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PubMedDate not supplied

Retinal changes in Otsuka long-evans Tokushima Fatty rats (spontaneously diabetic rat)--possibility of a new experimental model for diabetic retinopathy.

PURPOSE: To study retinal changes in the Otsuka Long-Evans Tokushima Fatty (OLETF) rat, a spontaneously diabetic rat, and evaluate it as a possible new diabetic retinopathy model. METHODS: We examined the retinas of OLETF rats and Long-Evans Tokushima Otsuka (LETO) rats as controls under both a transmission electron microscope (TEM) and a scanning electron microscope (SEM). RESULTS: We detected higher blood sugar level in the OLETF rats than in the LETO rats beginning at 5 months of age. The inner nuclear layers of the retina decreased from 3-4 rows to 2 rows, whereas the photoreceptor cell nuclei decreased from 8 rows to 3-6 rows. Retinal pigment epithelial cells decreased in height, and basal infoldings were poorly developed. Retinal capillary basement membranes were significantly thicker in the OLETF rats than in the LETO rats, and endothelial cell damage was observed. The SEM of vascular corrosion casts of OLETF rats showed tortuosity, microaneurysms, and loop formations. CONCLUSIONS: The development of spontaneous hyperglycemia in OLETF rats was associated with alterations in retina ultrastructure. Changes were similar to those seen in diabetic retinopathy, but did not include either hemorrhages or exudates. The OLETF rat may be a useful animal model for the study of ocular complications in humans.

Animals↗

PubMed2003

Long-Evans and Sprague-Dawley rats have similar skilled reaching success and limb representations in motor cortex but different movements: some cautionary insights into the selection of rat strains for neurobiological motor research.

Many rat strains are used for neurobiological studies of nervous system function and behavior. The most widely used strain for studies of the neural basis of movement is the out bred, pigmented Long-Evans strain, while the most widely used strains for the study of movement impairments in neurological disease are out bred albino rats, including Sprague-Dawley rats. Although previous research has indicated that there are strain differences in skilled movements displayed by different rat strains, there has been no explicit comparison of the Long-Evans and Sprague-Dawley strains. This was the purpose of the present study. The rats were video recorded as they learned to reach for single food pellets and the video records were subjected to frame-by-frame analysis. Component movements of reaching were scored using a system derived from Eshkol-Wachman Movement Notation (EWMN). The quality of movements was described using Laban Movement Analysis (LMA). Forelimb representations in motor cortex were defined electrophysiologically. Acquisition scores and success in reaching did not differ between the two strains, nor did the topographical representation of the forelimb in motor cortex. Long-Evans and Sprague-Dawley rats did differ in the movements used for reaching and on the quality of their movements. The movements of Sprague-Dawley rats resembled the movements of Long-Evans rats with motor system injury. That rat strains can show both quantitative and qualitative differences in movement is useful for the understanding of the genetic, neural, and behavioral organization of the motor system. The results are also relevant to the question of appropriateness of particular rat strains for studies of neurological diseases and the effects of albinism on motor behavior, and suggest that some of the most widely used rat strains for neurological investigations may be less than appropriate.

Animals↗

PubMed2003

Deficient prepulse inhibition of acoustic startle in Hooded-Wistar rats compared with Sprague-Dawley rats.

1. Prepulse inhibition of acoustic startle has been suggested as a model of sensorimotor gating and central sensory information processing. Prepulse inhibition is impaired in patients with schizophrenia and responses can be restored by antipsychotic drug treatment. In the present study, startle and prepulse inhibition of startle were compared in different rat strains. 2. Sprague-Dawley rats showed robust inhibition of startle responses by increasing intensities of prepulse delivered just before the startle stimulus. In contrast, at both 4 and 10 weeks of age, rats of the Hooded-Wistar line had markedly reduced prepulse inhibition, although startle responses were not different. 3. Treatment with the dopamine receptor agonist apomorphine (0.1 mg/kg) or the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801 (0.1 mg/kg) caused disruption of prepulse inhibition in Sprague-Dawley rats. In Hooded-Wistar rats, apomorphine further reduced the already low level of prepulse inhibition, but MK-801 treatment had no significant effect. This suggests that the impaired prepulse inhibition in Hooded-Wistar rats could be caused by changes in glutamatergic activity and/or NMDA receptors in these rats. 4. In photocell cages, spontaneous exploratory activity and inner zone activity were significantly lower in Hooded-Wistar rats than in Sprague-Dawley rats. Similarly, on the elevated plus-maze, Hooded-Wistar rats showed a lower propensity to visit the open arms. In contrast, amphetamine (0.5 mg/kg)-induced locomotor hyperactivity, an animal model of psychosis, was enhanced in Hooded-Wistar rats. 5. These data suggest that the Hooded-Wistar line could be a useful genetic animal model to study the interaction of glutamatergic and dopaminergic mechanisms in anxiety and schizophrenia.

