Synaptic transmission between vertebrate retinal photoreceptors and second order neurons is mediated by glutamate, but the postsynaptic receptors, as well as the intrinsic synaptic mechanisms, are different for each type of bipolar cell. In salamander retina it has been shown that depolarizing bipolars have a metabotropic receptor sensitive to the glutamate agonist APB which activates a second messenger cascade ending with the closing of cyclic GMP-gated cationic channels. On the other hand, at hyperpolarizing bipolars glutamate and various agonists such as kainate, open cationic channels by an ionotropic mechanism. Finally, it was reported recently that in some retinal bipolar cells of certain fishes, glutamate opens chloride channels that would appear to be associated with a glutamate transporter. In order to perform studies of the mechanisms associated with these various types of synaptic transmission, the responses to glutamate and kainate were recorded with patch electrodes from bipolar cells in slices of the zebrafish retina. Some of the bipolar cells respond to both substances with an increase in conductance and a current that reverses polarity at zero membrane potential; these cells are presumed to represent hyperpolarizing bipolars. In other instances, glutamate evokes an increase in conductance and a current that reverses at about -60 mV; further work is required to establish whether this effect is due to an increase in chloride conductance. Finally, a third type of bipolar cells shows a glutamate induced current that reverses polarity at potentials of -20 to -40 mV; such cells have not been observed in other retina and it will be necessary to determine whether the reversal potential represents an algebraic sum of effects on more than one kind of ionic conductance. Of special note is the fact that so far it has not been possible to find any instances in which glutamate induces a decrease in conductance, which is the action usually detected in depolarizing bipolar cells of other retinae.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Intramural Research (Z01)
Project #
1Z01NS001659-29
Application #
6162979
Study Section
Special Emphasis Panel (LNP)
Project Start
Project End
Budget Start
Budget End
Support Year
29
Fiscal Year
1997
Total Cost
Indirect Cost
City
State
Country
United States
Zip Code