Effects of HCN channel blockade on the intensity‑response function of electroretinographic ON and OFF responses in dark adapted frogs.

Hyperpolarization‑activated and cyclic nucleotide‑gated (HCN) channels are well expressed in the vertebrate retina. Their role in formation of electroretinographic (ERG) responses to stimulus onset (b‑wave) and stimulus offset (d‑wave) are largely unknown. In this study we investigated the effects of pharmacological blockade of HCN channels (with ZD7288 or ivabradine) on the ERG b‑ and d‑waves in dark adapted frog eyecup preparations.

Dopamine D2 receptor blockade differentially affects the light‑adapted turtle and frog electroretinogram.

The effects of dopamine D2-class receptor blockade by sulpiride on the electroretinographic (ERG) b-wave (ON response) and d-wave (OFF response) were investigated in light-adapted turtle (Trachemys scripta elegans) and frog (Rana ridibunda) eyecups. For turtle ERG, sulpiride (240 μM) produced an amplitude increase of the b- and d-waves, while the 40 μM and 120 μM of sulpiride were ineffective. Alternatively, for frog ERG, a well-developed and dose-dependent b- and d-wave amplitude decrease was obtained with 40 μM and 240 μM sulpiride.

Interaction between the serotoninergic and GABAergic systems in frog retina as revealed by electroretinogram.

Functional interactions between serotoninergic and GABAergic systems in the vertebrate retina are largely unknown. In this study, the effects of isolated or combined stimulation of the serotonin receptors (with 100 μM serotonin) and ionotropic GABAA and GABAC receptors (with 5 mM TACA) on the electroretinographic (ERG) ON (b‑wave) and OFF (d‑wave) responses were investigated in frog eyecup preparations. It was found that serotonin alone produced a significant enhancement of the b‑ and d‑wave amplitude, while TACA alone caused its marked diminution.

Purinergic modulation of frog electroretinographic responses: The role of the ionotropic receptor P2X7.

The contribution of the purinergic receptors P2X7 (P2X7Rs) to the electroretinographic (ERG) responses was studied by testing the effects of the selective P2X7R antagonist A438079 and the selective P2X7R agonist Bz-ATP on the electroretinograms obtained in perfused frog (Rana ridibunda) eyecup preparations under a variety of stimulation conditions. The P2X7R blockade by 200 µM A438079 diminished the amplitude of the photoreceptor components: the a-wave and the pharmacologically isolated mass receptor potential. In the pure rod-driven and pure cone-driven responses, the amplitude of the postreceptoral ON (b-wave) and OFF (d-wave) components was also diminished.

Effects of dopamine D receptor blockade on the ERG b- and d-waves during blockade of ionotropic GABA receptors.

Background: Some data indicate that the dopaminergic and GABAergic systems interact in the vertebrate retina, but the type of interactions is not well understood.

Methods: In this study we investigated the effect of dopamine D receptor blockade by 75 μM SCH 23390 on the electroretinographic ON (b-wave) and OFF (d-wave) responses in intact frog eyecup preparations and in eyecups where the ionotropic GABA receptors were blocked by 50 μM picrotoxin. Student's -test, One-way repeated measures ANOVA with Bonferroni post-hoc test and Two-way ANOVA were used for statistical evaluation of the data.

Ionotropic purinergic receptors P2X in frog and turtle retina: glial and neuronal localization.

Purinergic signaling is represented in both the peripheral and central nervous system (CNS), and in particular in the retina, which may be regarded as a part of the CNS. While purigenic signaling is relatively well studied in mammalian retinas, little is known about it in retinas of lower vertebrates. The aim of present study was to investigate, using immunocytochemistry, the distribution of purinoreceptors P2X in retinas of frog and turtle, which are appropriate models of the brain neuron-to-glia interactions.

Participation of the histamine receptor encoded by the gene hclB (HCLB) in visual sensitivity control: an electroretinographic study in Drosophila melanogaster.

Purpose: Histaminergic transmission in the first synapse of the visual system in Drosophila melanogaster is mediated by two types of histamine receptors: 1) encoded by the gene hclA (HCLA), which is expressed in the second-order neurons-the large monopolar cells of the lamina, and is absolutely required for forward signal transmission; and 2) encoded by the gene hclB (HCLB), which is expressed in epithelial glia, and is involved in modulation of synaptic transmission from photoreceptors to large monopolar cells. The aim of our study was to establish whether the HCLB receptor-mediated modulation of synaptic transmission 1) contributes to the process of light adaptation, and 2) is involved in the control of the dynamics of sensitivity recovery after short-term light adaptation.

Methods: The effects of mutations in the gene hclB, encoding the subunits of the histamine receptor HCLB, were studied on 1) the intensity-response (V/logI) function of electroretinographic (ERG) responses under dark adaptation, as well as under three levels of background illumination; and 2) the dynamics of the dark sensitivity recovery after short-term light adaptation.

GABAa and GABAc receptor-mediated modulation of responses to color stimuli: electroretinographic study in the turtle Emys orbicularis.

GABAergic transmission is involved in color coding in the retina. The specific contribution of different GABA receptors to spectral sensitivity of the retinal responses is not well characterized. We studied GABAa and GABAc receptor-mediated effects on the intensity-response functions of the electroretinographic ON (b-wave) and OFF (d-wave) responses to color stimuli.

Altered ivermectin pharmacology and defective visual system in Drosophila mutants for histamine receptor HCLB.

The Drosophila gene hclB encodes a histamine-gated chloride channel, which can be activated by the neurotoxin ivermectin when expressed in vitro. We have identified two novel hclB mutants, carrying either a missense mutation (P293S, allele hclB (T1)) or a putative null mutation (W111*, allele hclB (T2)), as well as a novel splice form of the gene. In survival studies, hclB (T1) mutants were more sensitive to ivermectin than wild-type, whereas hclB (T2) were more resistant.