Acoustic Stimulation↗

PubMed1993

A new genetic locus cosegregating with blood pressure in F2 progeny obtained from stroke-prone spontaneously hypertensive rats and Wistar-Kyoto rats.

BACKGROUND: Segregation studies using genomic polymorphisms on F2 progeny obtained from hypertensive rat models showed that a putative hypertensive gene is located close to the angiotensin converting enzyme (ACE) gene. However, it was suggested that additional major genes should contribute to the pathogenesis of hypertension. METHODS: F2 rats were obtained from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats of Izumo colony. Blood pressure was measured with a photoelectronic oscillometric tail-cuff method before and during salt loading. Genomic DNA was extracted from livers and digested with HaeIII or Rsal. DNA fingerprinting was performed with 26 32P-labelled human variable number of tandem repeats markers. RESULTS: Eighty-seven fingerprint bands polymorphic between SHRSP and WKY were obtained. When the distribution of these bands in the F2 progeny was studied, one fingerprint band (1/MCT96.1) showed a distorted distribution between the high- and low-blood pressure subpopulations of the F2 rats, suggesting that the band cosegregated with blood pressure. When blood pressure was compared between the F2 rats with [(+) rats] and without [(-) rats] the 1/MCT96.1 band, it was found that (-) rats had significantly higher basal and salt-loaded blood pressures than (+) rats. The 1/MCT96.1 locus was also shown to have no positive linkage with the ACE locus. CONCLUSION: The present study showed that examination of the allele distribution between subpopulations with extreme phenotype can be used in the screening of loci cosegregating with blood pressure. Furthermore, a locus not in the ACE region, showing cosegregation with blood pressure in F2 progeny from SHRSP and WKY rats, was found.

Animals↗

PubMed1993

Failure of the heat-shock protein 70 locus to cosegregate with blood pressure in spontaneously hypertensive rat x Wistar-Kyoto rat cross.

OBJECTIVE: To investigate the involvement of the heat-shock protein 70 (hsp70) locus, located in the rat major histocompatibility complex (RT1), in hypertension of the spontaneously hypertensive rat (SHR). Previous studies have shown abnormal expression of hsp70 in the SHR and an association of the SHR hsp70 allele with increased blood pressure in recombinant inbred strains derived from a cross of SHR with Brown-Norway rats. DESIGN: SHR were crossed with normotensive Wistar-Kyoto (WKY) rats to produce a large cohort of F2 rats segregating for blood pressure and hsp70 alleles. Two hundred and thirty-three rats were maintained on a normal-salt diet and 167 were put on a high-salt diet (1% sodium chloride in drinking water) from 16 to 26 weeks of age. METHODS: Blood pressure was measured indirectly at 12, 16 and 20 weeks of age in rats on the normal-salt diet and at 16 (pre-salt), 18 and 20 weeks in rats on the high-salt diet. Both groups had direct conscious blood pressure measurements at 25-26 weeks of age. Genotyping was carried out for a BamH1 polymorphism in the hsp70 gene by Southern blotting. RESULTS: The hsp70 genotype had no effect on any of the blood pressure measurements in rats on either diet. CONCLUSIONS: We find no evidence of linkage between the hsp70 gene locus, and by implication other genes located within the rat RT1 complex, and blood pressure in our cross of SHR and WKY rats.

Animals↗

PubMed1998

Dietary-sodium-induced cardiac remodeling in spontaneously hypertensive rat versus Wistar-Kyoto rat.

