Functions of insulin and insulin receptor signaling in retina: possible implications for diabetic retinopathy

Insulin action regulates the metabolic functions of the classically insulin-responsive tissues: liver, adipose, and skeletal muscle. Evidence also suggests that insulin acts on neural tissue and can modulate neural metabolism, synapse activity, and feeding behaviors. Insulin receptors are expressed on both the vasculature and neurons of the retina, but their functions are not completely defined. Insulin action stimulates neuronal development, differentiation, growth, and survival, rather than stimulating nutrient metabolism, e.g., glucose uptake as in skeletal muscle. Insulin receptors from retinal neurons and blood vessels share many similar properties with insulin receptors from other peripheral tissues, and retinal neurons express numerous proteins that are attributed to the insulin signaling cascade as in other tissues. However, undefined neuron-specific signals downstream of the insulin receptor are likely to also exist. This review compares retinal insulin action to that of peripheral tissues, and demonstrates that the retina is an insulin-sensitive tissue. The review also addresses the hypothesis that dysfunctional insulin receptor signaling in the retina contributes to cell dysfunction and death in retinal diseases.     

The fine structure of the pineal gland in the pocket gopher,Geomys bursarius

The morphology of the pineal gland of the pocket gopher, Geomys bursarius, is of special interest because this species is exposed to extremes of environmental lighting in its natural habitat. The pineal gland of the gopher has been studied in specimens collected as they were about to enter their winter dormant period. The gopher pineal is similar to other mammalian pineal glands in that it possesses light and dark parenchymal cells, glia, and pigment-containing-cells. Vascular-parenchymal relationships are similar to other species. Vesicles containing electron-opaque cores are infrequently encountered in the parenchymal cells. Parenchymal cells and pigment cells occasionally abut a lumen, suggesting an acinar arrangement. Large cytoplasmic vacuoles several microns in diameter are present in the parenchymal cells.     

Tin distribution in adult and neonatal rat brain following exposure to triethyltin

The uptake, distribution, and elimination of tin were determined in adult and neonatal (Postnatal Day 5) rat brain following ip administration of triethyltin bromide (TET). Groups of five adult CD rats were killed at 10 min, 1 hr, 4 hr, 24 hr, 5 days, or 10 days following acute exposure to 6.0 mg/kg TET; an additional group of adult animals was killed at 24 hr following exposure to either 3.0, 6.0, or 9.0 mg/kg (N = 5/dosage). The time course for tin distribution in 5-day-old rat pups was determined by killing pups 10 min, 30 min, 1 hr, 4 hr, 8 hr, 12 hr, 24 hr, 5 days, 10 days, or 22 days following exposure to either 3.0 or 6.0 mg/kg TET (N = 4/dosage/time). Tin analyses were performed by flameless atomic absorption spectrophotometry. The $\text{t}{}^{\mathrm{<mtext>1</mtext><mtext>2</mtext>}}$ for total tin in the adult rat brain following 6.0 mg/kg TET was determined to be 8.0 days. The maximum concentration in the adult was reached at 24 hr and corresponded to 4.6, 9.6, and 16.6 ng tin/mg protein for dosages of 3.0, 6.0, and 9.0 mg/kg, respectively. Tin was evenly distributed across all brain areas studied. For animals exposed to 6.0 mg/kg TET on Postnatal Day 5, the $\text{t}{}^{\mathrm{<mtext>1</mtext><mtext>2</mtext>}}$ for total tin in the brain was 7.3 days. A maximum concentration of 9.9 ng tin/mg protein was reached at 8 hr postexposure. The rate of elimination of tin from the brain (as measured by the elimination rate constant k_el) did not differ significantly between adults and neonates. However, due to a dilution effect by the rapid brain growth of the neonate, the concentration of tin in the neonatal brain following TET administration decreased significantly faster than that in the adult.     

Relative Efficacy of Melatonin and 5-Methoxytryptamine in Terms of Their Antigonadotrophic and Counterantigonadotrophic Actions in Male Syrian Hamsters

Antigonadotrophic and counterantigonadotrophic activities of melatonin and 5-methoxytryptamine (5-MT) were quantitatively compared in male Syrian hamsters. In long day conditions, the daily afternoon administration of either 5, 15, 25, 50, 100 or 200 μg melatonin induced testicular regression within 10 wk; under the same circumstances, only the 200-μg dosage of 5-MT was able to suppress testicular weights. Thus, 5-MT appears to have about one-tenth the antigonadotrophic action of melatonin in the male Syrian hamster. In short days, the subcutaneous implantation of either 50 or 100 μg melatonin (every 2 wk in beeswax) prevented testicular regression whereas it required much larger doses of 5-MT (1 mg every 2 wk in beeswax) to achieve the same counterantigonadotrophic action. In terms of both their antigonadotrophic and counterantigonadotrophic effects, hamsters seem to be more sensitive to melatonin than to 5-MT.     

The Influence of Various Irradiances of Artificial Light, Twilight, and Moonlight on the Suppression of Pineal Melatonin Content in the Syrian Hamster

The purpose of the present studies using artificial light was to determine how the timing and duration of exposure influence the light-induced suppression of pineal melatonin levels in hamsters. An 8-min exposure to 0.186 microW/cm2 of cool white fluorescent light caused a continued depression of pineal melatonin even when animals were returned to darkness. In addition, the pineal gland does not appear to change its sensitivity to light throughout the night. A 20-min exposure to 0.019 microW/cm2 of cool white fluorescent light did not significantly suppress pineal melatonin during any time of the melatonin peak, whereas a 20-min exposure to 0.186 microW/cm2 was capable of always suppressing melatonin. Furthermore, increasing the duration of 0.019-microW/cm2 exposure to 30, 60, 120, or 180 min does not increase the capacity of this irradiance to depress melatonin. Similar to artifical light, natural light has a variable capacity for suppressing nocturnal levels of pineal melatonin. Twilight irradiances of 0.138 microW/cm2 or less did not suppress nocturnal melatonin whereas twilight irradiances of 3.0 microW/cm2 or greater did suppress pineal melatonin. A few animals did have lower melatonin after a 40-min exposure to full moonlight during July (0.045 microW/cm2) or January (0.240 microW/cm2). However, pineal melatonin levels remained high in the majority of animals exposed to full moonlight.     

Hirnstammblutungen infolge kapillarer Telangiektasien — ein Substrat des plötzlichen Todes aus natürlicher Ursache

Zusammenfassung Blutungen in der Hirnbrücke aus kapillären Telangiektasien stellen selten zu beobachtende Verä nderungen dar. Es werden fünf Fälle vorgestellt, bei denen diese Blutungen auch als Todesursache gewertet werden konnten. Zweimal war es, infolge der Umstände des Falles, möglich auf einen äußerst raschen Bewußtseinsverlust und/oder sofortigen Tod zu schließen. In zwei Fällen bestand zusä tzlich eine urämische Stoffwechsellage, so daß diskutiert werden muß, ob die Blutungen nicht auch als Komplikation im Zuge der renalen Grunderkrankung aufgetreten sein könnten. Für den Gerichtsmediziner erscheint es wissenswert, daß kapilläre Telangiektasien unter Umständen auch auslösendes Substrat für ein Unfallgeschehen darstellen können.