ON bipolar cells invert the sign of light responses from hyperpolarizing to depolarizing before passing them on to ganglion cells. Light responses are generated when a cation channel, recently identified as Trpm1, opens. The amplitude of the light response rapidly decays due to desensitization of Trpm1 current. The role of Trpm1 desensitization in shaping light responses both in bipolar and downstream ganglion cells has not been well characterized. Here we show that two parameters, the amount and the rate of recovery from desensitization, depend on the strength of the presynaptic stimulus. Stimuli that activate less than 20% of the maximum Trpm1 current did not promote any detectable desensitization, even for prolonged periods. Beyond this threshold there was a linear relationship between the amount of desensitization and the fractional Trpm1 current. In response to stimuli that open all available channels, desensitization reduced the response to approximately 40% of the peak, with a time constant of 1 s, and recovery was slow, with a time constant of more than 20 s. In dye-filled bipolar cells classified as transient or sustained using morphological criteria, there were no significant differences in Trpm1 desensitization parameters. Trpm1 activation evoked robust EPSCs in ganglion cells, and removal of Trpm1 desensitization strongly augmented a sustained component of the ganglion cell EPSC irrespective of whether ganglion cells were of the ON or ON/OFF type. We conclude that Trpm1 desensitization impacts the kinetics of ganglion cell EPSCs, but does not underlie the sustained/transient dichotomy of neurons in the ON pathway.
ASJC Scopus subject areas