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An amacrine cell is a retinal interneuron that modifies signaling in the inner retina, including interactions between retinal bipolar cells and retinal ganglion cells. Different types contribute different spatial, temporal and inhibitory interactions.

This diversity makes the label an anatomical and circuit category rather than one universal computation. Comparing responses before and after a specific connection is perturbed can test a proposed function more directly than observing that an amacrine cell responds to moving light.

A bipolar neuron has two main processes extending from its soma, conventionally an axon and a dendrite. Retinal bipolar cells provide a sensory example connecting photoreceptors to downstream retinal circuitry. The anatomical label does not mean that the biological cell has two axons, and it does not imply that every signal must be an action potential.^[ref]

Catherine W. Morgans studies signalling between photoreceptors and retinal bipolar cells. A 2009 study led by Catherine W. Morgans connected TRPM1 to the depolarizing response controlled by mGluR6 in ON retinal bipolar cells.^[ref]

The team compared expression, localization and function. Mice lacking TRPM1 retained the photoreceptor-associated a-wave recorded by electroretinography but lacked the bipolar-cell-associated b-wave. Patch clamp recordings from retinal slices then tested individual retinal bipolar cells, rather than inferring their behaviour from the summed retinal signal alone.^[ref]

That combination illustrates how a molecular candidate becomes a functional explanation: localization establishes where a protein is found, whereas removing it and recording a changed current tests its contribution to signalling.

Electroretinography records electrical responses generated by the retina when it is stimulated with light. In full-field electroretinography, diffuse flashes stimulate a broad retinal area, and an electrode at or near the eye records a potential difference relative to a recording reference. The trace is a summed response of retinal tissue, rather than a recording of one photoreceptor or a direct report of perceived brightness.^[ref]

Dark-adapted and light-adapted recordings help distinguish response systems under controlled conditions. Standardization matters because flash strength, adaptation and electrode configuration change the trace. A simple experimental comparison uses the same flash and recording arrangement before and after an intervention: differences then become evidence about which retinal processes contribute, subject to the intervention's selectivity.^[ref]

The positive b-wave illustrates how component interpretation is tested. Richard A. Stockton and Malcolm M. Slaughter measured retinal field responses together with extracellular potassium changes in amphibian preparations. A drug that suppressed ON retinal bipolar cell responses also removed the b-wave; treatments suppressing OFF-pathway responses removed the light-offset d-wave while preserving the b-wave. This supported a central role for ON retinal bipolar cell activity in generating the b-wave, rather than treating all deflections as direct rod voltages.^[ref]

An independent example is the RPE65 knockout: disrupted visual cycle chemistry caused loss of normal rod responses on electroretinography, connecting pigment regeneration to a measurable tissue-level signal.^[ref]

An OFF retinal bipolar cell is a retinal bipolar cell whose central receptive response shows depolarization for an appropriate decrease in illumination. Its input synapse preserves the sign of a cone photoreceptor's voltage response through excitatory AMPA receptors or kainate receptors, rather than the sign-inverting arrangement of an ON retinal bipolar cell.^[ref]

In a 2000 experiment, simultaneous recordings from connected cone cells and OFF retinal bipolar cells, together with receptor-selective manipulations, distinguished receptor mechanisms in different morphological OFF types. Differences in recovery from receptor desensitization filtered the same cone signal into different temporal components.^[ref]

Thus two OFF types can agree on whether a light decrement excites them while differing in response timing. Response sign, temporal filtering and neuron identity are related measurements, not interchangeable labels. The result from the studied retina should not be taken as an identical receptor assignment for every OFF subtype in every species.

An ON retinal bipolar cell is a retinal bipolar cell whose central receptive response shows depolarization when illumination increases appropriately. At the input synapse, this reverses the response sign of a photoreceptor, which undergoes hyperpolarization in response to light and releases less glutamate.^[ref]

The postsynaptic glutamate-sensing receptor mGluR6 controls a current requiring TRPM1. In a 2009 study, TRPM1-deficient mice retained the rod-related electroretinogram a-wave but lacked the b-wave; direct recordings of bipolar responses provided evidence for a postsynaptic signaling defect.^[ref]

A local sign model makes the circuit transformation visible. If a small light increment $\delta L$ changes glutamate release by $\delta G=-a\delta L$ and the ON response obeys $\delta V=-b\delta G$, with $a,b>0$, then $\delta V=ab\delta L>0$. These are illustrative gains, not fitted measurements. The label describes response polarity under specified stimulation, not continuous firing or identical behaviour in every ON subtype.