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Retina bipolar cell

(Redirected fromRetinal bipolar cell)

As a part of theretina,bipolar cells exist betweenphotoreceptors (rod cells andcone cells) andganglion cells. They act, directly or indirectly, to transmit signals from the photoreceptors to the ganglion cells.

Retinal bipolar cell
Retina. Bipolar cells are shown in red.
Details
SystemVisual system
LocationRetina (inner nuclear layer)
Shapebipolar
FunctionConveygradients betweenphotoreceptor cells to retinal ganglion cells
NeurotransmitterGlutamate
Presynaptic connectionsRods,cones andhorizontal cells
Postsynaptic connectionsRetinal ganglion cells andamacrine cells
Identifiers
MeSHD051245
NeuroLex IDnifext_31
Anatomical terms of neuroanatomy

Structure

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Bipolar cells are so-named as they have a central body from which two sets of processes arise. They can synapse with either rods or cones (rod/cone mixed input BCs have been found in teleost fish but not mammals), and they also accept synapses fromhorizontal cells.[disputeddiscuss] The bipolar cells then transmit the signals from the photoreceptors or the horizontal cells, and pass it on to the ganglion cells directly or indirectly (viaamacrine cells). Unlike most neurons, bipolar cells communicate viagraded potentials, rather thanaction potentials.

Function

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Bipolar cells receive synaptic input from either rods or cones, or both rods and cones, though they are generally designated rod bipolar or cone bipolar cells. There are roughly 10 distinct forms of cone bipolar cells, however, only one rod bipolar cell, due to the rod receptor arriving later in the evolutionary history than the cone receptor[attribution needed].

In the dark, a photoreceptor (rod/cone) cell will release glutamate, which inhibits (hyperpolarizes) the ON bipolar cells and excites (depolarizes) the OFF bipolar cells. In light, however, light strikes the photoreceptor cell which causes it to be inhibited (hyperpolarized) due to the activation ofopsins which activateG-Proteins that activate phosphodiesterase (PDE) which cleaves cGMP into 5'-GMP. In photoreceptor cells, there is an abundance of cGMP in dark conditions, keeping cGMP-gated Na channels open and so, activating PDE diminishes the supply of cGMP, reducing the number of open Na channels and thus hyperpolarizing the photoreceptor cell, causing less glutamate to be released. This causes the ON bipolar cell to lose its inhibition and become active (depolarized), while the OFF bipolar cell loses its excitation (becomes hyperpolarized) and becomes silent.[1]

Rod bipolar cells do not synapse directly on to ganglion cells. Instead, rod bipolar cells synapse on to aRetina amacrine cell, which in turn excite cone ON bipolar cells (via gap junctions) and inhibit cone OFF bipolar cells (viaglycine-mediated inhibitory synapses) thereby overtaking the cone pathway in order to send signals to ganglion cells at scotopic (low) ambient light conditions.[2]

OFF bipolar cells synapse in the outer layer of the inner plexiform layer of the retina, and ON bipolar cells terminate in the inner layer of the inner plexiform layer.

Signal transmission

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Bipolar cells effectively transfer information from rods and cones to ganglion cells. The horizontal cells and the amacrine cells complicate matters somewhat. The horizontal cells introducelateral inhibition to the dendrites and give rise to the center-surround inhibition which is apparent in retinalreceptive fields. Theamacrine cells also introducelateral inhibition to the axon terminal, serving various visual functions including efficient signal transduction with high signal-to-noise ratio.[3]

The mechanism for producing the center of a bipolar cell'sreceptive field is well known: direct innervation of thephotoreceptor cell above it, either through ametabotropic (ON) orionotropic (OFF) receptor. However, the mechanism for producing the monochromatic surround of the same receptive field is under investigation. While it is known that an importantcell in the process is thehorizontal cell, the exact sequence ofreceptors andmolecules is unknown.

See also

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Notes

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  1. ^Kevin S. LaBar; Purves, Dale;Elizabeth M. Brannon; Cabeza, Roberto; Huettel, Scott A. (2007).Principles of Cognitive Neuroscience. Sunderland, Mass: Sinauer Associates Inc. p. 253.ISBN 978-0-87893-694-6.
  2. ^Bloomfield Stewart A.; Dacheux Ramon F. (2001). "Rod Vision: Pathways and Processing in the Mammalian Retina".Progress in Retinal and Eye Research.20 (3):351–384.doi:10.1016/S1350-9462(00)00031-8.PMID 11286897.S2CID 43225212.
  3. ^Tanaka M, Tachibana M (15 August 2013)."Independent control of reciprocal and lateral inhibition at the axon terminal of retinal bipolar cells".J Physiol.591 (16):3833–51.doi:10.1113/jphysiol.2013.253179.PMC 3764632.PMID 23690563.

References

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External links

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