OBJECTIVE: To study the effects of short-term and long-term high sodium intake on cardiac mass and design in sodium-sensitive spontaneously hypertensive rats versus sodium-resistant Wistar-Kyoto rats. METHODS: Young spontaneously hypertensive rats and Wistar-Kyoto rats were randomly allocated to control diet, 2 or 8% dietary sodium for 2-12 weeks and changes in resting hemodynamics, cardiac angiotensin II level, sympathetic activity and cardiac structure evaluated. Sympathetic activity was assessed by measuring levels of plasma catecholamines, responses of blood pressure to ganglionic blockade, and rates of cardiac turnover of norepinephrine. RESULTS: High sodium intake for 4 weeks increased left ventricle weight of Wistar-Kyoto rats aged 4 weeks (by 11 and 25% for 2 and 8% NaCl diets, respectively). This hypertrophic response was temporary, however, had already diminished after 6 weeks, and was absent after 12 weeks of a high sodium intake. However, after prolonged exposure concentric remodeling occurred (i.e. left ventricle wall thickness : radius ratio increased with no change in left ventricle mass). High sodium intake did not affect resting blood pressure, cardiac index, cardiac angiotensin II level, and general sympathetic activity of Wistar-Kyoto rats. Short-term high sodium intake did not increase left ventricle mass of young spontaneously hypertensive rats, unless sodium intake was so high (8% NaCl) that blood pressure and general sympathetic activity increased, too. However, a prolonged moderate (2%) increase in sodium intake also caused concentric remodeling in spontaneously hypertensive rats without increasing left ventricle mass, blood pressure, cardiac index, and general and cardiac sympathetic activities. CONCLUSIONS: The blood pressure in young Wistar-Kyoto rats is sodium-insensitive but the heart structure is sodium-sensitive and high dietary sodium intake causes an early hypertrophic response, and then concentric remodeling. In contrast, hypertrophic response appears to occur after the response of blood pressure in spontaneously hypertensive rats, whereas the remodeling is similar to that in Wistar-Kyoto rats.

Angiotensin II↗

PubMed1993

Specific unresponsiveness in rats with prolonged cardiac allograft survival after treatment with cyclosporine. VI. In vitro alloreactivity of T cell subsets from rats with long-surviving allografts.

DA rats treated with a short course of cyclosporine develop specific unresponsiveness to RT1-incompatible PVG donor heart allografts. CD4+ cells, not CD8+ cells, transfer unresponsiveness to irradiated rats. However, host-derived CD8+ cells are important in reestablishing unresponsiveness. In this study, unfractionated lymphoid cells and W3/25+ (CD4+) cells from CsA-treated rats with long-surviving PVG allografts demonstrated normal alloreactivity to PVG alloantigen in the mixed lymphocyte culture and failed to suppress the proliferative response of naive W3/25+ cells to donor-specific alloantigen. MRC OX8+ (CD8+) cells did not proliferate. Sera from CsA-treated rats had no effect on the MLC reactivity of cells from CsA-treated rats, suggesting that blocking or antiidiotypic antibodies did not diminish alloreactivity. IL-2 production by W3/25+ cells from CsA-treated rats was similar to that by W3/25+ cells from naive rats. Specific cytotoxic T cells to PVG were generated in MLC, and the frequency of precursor cytotoxic lymphocytes in CsA-treated rats was similar to that in naive DA rats. In an in vitro assay testing response to idiotype, neither W3/25+ or MRC OX8+ cells from unresponsive rats proliferated. As CD4+ cells from CsA-treated rats lose their capacity to adoptively transfer specific unresponsiveness unless maintained in a cytokine-rich supernatant, all in vitro assays were performed with and without added cytokines, but no change in reactivity consistent with suppression was observed in any assay. CD4+ suppressor cells had no effect on conventional in vitro assays of alloreactivity, preventing the detection of the unresponsiveness in vitro.

Animals↗

PubMed1991

Normotensive Wistar rats differ from spontaneously hypertensive and renal hypertensive rats in their cardiovascular responses to opioid agonists.

