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PubMedDate not supplied

Coexistence of neurofilaments and vimentin in a neurone of adult mouse retina.

Different classes of intermediate filaments are restricted to particular cell types. For example, neurofilaments are found only in neurones, whereas filaments that contain the protein vimentin, which were found in some cells of mesenchymal origin and some forms of glia, are thought to be absent from mature neurones, and present only transiently in early embryonic neurones. However, evidence is presented here of an exception to that rule in the outer plexiform layer of the mouse retina. Double-labelling with antibodies to neurofilaments and vimentin showed that both types of intermediate filaments coexisted in the axonless horizontal cell of that retinal layer, recalling the previous notion that these cells are glial or intermediate between neuronal and glial (reviewed in ref. 10).

Animals↗

PubMed1987

Signal transmission in the catfish retina. V. Sensitivity and circuit.

1. We analyzed the light-evoked responses of retinal neurons by means of a white-noise technique. Horizontal and bipolar cells produced a modulation response that was linearly related to a modulation of the mean luminance of a large field of light. The first-order kernels were capable of reproducing the cells' modulation response with a fair degree of accuracy. The amplitude as well as the waveform of the kernels changed with the change in the mean luminance. This is a parametric change and is a form of field adaptation. As the time constant of the parametric change was much longer than that of the modulation response (memory), neurons were assumed to be at a dynamic steady state at a given mean luminance. 2. With the presence of a steady annular illumination, the first-order kernel derived from stimulation with a small spot of light became faster in peak response time and larger in amplitude. For horizontal-cell somas and bipolar cells, the surround also linearized their modulation response. This surround enhancement has been seen in all the cone-driven retinal cells except the receptor and horizontal cell axon, in which a steady surround decreased the amplitude of the spot-evoked kernel but shortened the peak response time. 3. A change in the modulation depth did not affect either the amplitude or the wave-form of the first-order kernels from the horizontal and bipolar cells. In the amacrine and ganglion cells, on the other hand, the amplitude of kernels was related inversely to the depth of modulation. These cells were more sensitive to the modulation of a small modulation depth. 4. A static nonlinearity appeared when signals were transmitted to the amacrine cells. The nonlinearity was first produced in the type-C amacrine cells by a process, which could be modeled by squaring the bipolar cell response. A gamut of more complex second-order nonlinearities found in type-N amacrine cells could be modeled by a band-pass filtering of the type-C cell response. Linear components in the bipolar cells and nonlinear components in the amacrine cells are encoded into spike trains in the ganglion cells. Thus, under our simple stimulus regimen, the ganglion cells transformed the results of the preganglionic signal processing into a spike train without much modification. 5. We propose a tentative diagram of the signal flow in the cone-driven catfish retinal neurons based on this and previous studies.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

A set of early-born neurons is distinctly labeled by several defined antibodies in the adult rabbit retina.

Retinal ganglion cells, cone photoreceptor cells, and horizontal cells arise earlier in ontogenesis than the other retinal cell types. Although during the first postnatal week of life much cell proliferation occurs in the rabbit retina, 3H-thymidine labeling shows that these particular neurons are already postmitotic in neonatal animals. We show here that, in the adult retina, these early-born neurons express antigens as neuron-specific enolase, HNK-1 epitope of N-CAM, and PGP 9.5 antigen, which are not expressed by the neurons later born. It is concluded that the mammalian retina contains two genotypically different sets of neuronal cells which can be distinguished by immunocytochemistry.

Aging↗

PubMed1992

Organization and development of horizontal cells in the goldfish retina, II: Use of monoclonal antibody MH1.

We have produced and characterized a monoclonal antibody, MH1, which selectively labels rod horizontal cells and Müller cells in the goldfish retina. Biochemical and tissue distribution studies indicate that MH1 may recognize four out of five classes of intermediate filament proteins in goldfish: vimentin, desmin, glial fibrillary acidic protein (GFAP), and keratin, but not neurofilament. The intermediate filament which is labeled strongest in the retina is vimentin. In the goldfish retina, the only type of horizontal cells recognized by MH1 appear to be rod horizontal cells. This result suggests that the rod horizontal cell, an interneuron, and Müller (glial) cells share a common antigen: vimentin, which is usually only expressed in mesenchymal origin cells. The development of rod horizontal cells in the goldfish retina was also studied using MH1. The cells were not labeled by MH1 until 4-6 weeks posthatching, a stage in which the animals are already visually active. MH1 also did not label any horizontal cell in the region close to the ora terminalis in the goldfish retina. These results suggest that either the emergence and maturation of rod horizontal cells occur late during goldfish retinal development or the expression of vimentin itself occurs late in the development of rod horizontal cells.

