoreceptors Exprmentioning

confidence: 99%

Calcium regulation in photoreceptors

2002

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In this review we describe some of the remarkable and intricate mechanisms through which the calcium ion (Ca 2+ ) contributes to detection, transduction and synaptic transfer of light stimuli in rod and cone photoreceptors. The function of Ca 2+ is highly compartmentalized. In the outer segment, Ca 2+ controls photoreceptor light adaptation by independently adjusting the gain of phototransduction at several stages in the transduction chain. In the inner segment and synaptic terminal, Ca 2+ regulates cells' metabolism, glutamate release, cytoskeletal dynamics, gene expression and cell death. We discuss the mechanisms of Ca 2+ entry, buffering, sequestration, release from internal stores and Ca 2+ extrusion from both outer and inner segments, showing that these two compartments have little in common with respect to Ca 2+ homeostasis. We also investigate the various roles played by Ca 2+ as an integrator of intracellular signaling pathways, and emphasize the central role played by Ca 2+ as a second messenger in neuromodulation of photoreceptor signaling by extracellular ligands such as dopamine, adenosine and somatostatin. Finally, we review the intimate link between dysfunction in photoreceptor Ca 2+ homeostasis and pathologies leading to retinal dysfunction and blindness. KeywordsRetina; Photoreceptor; Rod; Cone; Calcium; Plasma Membrane Calcium Atpase; Na-Ca Exchange; Calcium Store; Calcium Buffering; Calcium Channel; Calcium Extrusion; Ryanodine; Inner Segment; Dystrophy; Synaptic Transmission; Review INTRODUCTIONThe calcium ion (Ca 2+ ) is a major messenger for coordinating activity of eukaryote cells. Its extensive distribution and functioning as a control ion is common to a huge range of eukaryote cell types from animal, plant or fungal sources which diverged billions of years ago. The signaling potential of Ca 2+ is linked to the ability of cells to maintain a large concentration gradient between the cytosol (with basal Ca 2+ levels typically ~ 50 nM) and the extracellular media (with Ca 2+ ~ 1.5 mM). Because of this 10,000-fold difference in [Ca 2+ ]i between the cytosol and the extracellular space, Ca 2+ influx across the plasma membrane and Ca 2+ release from intracellular stores may produce large fluctuations of free cytosolic Ca 2+ (1). Another important feature of Ca 2+ homeostasis is that [Ca 2+ ]i elevations in the cell can be highly localized. We now know that the diffusion of Ca 2+ within the cytosol is much slower than that of other intracellular messengers (2,3). Ca 2+ is thus able to regulate a variety of different functions in different parts of the cell. Such selective action of Ca 2+ is facilitated by Ca 2+ -binding proteins which are often localized to specific sites mediating individual functions (4). To understand Ca 2+ signaling, it is therefore essential to map the spatial distribution of Ca 2+ effector proteins such as Ca 2+ channels, Ca 2+ pumps, cytoplasmic buffers and intracellular Anatomically, primary sensory neurons are notable for their compartmentalization into input ...

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Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

Cited by 26 publications

References 23 publications

Synaptic transmission at retinal ribbon synapses

Synaptic transmission at retinal ribbon synapses

Kinetics of Synaptic Transmission at Ribbon Synapses of Rods and Cones

Calcium regulation in photoreceptors

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