1. The effects of three opioid receptor agonists on the blood pressure and heart rate of anaesthetized normotensive, spontaneously hypertensive and renal hypertensive rats were measured. 2. Mu agonist morphiceptin i.c.v. induced a pressor response and increase in heart rate in hypertensive rats, but hypotension in normotensive rats. After intravenous (i.v.) injection, morphiceptin produced a hypotensive response in all three groups of rats. 3. In contrast, the delta agonist DTLET i.c.v. decreased blood pressure and heart rate in hypertensive rats, but increased both pressure and beat rate in normotensive rats. After i.v. injections DTLET produced a hypertensive response and increase in heart rate in all groups of rats. 4. Kappa agonist U-50, 488H given i.c.v. induced effects similar to morphiceptin: an increase in blood pressure and heart rate in hypertensive and a decrease in normotensive rats. After i.v. injections U-50, 488H produced decreases in blood pressure and heart rate in all treated groups of rats. 5. Pretreatment with naloxone antagonized the activity of morphiceptin but prevented only the stimulating effect of DTLET in normotensive rats. Cardiovascular actions of U-50, 488H were not blocked by naloxone. 6. The results suggest that opioid agonists exert similar changes in cardiovascular function at central and peripheral sites in both models of experimental hypertension and these effects are different in normotensive rats.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed2006

Experimental stroke: ischaemic lesion volume and oedema formation differ among rat strains (a comparison between Wistar and Sprague-Dawley rats using MRI).

Investigating focal cerebral ischaemia requires animal models that are relevant to human stroke. This study was designed to evaluate the influence of early reperfusion and choice of rat strains on infarct volume and oedema formation. Thirty-six Wistar and Sprague-Dawley rats were subjected to temporary middle cerebral artery occlusion (MCAO) for 90 min (groups I and II) or to permanent MCAO (groups III and IV) using the suture technique. Ischaemic lesion volume and oedema formation were quantified 24 h after MCAO using 7T-magnetic resonance imaging (MRI). Impact of rat strains: Reperfusion led to significant larger ischaemic lesion volumes in Wistar rats as compared to Sprague-Dawley rats (P<0.0005). Oedema formation was similar in both rat strains. Permanent MCAO led to significantly larger ischaemic lesion volumes in Sprague-Dawley rats (P<0.05). Oedema formation, however, was significantly more accentuated in Wistar rats (P<0.005). Impact of reperfusion: Reperfusion did not cause any changes in ischaemic lesion volume in Wistar rats. Oedema formation, however, was significantly reduced (P<0.0005). In Sprague-Dawley rats, reperfusion caused a significant reduction of ischaemic lesion volume (P<0.00005), but did not modify oedema formation. These findings emphasize the critical importance of rat strain differences in experimental stroke research.

Animals↗

PubMed1985

Oxytocin and vasopressin in rat hypophysial portal blood: experimental studies in normal and Brattleboro rats.

Oxytocin (OT) and vasopressin (VP) were measured by radioimmunoassay in hypophysial portal and peripheral blood from male Wistar rats and heterozygous and homozygous Brattleboro rats anaesthetized with urethane. In Wistar rats the concentrations of OT and VP were about 50 times greater than the concentrations in peripheral blood, whether or not the pituitary gland was left in situ during collection, and also considerably greater than the reported concentrations of the peptides in the cerebrospinal fluid. The release of both peptides was increased significantly by a lesion of the supraoptico-hypophysial tract that led to diabetes insipidus, but which left intact the external layer of the median eminence (ME). Concentrations of VP were undetectable in plasma from homozygous Brattleboro rats, but the portal plasma concentrations of VP in heterozygous Brattleboro rats were not significantly lower than in Wistar rats. The concentrations of OT in portal plasma from both types of Brattleboro rat were significantly higher than in Wistar rats. The output of VP and OT into hypophysial portal blood of Wistar rats was not significantly affected by electrical stimulation of the suprachiasmatic, supraoptic or paraventricular nuclei or the ME using two types of stimuli, one of which produced an increase in peripheral plasma concentrations of VP and OT in intact rats and a significant increase in the release of LH-releasing hormone into hypophysial portal blood. The output of VP and OT into portal blood was also not significantly affected by either adrenalectomy with or without injection of dexamethasone or the injection of either the 5-hydroxytryptamine (5-HT) synthesis blocker, parachlorophenylalanine, or the 5-HT uptake blockers, alaproclate or zimelidine. These results show that large amounts of OT as well as VP are released into hypophysial portal blood from fibres of the hypothalamo-neurohypophysial system that terminate in the external layer of the ME. Although distinct from the fibres that terminate in the pars nervosa (PN), the findings in Brattleboro rats show that the VP fibres of the ME system originate in neurones with a genomic mechanism for VP synthesis similar to that of the VP neurones that project to the PN. The lack of effect of adrenalectomy and the administration of 5-HT synthesis and uptake blockers must be interpreted with caution since the results obtained with electrical stimulation suggest that when the pituitary stalk is cut the release of OT and VP into portal blood approaches a maximum and may therefore be difficult to alter by experimental manipulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗

PubMed1983

Rat natural killer cell activity against lymphoid and nonlymphoid tumor cells and normal rat cell lines.