Animals↗

PubMed2003

Kinetics of synaptic transfer from rods and cones to horizontal cells in the salamander retina.

We examined synaptic transmission between rods or cones and horizontal cells, using perforated patch recording techniques in salamander retinal slices. Experimental conditions were established under which horizontal cells received nearly pure rod or pure cone input. The response-intensity relation for both photoreceptors and horizontal cells was described by a Michaelis-Menten function with an exponent close to 1. A dynamic model was developed for the transduction from photoreceptor voltage to postsynaptic current. The basic model assumes that: (i) photoreceptor light-evoked voltage controls Ca2+ entry according to a Boltzmann relation; (ii) the rate of glutamate release depends linearly on the voltage-gated Ca2+ current (ICa) in the synaptic terminal; (iii) glutamate concentration in the synaptic cleft reflects the balance of release and reuptake in which reuptake obeys first order kinetics; (iv) the binding of glutamate to its receptor and channel gating are fast compared with glutamate kinetics in the synaptic cleft. The good fit to the model confirms that these are the key features of synaptic transmission from rods and cones. The model accommodated changes in kinetics induced by the glutamate uptake blocker, dihydrokainate. The match between model and response was not improved by including an estimate of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor desensitization or by making glutamate uptake voltage dependent.

Animals↗

PubMed1981

Changes in ERG b-wave and Müller cell structure induced by alpha-aminoadipic acid.

The role of the Müller cell in the generation of the ERG b-wave was studied in the skate eye by examining the effects of a gliotoxic agent (alpha-aminoadipic acid; alpha-AAA) on retinal structure and function. Superfusing the eyecup for 1 h in 50 mM alpha-AAA resulted in the loss of the b-wave and extensive damage to glial cells, i.e. disruption of the cells' plasma membranes, and a marked loss of cytoplasmic substance. Of the other retinal elements, only the horizontal cells showed some signs of injury in alpha-AAA. On returning the retina to a normal Ringer solution, the widespread loss of cytoplasmic electron density persisted, but the Müller cell membranes appeared to have undergone repair, and the b-wave recovered fully its normal amplitude and waveform.

Adipates↗

PubMed1999

Expression of mt1 melatonin receptor in rat retina: evidence for multiple cell targets for melatonin.

Melatonin is synthesized in the retina at night and acts as a local modulator within this tissue by mediating the effects of darkness. We investigated the expression and localization of the mt1 (Mel1a) melatonin receptor in rat retina in order to disclose the cellular and molecular bases of melatonin's action in the mammalian retina. Western blotting of the mt1 receptor in rat retina exhibited a single immunoreactive band of approximately 37,000 mol. wt, which corresponds to the predicted molecular size of the receptor. The mt1 receptor was immunocytochemically localized to both the inner and outer plexiform layers. During postnatal development, retina from two-week-old rats showed the highest mt1 immunoreactivity; the outer plexiform layer and horizontal cell bodies were strongly immunolabeled, with weaker labeling in the inner plexiform layer. Expression of mt1 receptor messenger RNA in the rat retina was demonstrated by reverse transcription-polymerase chain reaction and in situ hybridization. mt1 receptor transcripts were localized to ganglion cells, amacrine cells and horizontal cells. These results suggest that melatonin influences retinal physiology by acting on multiple retinal cell types, including ganglion, amacrine and horizontal cells, via the mt1 receptor expressed in their processes.

Animals↗

PubMed2002

Cellular and developmental distribution of human homologues of the Drosophilia rdgB protein in the rat retina.

