Contrast is computed throughout the nervous system to encode changing inputs efficiently. The retina encodes luminance and contrast over a wide range of visual conditions and so must adapt its responses to maintain sensitivity and avoid saturation. Here we show how one type of adaptation allows individual synapses to compute contrast and encode luminance in biphasic responses to step changes in light levels. Light-evoked depletion of the readily releasable vesicle pool (RRP) at rod bipolar cell (RBC) ribbon synapses in rat retina limits the dynamic range available to encode transient but not sustained responses, thereby allowing the transient and sustained components of release to compute temporal contrast and encode mean light levels, respectively. A release/replenishment model shows that a single, homogeneous pool of synaptic vesicles is sufficient to generate this behavior and reveals that the dominant mechanism shaping the biphasic contrast/luminance response is the partial depletion of the RRP.

Dendritic spikes that propagate toward the soma are well documented, but their physiological role remains uncertain. Our in vitro patch-clamp recordings and two-photon calcium imaging show that direction-selective retinal ganglion cells (DSGCs) utilize orthograde dendritic spikes during physiological activity. DSGCs signal the direction of image motion. Excitatory subthreshold postsynaptic potentials are observed in DSGCs for motion in all directions and provide a weakly tuned directional signal. However, spikes are generated over only a narrow range of motion angles, indicating that spike generation greatly enhances directional tuning. Our results indicate that spikes are initiated at multiple sites within the dendritic arbors of DSGCs and that each dendritic spike initiates a somatic spike. We propose that dendritic spike failure, produced by local inhibitory inputs, might be a critical factor that enhances directional tuning of somatic spikes.

ToxB, a gene that encodes a 6.6-kDa host-selective toxin (HST), is present in several races of the wheat pathogen Pyrenophora tritici-repentis. To learn more about the multiple ToxB open reading frames (ORFs), six of the estimated nine copies from a race 5 isolate were cloned and analyzed. All six copies of ToxB have identical 261-bp ORFs and thus encode the same form of Ptr ToxB. Sequence analysis of regions flanking the cloned ToxB loci revealed that the majority of loci are associated with portions of retrotransposons and a transposon-like sequence. Data indicate that ToxB loci reside on two chromosomes, 3.5 and 2.7 Mb, with the majority of copies located on the 2.7 Mb chromosome. A related gene, referred to as toxb, from a nonpathogenic race 4 isolate was also cloned and characterized. This is interesting because, until now, HST genes have only been found in toxin-producing, pathogenic isolates of plant pathogenic fungi. The toxb gene from nonpathogenic isolates is 86% similar to ToxB, and data suggest that toxb is a single-copy gene. No toxb transcript was detected under culture conditions that favor the expression of ToxB; therefore, these genes differ in their transcriptional regulation.

The genetic locus for incomplete congenital stationary night blindness (CSNB2) has been identified as the CACNA1f gene, encoding the alpha 1F calcium channel subunit, a member of the L-type family of calcium channels. The electroretinogram associated with CSNB2 implicates alpha 1F in synaptic transmission between retinal photoreceptors and bipolar cells. Using a recently developed monoclonal antibody to alpha 1F, we localize the channel to ribbon active zones in rod photoreceptor terminals of the mouse retina, supporting a role for alpha 1F in mediating glutamate release from rods. Detergent extraction experiments indicate that alpha 1F is part of a detergent-resistant active zone complex, which also includes the synaptic ribbons. Comparison of native mouse rod calcium currents with recombinant alpha 1F currents reveals that the current-voltage relationship for the native current is shifted approximately 30 mV to more hyperpolarized potentials than for the recombinant alpha 1F current, suggesting modulation of the native channel by intracellular factors. Lastly, we present evidence for L-type alpha 1D calcium channel subunits in cone terminals of the mouse retina. The presence of alpha 1D channels in cones may explain the residual visual abilities of individuals with CSNB2.