Natural cytotoxicity in the rat was assessed against solid tumors and normal and embryonic rat monolayer culture lines, and the results were compared with rat natural killer activity towards syngeneic, allogeneic, and xenogeneic lymphoma targets. The targets tested showed a very wide range of susceptibility to lysis by peripheral blood and spleen effector cells in both 4- and 18-hr cytotoxicity assays. Cytotoxicity toward the mouse lymphoma, YAC-1, and rat sarcoma LT1 targets was relatively high in a 4-hr assay, compared with that toward the other cell lines used in the study. At 18 hr, increased killing was seen against YAC-1, LT1, SP3 (rat pheochromoblastoma), F2304 (rat embryonic cells), and normal rat kidney cells, while a significant increase in susceptibility with time was not observed with other rat targets: W/Fu-T (sarcoma); ERTh/V-G (sarcoma); R35 (mammary tumor); and W/Fu-P21 (embryo fibroblasts) targets. The cytotoxicity against all of the targets tested was not age restricted and was potentiated by rat interferon. Natural cytotoxic reactivity was seen with effector cells from the blood, spleen, and peritoneal cavity of both W/Fu (euthymic) and Rowett nude (congenitally athymic) rats. Cytotoxic effector cells from the blood were present in the low-density fractions recovered from discontinuous Percoll density gradients and, as shown previously for lymphoma target cells, a strong correlation was observed between the killing of embryonic, normal, and solid tumor targets and the presence of large granular lymphocytes. These results indicate that the naturally cytotoxic rat effector cells for normal fibroblast and bone marrow targets, lymphomas-leukemias, embryonic cell lines, and solid tumor targets are all included in the large granular lymphocyte subpopulation.

Aging↗

PubMed1993

Comparison of anxiety measured in the elevated plus-maze, open-field and social interaction tests between spontaneously hypertensive rats and Wistar EPM-1 rats.

On the basis of open-field and plus-maze results it has been proposed that spontaneously hypertensive (SHR) rats are less emotionally reactive than their normotensive controls, Wistar-Kyoto (WKY). However, the proposed "anxiolytic characteristics" of SHR rats may be questioned in view of the significant hypoactivity presented by WKY rats. In the present study, the behavioral response of spontaneously hypertensive (SHR) and equally active normotensive Wistar EPM-1 (EPM-1) rats (4-month old males, 10-13 animals per group) were evaluated in the open-field, social interaction and elevated plus-maze tests. In the open-field study, no differences were observed for total locomotion frequency and immobility duration, but SHR rats presented a higher central square locomotion frequency (23.8 +/- 2.1 vs 10.3 +/- 1.6) as compared to EPM-1. SHR rats also exhibited a greater duration of social interaction when compared to EPM-1 rats (mean +/- SEM values were 113.9 +/- 8.7 s for SHR vs 72.7 +/- 8.6 s for EPM-1 rats after 8-min observation). In the elevated plus-maze test, SHR rats presented an increased percent of entries (52.8 +/- 3.3 vs 28.3 +/- 4.5) and time in the open arms (65.6 +/- 6.0 vs 11.1 +/- 1.9) as compared to EPM-1 rats, although the total number of arm entries (9.2 +/- 0.9 vs 9.7 +/- 1.0) was unchanged. These results suggest that the "anxiolytic behavior" of SHR rats in relation to normotensive controls is not related to differences in motility levels.

Animals↗

PubMed1998

Inhibition of dopamine and choline acetyltransferase concentrations in rat CNS neurons by rat alpha 1- and alpha 2-macroglobulins.