PURPOSE: The Nirs (Nir1, Nir2, and Nir3), human homologues of Drosophila retinal degeneration B (rdgB), have been considered candidate genes for human inherited retinal degeneration diseases. To gain a better understanding of their functions in the retina and their putative roles in retinal degeneration diseases, this study was undertaken to determine their distribution profile in developing and mature rat retinas. METHODS: Specific antibodies against each of the Nir proteins were raised in rabbits and used in indirect immunofluorescence analysis to determine the distribution profile of the three proteins. Eyes from Wistar rats at various developmental stages (embryonic day [E]18 to postnatal day [P]16) were sectioned vertically and immunostained with anti-Nir antibodies. Coimmunostaining for Nirs and several specific cellular and subcellular markers was used to determine precisely the cellular and subcellular distribution of the Nirs. Sections were observed under a confocal laser microscope, and image analysis was performed with the standard operating software provided with the microscope. RESULTS: Confocal microscopic analysis of Nir1 immunoreactivity revealed that it was predominantly expressed in premature Müller cells at birth and that it was upregulated during Müller cell maturation. In contrast, Nir2 and Nir3 were homogeneously distributed in undifferentiated neuroblasts and ganglion cells at birth and later became distinctly distributed in newly differentiated neuronal cells. From P4, Nir2 and Nir3 were highly expressed in neuronal cells and their processes, coinciding with the formation of synaptic layers and ongoing synaptogenesis. From P12, Nir2 was uniformly expressed in all classes of retinal neuronal cells, including ganglion cells, horizontal cells, amacrine cells, bipolar cells, and photoreceptor cells. In the adult rat retina, Nir2 was preferentially localized to the somata of all classes of retinal neurons, whereas Nir3 was highly expressed in the synaptic terminals. This specific localization of Nir3 was confirmed by double immunostaining with the presynaptic protein synaptosomal-associated protein (SNAP)-25. In photoreceptor cells, both Nir2 and Nir3 were found to be highly expressed in the inner segments but were not detectably expressed in the outer segments. CONCLUSIONS: These findings suggest that the three Nir proteins are highly expressed in the developing retina, each exhibiting a distinct distribution profile. The different distribution patterns of these closely related proteins during development and at maturity may reflect their different cellular functions in vivo and their different roles in retinal cell survival or degeneration.

Animals↗

PubMed1995

Contactin/F11 and tenascin-C co-expression in the chick retina correlates with formation of the synaptic plexiform layers.

The neural immunoglobulin-like cell adhesion molecule contactin/F11 and the extracellular matrix glycoprotein tenascin-C are prominent molecules in the developing nervous system which interact in in vitro assays (Zisch et al., J. Cell Biol. 119, 203-213). To determine their potential role in neural development, the distribution of tenascin-C and contactin/F11 was examined in the developing chick retina. The onset of both tenascin-C and contactin/F11 expression coincides with the appearance of ganglion cell dendrides and neurites from bipolar and amacrine cells in the inner layer (IPL) at E8, and the extension of bipolar and horizontal cell processes in the outer plexiform layer (OPL) at E9. Contactin/F11 expression is co-ordinately upregulated with the TN190 and TN200 tenascin-C isoforms between embryonic day 8 (E8) and E17, while little, if any, of the TN220 isoform, which does not bind contactin/F11, is detected. In situ hybridization reveals that tenascin-C and contactin/F11 mRNAs are synthesized by different neuronal types. Tenascin-C mRNA probes hybridize to amacrine and displaced amacrine neurons, and horizontal neurons. In cultured retinal cells, tenascin-C is also present on process-bearing neurofilament-positive cells. Contactin/F11 mRNA is detected in bipolar cells or their precursors from E8-9, and later in horizontal and ganglion neurons. The highest levels and greatest overlap in the synaptic IPL and OPL are reached at E17, when the stratification of the retina is nearly complete. These results are consistent with a putative role for contactin/F11-tenascin-C interactions in the establishment of synaptic layers in the retina.

Animals↗

PubMed2003

Prox1 function controls progenitor cell proliferation and horizontal cell genesis in the mammalian retina.

Retinal progenitor cells regulate their proliferation during development so that the correct number of each cell type is made at the appropriate time. We found that the homeodomain protein Prox1 regulates the exit of progenitor cells from the cell cycle in the embryonic mouse retina. Cells lacking Prox1 are less likely to stop dividing, and ectopic expression of Prox1 forces progenitor cells to exit the cell cycle. During retinogenesis, Prox1 can be detected in differentiating horizontal, bipolar and AII amacrine cells. Horizontal cells are absent in retinae of Prox1-/- mice and misexpression of Prox1 in postnatal progenitor cells promotes horizontal-cell formation. Thus, Prox1 activity is both necessary and sufficient for progenitor-cell proliferation and cell-fate determination in the vertebrate retina.

