2005
DOI: 10.1523/jneurosci.2735-04.2005
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Group III Metabotropic Glutamate Receptors and Exocytosed Protons Inhibit L-Type Calcium Currents in Cones But Not in Rods

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Cited by 56 publications
(39 citation statements)
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References 91 publications
(109 reference statements)
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“…Since glutamate is the main neurotransmitter in the retina, various mGluRs can be found in the eye of vertebrates, where they have been shown to be involved in signal modulation at the first visual synapse (Rothe et al, 1994;Linn and Gafka, 1999;Hirasawa et al, 2002;Hosoi et al, 2005;Fan and Yazulla, 2007). However, we found expression for most zebrafish mglurs in the inner retina but not in the outermost layers where photoreceptors (ONL) and horizontal cell bodies (outermost INL close to OPL) are located.…”
Section: Retinamentioning
confidence: 60%
“…Since glutamate is the main neurotransmitter in the retina, various mGluRs can be found in the eye of vertebrates, where they have been shown to be involved in signal modulation at the first visual synapse (Rothe et al, 1994;Linn and Gafka, 1999;Hirasawa et al, 2002;Hosoi et al, 2005;Fan and Yazulla, 2007). However, we found expression for most zebrafish mglurs in the inner retina but not in the outermost layers where photoreceptors (ONL) and horizontal cell bodies (outermost INL close to OPL) are located.…”
Section: Retinamentioning
confidence: 60%
“…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].…”
Section: Synaptic Depression and Vesicle Replenishmentmentioning
confidence: 99%
“…This could reflect differences in Ca 2ϩ entry or removal from the cytoplasm. Although rods and cones exhibit some differences in L-type Ca 2ϩ -channel subtypes (Morgans et al, 2005), the voltage dependence of activation is similar in dissociated rods and cones (Corey et al, 1984;Maricq and Korenbrot, 1988;Barnes and Hille, 1989;Rieke and Schwartz, 1994;Wilkinson and Barnes, 1996;Savchenko et al, 1997;Hosoi et al, 2005). However, the Ca 2ϩ current in cone, but not rod terminals is modulated by horizontal cell feedback (Verweij et al, 1996;Cadetti and Thoreson, 2006), so in the intact retina, the voltagedependent activation of rod and cone Ca 2ϩ current may differ substantially.…”
Section: Mechanisms Underlying Slower Dark Release From Rodsmentioning
confidence: 99%
“…However, the Ca 2ϩ current in cone, but not rod terminals is modulated by horizontal cell feedback (Verweij et al, 1996;Cadetti and Thoreson, 2006), so in the intact retina, the voltagedependent activation of rod and cone Ca 2ϩ current may differ substantially. Moreover, group III metabotropic glutamate receptors and exocytosed protons can modulate the Ca 2ϩ current of cones, but not rods (Hosoi et al, 2005). L-type Ca 2ϩ channels are the sole pathway for extracellular Ca 2ϩ entry in rods, but cyclic nucleotide-gated channels also contribute to Ca 2ϩ influx in cones (Rieke and Schwartz, 1994;Savchenko et al, 1997).…”
Section: Mechanisms Underlying Slower Dark Release From Rodsmentioning
confidence: 99%