Visual behavior of adult goldfish with regenerating retina.

To determine whether regenerating neural pathways can support visual behavior, adult goldfish (Carassius auratus) were injected intraocularly with ouabain and tested for the presence of reflexive visual behaviors (dorsal light reflex and optokinetic nystagmus) and the ability to respond to visual stimuli in a classical conditioning paradigm. All visual behaviors were absent or greatly diminished until 8 to 10 weeks, when retinal layering had returned. At 10 weeks post-ouabain, reflexive behaviors to supra-threshold stimuli were near normal; however the ability to detect supra-threshold stimuli in the conditioning paradigm did not recover until 13 weeks. Absolute dark-adapted threshold and light-adapted spectral sensitivity measured at 13 to 17 weeks were abnormal: Dark-adapted threshold was elevated by 1.5 log units and light-adapted spectral sensitivity was markedly narrower than normal. No responses to 50% contrast sinusoidal gratings could be obtained through ouabain-treated eyes using the classical conditioning technique, even though responses through the untreated eye remained. Results demonstrate that: (a) visually mediated behaviors return in goldfish with ouabain-treated retinas; (b) the time course of recovery of reflexive responses in luminance and spatial domains parallels return of ERG function and of tectal activity; and (c) visual function that is mediated by regenerating retina appears not to be as sensitive as vision via normally developed retinal pathways.

Intestinal lipoproteins in the rat with D-(+)-galactosamine hepatitis.

D-(+)-galactosamine (GalN) induces severe reversible hepatocellular injury in the rat accompanied by lecithin: cholesterol acyltransferase (LCAT) deficiency, defective chylomicron (CM) catabolism, and accumulation of abnormal plasma lipoproteins (Lps), including discoidal high density lipoproteins (HDL). These abnormalities are presumed to result from hepatic injury alone, but the effect of GalN on intestinal Lps has not been studied. To assess possible effects on intestinal Lp formation and secretion, mesenteric lymph fistula rats were injected with GalN or saline. Twenty-four hours later a 2-hr fasting lymph sample was collected; this was followed by an 8-hr duodenal infusion of a lipid emulsion containing 17.7 mM [3H]triolein at 3 ml/hr. Fasting lymph and fat-infused lymph flow rates, 3H, triglyceride, and cholesterol output, residual 3H in intestinal lumen and mucosa, total 3H recovery, and d less than 1.006 g/ml Lp size and lipid composition were unchanged by GalN treatment, but d less than 1.006 g/ml Lps were depleted of apoE and C. Fat-infused lymph phospholipid (PL) output was higher in GalN rats due to PL-enriched d greater than 1.006 g/ml Lps. Electron microscopy of lymph and plasma LDL and HDL revealed spherical Lps in all samples. GalN plasma, fasting lymph, and fat-infused lymph also contained large abnormal LDL and discoidal HDL. Control lymph LDL and HDL did not differ in size from control plasma LDL and HDL. Control lymph LDL contained both apoB240K and B335K. However, spherical LDL and discoidal HDL in fasting lymph from GalN rats differed significantly in size from the corresponding plasma particles and became closer in size to the plasma particles with fat infusion. GalN lymph LDL contained only apoB240K and had a lower PL/CE than GalN plasma LDL. GalN fasting lymph HDL, depleted of apoC and having a PL/CE of 5, became enriched in apoE and the PL/CE increased to 10 with fat infusion to closely resemble GalN plasma HDL. GalN reduces apoE and C (mainly of hepatic origin) in d less than 1.006 g/ml gut Lps, which may contribute to the CM catabolic defect in GalN rats. Lymph LDL and HDL, especially in fasting lymph, may be partially gut-derived with increased filtration of plasma Lps into lymph with fat infusion. GalN fat-infused lymph HDL is enriched in apoE, but unable to transfer apoE to d less than 1.006 g/ml intestinal Lps. We conclude that GalN hepatitis is a model that allows study of intestinal Lps with normal lipid digestion and absorption in the face of severe hepatic injury and LCAT deficiency.

Erythrocyte alterations in praseodymium-induced lecithin:cholesterol acyltransferase (LCAT) deficiency in the rat: comparison with familial LCAT deficiency in man.

The intravenous administration of praseodymium nitrate (PrN) to rats was associated with parallel decreases in plasma lecithin: cholesterol acyltransferase (LCAT) activity and erythrocyte osmotic fragility at low doses (20 and 40 mg/kg) while higher doses (80 mg/kg) resulted in increases in both. Erythrocyte membranes from rats with PrN-induced LCAT deficiency exhibited small increases in cholesterol content, but not other alterations (e.g., in phospholipid profiles and sulfhydryl group latency) which characterize erythrocytes in familial LCAT deficiency in man. The administration of PrN caused a time- and dose-dependent accumulation of praseodymium in liver with hepatic levels being substantially greater in animals given the high (protective) as compared with the low (toxic) doses of PrN. Hepatic levels of glutathione were not altered by PrN administration, but hexobarbital sleeping time was markedly prolonged in animals receiving a toxic dose of PrN. It is suggested that dose-dependent alterations in the subcellular distribution of praseodymium may explain the paradoxical pathophysiological effects of high and low doses of PrN.