Animals↗

PubMed1996

Dopaminergic control of light-adaptive synaptic plasticity and role in goldfish visual behavior.

Dopamine has been implicated in processes of retinal light and dark adaptation. In goldfish retina, horizontal cell dendrites elaborate neurite processes (spinules) into cone terminals, in a light- and dopamine-dependent manner. However, the functions of retinal dopamine and the horizontal cell spinules in visual behavior are unknown. These issues were addressed in behavioral, electroretinographic, and anatomical studies of normal fish and those with unilateral depletion of retinal dopamine induced by intraocular (i.o.) injections with 6-hydroxydopamine (6-OHDA). Dopamine interplexiform cells (DA-IPC) disappear within 2 weeks after 6-OHDA injection; cell bodies appear at the marginal zone within 6 weeks at which time neurites slowly reinnervate the retina with a sparse plexus over the next 12 months. We found that dopamine depletion increased light sensitivity at photopic but not scotopic backgrounds by 2.5 log units, an effect mimicked by i.o. injections of dopamine D1 and D2 antagonists. The ERG b-wave increment thresholds were the same for control and dopamine depleted eyes, indicating a normal transition from rod to cone systems in the ON pathway. Light-dependent spinule formation was reduced by about 60% in dopamine-depleted retinas, but returned to normal by 3 months and 9 months after injection in the entire retina, even areas not directly innervated with DA-IPC processes. Spinule formation in vivo was inhibited 50% with i.o. injection of SCH 23390 in control retinas as well as throughout 3 month 6-OHDA injected retinas, including DA-IPC free areas. This latter result indicates a volume effect of dopamine, diffusing laterally through the retina over several millimeters, in regulating spinules. We conclude that DA-IPCs regulate sensitivity to background at photopic levels not via the ON pathway, but perhaps the OFF pathway. Goldfish display both increased sensitivity to light and a normal Purkinje shift in the ERG b-wave whether or not horizontal cell spinules are present, indicating that dopamine control of photopic vision in fish is not mediated through light-induced spinule formation of horizontal cell dendrites.

Adaptation, Ocular↗

PubMed1984

Pharmacological properties of isolated horizontal and bipolar cells from the skate retina.

Retinal neurons were enzymatically and mechanically dissociated from adult skate retinas and maintained in cell culture for up to 14 days. Intracellular recordings were made from isolated horizontal and bipolar cells while neurotransmitters were applied via pressure ejection. L-Glutamate, quisqualate, kainate, and gamma-amino-butyric acid (GABA), when applied to horizontal cells, produced large (60 to 70 mV), long-lasting depolarizations. These responses appear to consist of at least two components: a graded depolarization and a Ca++-dependent regenerative component. As regards bipolar cells, L-glutamate and its analogues depolarized about 30% of the cells tested, while GABA hyperpolarized most of these neurons. Both agents acted on bipolar cells by increasing conductance. Repeated applications of L-glutamate, quisqualate, kainate, and GABA to horizontal cells produced no desensitization, but in these circumstances the glutamate analogues, kainate and quisqualate, induced certain morphological changes, most notably a retraction of cell processes and the appearance of blebs on the cell surface.

Animals↗

PubMed1990

The physiology of somatostatin in the rabbit retina.

The neuropeptide somatostatin (SS) has been localized to neurons of the rabbit retina by immunochemical and biochemical methods (Sagar et al., 1982, 1986; Marshak and Yamada 1984). We examined the effects of bath-applied SS on neurons of the rabbit retina, using intra- and extracellular electrophysiological techniques in an in vitro retina eyecup preparation. All commonly encountered ganglion cell receptive field types were affected by SS, and the effects were of 3 kinds: The first was a general excitation, occurring with a threshold concentration of about 100 nM; the onset of the excitation was too slow (seconds) for SS to participate in any rapid light-evoked responses. The second SS effect was an increase in the "signal-to-noise ratio," defined here as the ratio of light-evoked to spontaneous spiking, which resulted from a decrease in spontaneous activity and, usually, a concomitant increase in light-evoked spiking. The third effect was a shift in center-surround balance towards a more dominant center. The signal-to-noise and center-surround effects were evident at concentrations as low as 0.5 nM; both were slow onset (tens of seconds) and long lasting (tens of minutes). SS acted at multiple levels within the retinal circuitry to produce the observed changes in ganglion cell output. These effects included direct actions on ganglion and amacrine cells, and a decrease in the efficiency with which horizontal cells could drive the retinal network. At least part of these SS actions on third-order neurons resulted from a decrease in conductance to ions with an equilibrium potential more positive than dark membrane potential. The degradation-resistant SS agonist SMS201-995 had effects qualitatively and quantitatively similar to those of SS, suggesting that SS may be degraded slowly enough to act at a distance from its sites of release. While no adequate SS antagonist is available, the greater sensitivity to exogenous SS, in retinas depleted of their SS content (with cysteamine), suggests a role for endogenous SS. The potency of SS also reinforces this view. The results of this study suggest that SS may be a neuromodulator in the rabbit retina, producing long-lasting changes in the "signal-to-noise" discharge pattern and center-surround balance of ganglion cells.

