In that year Japanese 
neurophysiologist Tsuneo 
Tomita, working at Keio 
University in Tokyo, first 
succeeded in getting a 
microelectrode inside the 
cones of a fish, with a result so 
surprising that many 
contemporaries at first 
seriously doubted it. In the 
dark, the potential across the 
cone membrane was 
unexpectedly low for a nerve 
cell: roughly 50 millivolts 
rather than the usual 70 
millivolts. When the cone was 
illuminated, this potential 
increased--the membrane 
became hyperpolarized--just 
the reverse of what everyone 
had assumed would happen. In 
the dark, vertebrate light 
receptors are apparently more 
depolarized (and have a lower 
membrane potential) than 
ordinary resting nerve cells, 
and the depolarization causes a 
steady release of transmitter at 
the axon terminals, just as it 
would in a conventional 
receptor during stimulation. 
Light, by increasing the 
potential across the receptor-
cell membrane (that is, by 
hyperpolarizing it), cuts down 
this transmitter release. 
Stimulation thus turns the 
receptors off, strange as that 
may seem. Tomita's discovery 
may help us to understand why 
the optic-nerve fibers of 
vertebrates are so active in the 
dark: it is the receptors that are 
spontaneously active; 
presumably, many of the 
bipolar and ganglion cells are 
simply doing what the receptors 
tell them to do.

    In the ensuing decades, the 
main problems have been to 
learn how light leads to 
hyperpolarization of the 
receptor, especially how 
bleaching as little as a single 
molecule of visual pigment, by a 
single photon of light, can lead, 
in the rod, to a measureable 
change in membrane potential. 
Both processes are now 
reasonably well understood. 
Hyperpolarization by light is 
caused by the shutting off of a 
flow of ions. In darkness, part 
of the receptor membrane is 
more permeable than the rest of 
the membrane to sodium ions. 
Consequently, sodium ions 
continually flow into the cell 
there, and potassium ions flow 
out elsewhere. This flow of ions 
in the dark, or dark current, 
was discovered in 1970 by 
William Hagins, Richard Penn, 
and Shuko Yoshikami at the 
National Institute of Arthritis 
and Metabolic Diseases in 
Bethesda. It causes 
depolarization of the receptor 
at rest, and hence its continual 
activity. As a result of the 
bleaching of the visual pigment 
in response to light, the sodium 
pores close, the dark current 
decreases, and the membrane 
depolarization declines--the 
cell thus hyperpolarizes. Its 
rate of activity (that is, 
transmitter release) decreases.