Final answer:
In darkness, photoreceptors are depolarized and release glutamate, inhibiting bipolar cells. Upon light stimulation, rhodopsin activation leads to hyperpolarization of photoreceptors, reducing glutamate release. These events affect visual signal transmission to the brain.
Step-by-step explanation:
In the dark, the photoreceptor cells in the retina are depolarized, which means they have a less negative charge inside compared to the outside of the cell. This depolarization occurs due to the action of certain cellular machinery which keeps sodium (Na+) channels open allowing a steady influx of Na+ ions. This inflow helps to maintain a depolarized state. Photoreceptor cells release the neurotransmitter glutamate onto bipolar cells, inhibiting them under these conditions. However, it is important to note that the statement 'the cell is hyperpolarized to about -80mV' is incorrect for a photoreceptor in the dark. Instead, photoreceptors become hyperpolarized when they are stimulated by light due to the closure of sodium channels.
When light strikes the photoreceptor, a molecule called rhodopsin gets activated which in turn activates the G protein known as transducin. This protein activates phosphodiesterase, which converts cyclic guanosine monophosphate (cGMP) to guanosine monophosphate (GMP). This results in the closing of sodium channels, and hence, the photoreceptor membrane becomes hyperpolarized. As a consequence, less glutamate is released onto the bipolar cells.