Action Potentials↗

PubMed2006

Expression of the basic helix-loop-factor Olig2 in the developing retina: Olig2 as a new marker for retinal progenitors and late-born cells.

In this study, we examined the spatiotemporal expression patterns of Olig2, a basic helix-loop-helix transcription factor, in the developing mouse retina. Expression of Olig2 was initially detected on embryonic day 12.5 (E12.5). The majority of Olig2-positive cells were identified as retinal progenitor cells throughout embryogenesis. During later embryonic stages, the number of Olig2-positive retinal progenitor cells increased, and Olig2-positive cells were confined only to the neuroblast layer (NBL). Olig2 expression was not observed in the ganglion cell layer (GCL) nor in the inner nuclear layer (INL) that contain the differentiated retinal cell types, indicating that Olig2 is not expressed in differentiated cells in prenatal retina. In later postnatal stages, Olig2 expression was retained in mature neurons and glial cells, namely retinal ganglion cells (RGCs), amacrine cells (ACs), horizontal cells, bipolar cells and Müller glial cells. Thus, Olig2 is an marker both for retinal progenitor cells during embryonic stages, and also for differentiated retinal subpopulations within the GCL and INL during postnatal stages.

Animals↗

PubMed1997

Reducing extracellular Cl- suppresses dihydropyridine-sensitive Ca2+ currents and synaptic transmission in amphibian photoreceptors.

A reduction in extracellular chloride suppresses light-evoked currents of second-order retinal neurons (bipolar and horizontal cells) by reducing release of glutamate from photoreceptors. The underlying mechanisms responsible for this action of reduced extracellular Cl- were studied with a combination of electrophysiological recordings from single neurons in a retinal slice preparation and image analyses of intracellular Ca2+ (Fura-2) and pH [2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein, acetoxymethyl ester] in dissociated photoreceptors. The results show that reducing extracellular Cl- suppresses a dihydropyridine (DHP)-sensitive Ca2+ current (I(Ca)) in photoreceptors. It is proposed that suppression of I(Ca) results in suppression of photoreceptor neurotransmission. The suppressive effect of low Cl- on I(Ca) is not due to antagonism by the substituting anion nor is it mediated by changes in extracellular or intracellular pH. We conclude that normal extracellular levels of Cl- are important for maintenance of the voltage-gated Ca2+ channels that support neurotransmission from photoreceptors. Several ideas are presented about the mechanisms by which Cl- supports photoreceptor neurotransmission and the possibility that modulations of Cl- might play a physiological role in the regulation of Ca2+ channels in photoreceptors and, hence, photoreceptor function.

Ambystoma↗

PubMed2002

Retinal voltage-dependent anion channel: characterization and cellular localization.

