8.5 - Rods, light and retinal signalling

Rods and their light-sensitive pigment

A rod is a specialised receptor cell in the mammalian retina that detects light, particularly at low light intensities.

A rod's outer segment contains many membrane discs with the light-sensitive pigment rhodopsin. Rhodopsin consists of opsin, a protein, combined with retinal, a light-absorbing molecule derived from vitamin A. Retinal is the molecule bound in this pigment; do not substitute the related vitamin A molecule retinol.

In the unactivated pigment, retinal has the 11-cis arrangement. When it absorbs a photon, retinal changes to the all-trans arrangement. This change in molecular shape changes the conformation of the opsin protein, producing an activated state of rhodopsin. The activated pigment starts an intracellular signalling sequence; it is not itself an ion channel.

Activated rhodopsin subsequently breaks down into opsin and retinal, a process called bleaching. The key trigger is the light-induced shape change and pigment activation, rather than free retinal physically plugging a channel. To regenerate light-sensitive rhodopsin, the visual cycle restores 11-cis retinal, which combines with opsin again. Regeneration restores sensitivity after bleaching; spending time in the dark allows this to contribute to dark adaptation. The detailed enzyme sequence of this recycling process is not needed here.

The rod's dark current

A rod is electrically active in darkness because some cation channels in its outer-segment plasma membrane are open.

A cation is a positively charged ion. These channels allow sodium ions, $\mathrm{Na}^{+}$, to enter the rod down their electrochemical gradient. They also admit calcium ions, but sodium entry is the main ion movement to follow in this explanation. The inward movement of positive charge is part of the dark current.

The channels are held open by an intracellular signalling molecule called cyclic GMP, or cGMP. They are different from the voltage-gated sodium channels that produce the rising phase of an axonal action potential. The rhodopsin-containing disc membranes and the plasma membrane containing these cation channels are also different structures.

At the same time, potassium ions leave through channels in the rod's inner-segment membrane. The membrane potential depends on the balance of inward and outward currents. In darkness, the inward cation current keeps the rod relatively depolarised: its inside is less negative than it becomes in light. Ion pumps and other transporters maintain the concentration gradients that make these currents possible.

This dark membrane potential keeps voltage-gated calcium channels at the rod's synaptic terminal relatively active. Calcium entry there supports continuous release of the neurotransmitter glutamate. The terminal calcium channels controlling release are distinct from the outer-segment cation channels responding to the light-signalling sequence.

This provides a baseline that can be changed. Detecting light will reduce a signal the rod is already sending, rather than simply switch an electrically silent cell on.

Light closes cation channels

Light changes the rod's membrane potential by reducing its inward cation current.

Activated rhodopsin starts a signalling cascade that lowers the concentration of cGMP. With less cGMP available, fewer cation channels remain open in the outer-segment plasma membrane. Sodium entry therefore falls. Rhodopsin is not a sodium pump, and light does not have to make sodium flow out through these channels.

Potassium continues to leave the inner segment while the inward positive current is reduced. The inside consequently becomes more negative relative to the outside: the rod hyperpolarises.

The voltage change spreads to the synaptic terminal. Hyperpolarisation reduces opening of the terminal's voltage-gated calcium channels, so less calcium enters there and less glutamate is released. A strong light response can suppress release greatly; “reduced release” is the useful general statement, rather than claiming every light stimulus always produces exactly zero transmitter.

The rod's response is a graded potential. Its size varies with stimulation over the rod's working range, until the response approaches saturation. It is not an all-or-nothing action potential. Closing the outer-segment channels changes the membrane current and voltage; it does not create a train of spikes in the rod.