Photoreceptors are the first in the chain of neurons that process visual information. In lateral eyes of vertebrates, light hyperpolarizes rod and cone photoreceptors that synapse onto bipolar and horizontal cells in the first synaptic layer of the retina. The sign of the photoreceptor signal is either conserved or inverted in bipolar cells, resulting in chromatically dependent depolarizing and hyperpolarizing responses to visual stimuli. Visual information is then conveyed to the second synaptic layer for encoding and transmission to the brain by ganglion cells. The parietal (third) eye of lizards does not contain bipolar cells or other interneurons. Photoreceptors synapse directly onto ganglion cells and yet, even in the absence of interneurons, antagonistic chromatic mechanisms modulate the ganglion cell responses. We report here that chromatic antagonism in the third eye originates in the chromatically dependent hyperpolarizing and depolarizing response of the photoreceptors to light. We also suggest that the antagonistic nature of these photoresponses may provide lizards with a mechanism for the enhanced detection of dawn and dusk.
The retina is among the most metabolically active tissues in the body, requiring a constant supply of blood glucose to sustain function. We assessed the impact of low blood glucose on the vision of C57BL/6J mice rendered hypoglycemic by a null mutation of the glucagon receptor gene, Gcgr. Metabolic stress from moderate hypoglycemia led to late-onset loss of retinal function in Gcgr ؊/؊ mice, loss of visual acuity, and eventual death of retinal cells. Retinal function measured by the electroretinogram b-wave threshold declined >100-fold from age 9 to 13 months, whereas decreases in photoreceptor function measured by the ERG a-wave were delayed by 3 months. At 10 months of age Gcgr ؊/؊ mice began to lose visual acuity and exhibit changes in retinal anatomy, including an increase in cell death that was initially more pronounced in the inner retina. Decreases in retinal function and visual acuity correlated directly with the degree of hypoglycemia. This work demonstrates a metabolic-stress-induced loss of vision in mammals, which has not been described previously. Linkage between low blood glucose and loss of vision in mice may highlight the importance for glycemic control in diabetics and retinal diseases related to metabolic stress as macular degeneration.C57BL/6J mice ͉ cell death ͉ glucagon receptor gene ͉ retinal function ͉ visual acuity C hanges in metabolism can affect vision. Lowering blood glucose (BG) can decrease human visual sensitivity (1-3) as does reducing the partial pressure of inhaled oxygen (4). Natural nighttime decreases in glucose availability (5, 6) parallel a decline in visual sensitivity that can be restored by glucose ingestion (7). In the cat, acute decreases in glucose supply can transiently reduce retinal sensitivity (8) and exacerbate the effects of hypoxia on the retina (9). The effects of metabolite supply on vision are not surprising in view of the high energy consumption by the retina (10, 11). Although the retina's high metabolic activity has been known for Ͼ40 years (12), the consequences of an inadequate supply of metabolites are not completely understood.We report here that a chronic decrease in BG in mice decreases retinal function, leading to a loss of vision and eventual degeneration of the retina. We observed decreases in both electroretinogram (ERG) a-and b-waves, as well as a loss in visual acuity. Retinal cell death, assayed by TUNEL, was increased in Gcgr Ϫ/Ϫ mice, and decreases in cell number were detected. These data indicate that a chronic decrease in BG leads to loss of vision and cell death in mice and highlight the possibility that the human retina may likewise be susceptible to hypoglycemia. ResultsGlucagon Receptor and Changes in BG. Hypoglycemia was induced in C57BL/6J mice by a null mutation of the glucagon receptor gene, Gcgr (13). Among its actions, the glucagon receptor under control of glucagon regulates gluconeogenesis to increase BG levels. Liver and kidney abundantly express Gcgr, and PCR analysis reveals trace levels of receptor mRNA in the retina of wi...
Histochemical and autoradiographic analyses of the axonal transport of horseradish peroxidase and tritiated amino acids were employed to study the central connectivity of the lizard parietal eye. Somata and processes of centrifugal fibers to the parietal eye were localized in tissue of the dorsal sac and in the leptomeningeal sheath of the pineal gland. Analyses of series of transverse sections of the brain showed the left medial habenular nucleus to be subdivided into pars dorsolateralis and pars ventromedialis, and the right medial habenular nucleus not to be so subdivided. Centripetal fibers of parietal eye ganglion cells project to only the pars dorsolateralis of the left medial habenular nucleus and terminate there in two distinct fields. The asymmetry of the lizard habenula may be a specialization associated with the unilateral projection from the parietal eye.
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