PURPOSE: To characterize and localize retinal voltage-dependent anion channel (VDAC) and to understand its possible contribution to mitochondrial function and dysfunction. METHODS: VDAC was characterized by a method involving purification from isolated mitochondria and reconstitution into a planar lipid bilayer (PLB). The permeability transition pore (PTP) was monitored by Ca(2+) accumulation in isolated mitochondria and swelling of mitochondria. Localization was studied by immunocytochemistry and in situ hybridization. RESULTS: Retinal VDACs exhibited the electrophysiological fingerprint of the VDAC superfamily. It had a maximal chord conductance of 3.7 +/- 0.1 nanosiemens (nS) in 1 M NaCl, and a voltage-dependent conductance that was highest at transmembrane potential close to zero. It was modulated by glutamate, which decreased the channel's open probability, and by La(3+) and ruthenium amine binuclear complex (Ru360), which closed the channel. Energized and freshly prepared retinal mitochondria accumulated Ca(2+) that is inhibited by La(3+) ruthenium red and Ru360. Subsequent to Ca(2+) accumulation, mitochondria released the accumulated Ca(2+), probably through activation of the PTP. Ru360 inhibited Ca(2+) release and mitochondrial swelling. VDAC was present in mitochondria of all retinal cell types: photoreceptor, bipolar, horizontal, amacrine, and ganglion cells. Most cells primarily expressed VDAC-1, but they also expressed VDAC-2 and -3. CONCLUSIONS: These results suggest that VDAC is involved in PTP activity and/or regulation and thus is an important player in retinal degeneration associated with PTP-mediated mitochondrial dysfunction.

Animals↗

PubMed1995

The extracellular matrix molecule tenascin: expression in the developing chick retinotectal system and substrate properties for retinal ganglion cell neurites in vitro.

To investigate the molecular mechanisms involved in the outgrowth of retinal ganglion cell axons in the tectum, the expression of the extracellular matrix molecule tenascin was analysed in the tectum and retina of chickens by immunocytochemistry and in situ hybridization. Tissue was analysed between embryonic days 4 and 12, just before and during the period when retinal ganglion cell axons innervate their target region, the optic tectum. In the tectum, tenascin immunoreactivity becomes detectable at the anterior pole at embryonic day 4, 2 days before retinal ganglion cell axons arrive, and spreads caudally with increasing age. At early stages, tenascin is predominantly accumulated in the stratum opticum, the zone of ingrowing retinal ganglion cell axons, and along their prospective pathway. In the stratum opticum, the molecule is associated with radial glial fibres, glial endfeet and retinal ganglion cell axons located in the immediate neighbourhood of radial glial fibres. At all ages investigated, tenascin mRNA is mainly restricted to cells located in the periventricular region, suggesting that the molecule is synthesized by radial glial cells. In the retina, tenascin is expressed by amacrine, displaced amacrine and horizontal cells but not by retinal ganglion cells. To investigate whether the accumulation of tenascin in the developing and prospective pathway of retinal ganglion cell axons may affect their rate of growth we assayed the substrate properties of tenascin for retinal ganglion cell neurites in vitro. When retinal ganglion cell suspensions from 6-day-old chick embryos were maintained on homogeneous mouse or chick tenascin/polyornithine substrates, neurite length was significantly increased when compared to polyornithine substrates at coating concentrations of 10 or 20 micrograms/ml. Higher coating concentrations (35 or 70 micrograms/ml) resulted in neurite lengths comparable to control values. Together, these observations suggest that tenascin in the developing and prospective stratum opticum might serve as a performed pathway to support growth of retinal ganglion cell axons in the tectum.

Animals↗

PubMed1989

The effect of dark adaptation on the responses of cat retinal ganglion cells to eyeball deformation.

Eyeball deformation in total darkness leads to an activation of on-center ganglion cells and an inhibition of off-center ganglion cells. After "deformation off" most on-center ganglion cell activity decreased slowly to the normal spontaneous dark level, while in off-center ganglion cells some returned according to an exponential function to normal dark activity, while others had a transient postinhibitory activation period. In general, the response type of latency class I and latency class II neurons was the same. Dark adaptation of 30-45 min duration only changed this neuronal response pattern slightly, if at all. A detailed statistical analysis is provided for the four classes of retinal ganglion cells recorded: latency class I on-center and off-center neurons and latency class II on-center and off-center neurons. The missing effects of dark adaptation on neuronal responses evoked by eyeball deformation are explained by three possible models. The more plausible one assumes that horizontal cells are depolarized by retinal stretch. Their interaction with cone on-bipolars or cone off-bipolars is fairly independent of photoreceptor adaptation or transmitter release at the cone pedicles and is still effective when all molecular receptor sites at cone/bipolar cell synapses are occupied during scotopic states of dark adaptation. In psychophysical experiments (two subjects), as in the neuronal responses, we also could not find any indication that the "pressure phosphenes" evoked by lateral eyeball indentation are altered during dark adaptation.

Action Potentials↗