Previous studies have implicated human alpha-2-macroglobulin (alpha2M) as a potential regulator of neuronal development and function. Rat alpha-1-macroglobulin (alpha1M) and acute-phase alpha-2-macroglobulin (alpha2M) are murine homologues of human alpha2M. In this report, we tested the effect of intracranially infused serotonin-activated rat alpha1M (5HT-alpha1M) on the concentration of dopamine (DA) in the corpus striatum in vivo and the effect of 5HT-activated rat alpha1M and alpha2M on the choline acetyltransferase (ChAT) activity upon embryonic basal forebrain neurons in culture. The results show that direct infusion of 0.65 nmole rat 5HT-alpha1M into the adult rat corpus striatum produced a consistent attenuation upon striatal DA concentrations. This decrease was particularly prominent at 5-7 days post-infusion. In addition, rat 5HT-alpha1M and rat 5HT-alpha2M, like human 5HT-alpha2M, all significantly inhibited ChAT activity of embryonic rat cerebral cortex neurons. Although normal human alpha2M and rat alpha2M were either marginally or insignificantly inhibitory in this preparation, normal rat alpha1M dose-dependently inhibited ChAT activity. These results demonstrate that monoamine-activated alpha-macroglobulins from rat depress dopaminergic and cholinergic neurotransmitter systems in the CNS, and this suggests a potential regulatory role of these alpha-macroglobulins in neurotransmitter metabolism.

Animals↗

PubMed1994

RCS rat retinal rod outer segment membranes exhibit different cholesterol distributions than those of normal rats.

Royal College of Surgeons (RCS) rats exhibit an hereditary defect in phagocytosis of the tips of the photoreceptor cell rod outer segments (ROS) which leads to degeneration of the retinal visual cells. The lipid composition of outer segment membranes of these rats was analysed and compared to those of normal rats to determine whether there are differences between the normal and mutant rat ROS. The cholesterol distribution in ROS disk membranes from normal and RCS rats was investigated using a digitonin induced change in membrane density. Normal rat ROS disks varied in cholesterol to phospholipid mole ratio from 0.36 to 0.03. The disk membranes from RCS rats, however, do not exhibit the same marked cholesterol heterogeneity. The mean molar ratio of cholesterol to phospholipid in the disk membranes of normal rats is 0.11 while that found in the RCS rats is 0.14. The ROS plasma membrane of dystrophic rats also has a lower cholesterol to phospholipid ratio (0.20) than is found in the normal rat (0.40). The phospholipid headgroup composition of RCS disks and plasma membrane were determined. RCS disks were shown to differ from those of normal animals. The cholesterol content of ROS disks may be governed by the phospholipid composition.

Animals↗

PubMed1994

Acetyl-L-carnitine prevents age-dependent structural alterations in rat peripheral nerves and promotes regeneration following sciatic nerve injury in young and senescent rats.

Morphologic and morphometric alterations of the sciatic nerve from old Sprague-Dawley rats and of lesioned tibial nerve from young and senescent Sprague-Dawley rats were studied. The possible therapeutical effects of treatment with acetyl-L-carnitine (ALCAR) were also investigated, ALCAR being a compound shown to exert a beneficial pharmacological action on diabetic neuropathies. Nerve sections from animals sacrificed under anesthesia were stained with toluidine blue. In old rats, a 6-month treatment with ALCAR markedly reduced the percentage of myelinated fibers (MF) characterized by age-dependent morphologic alterations (4% in treated rats versus 11% in untreated ones), such as myelin balloons, infolded loops of myelin, myelin reduplication, and ovoids. In the lesioned animals, ALCAR-treatment (15-60 days for young rats and 6-9 months for senescent rats) produced a significant increase versus controls in the density of regenerating myelinated fibers (RMF) at 15 days (young rats) and at 30 days (senescent rats) after crush, as well as an increase in the axon diameter in both young and senescent rats at 60 days after nerve crush. The MF diameter (sheath + axons) was significantly larger in treated senescent rats than in controls at 100 days after nerve crush. In ALCAR-treated rats, both young and senescent, the density of degenerative elements was lower and the RMF ratio (RMF density/RMF density + density of degenerative elements) was higher than that in controls at all detection times.

Acetylcarnitine↗

PubMed1993

Cultured retinal pigment epithelial cells from RCS rats express an increased calcium conductance compared with cells from non-dystrophic rats.

The Royal College of Surgeon (RCS) rats suffer from a retinal dystrophy that is caused by a malfunction of the retinal pigment epithelium (RPE). We compared the membrane currents of cultured RPE cells from non-dystrophic and RCS rats by using the whole-cell configuration of the patch-clamp technique. Cultured RPE cells from RCS rats showed voltage-dependent, barium- and 4-aminopyridine-sensitive outward currents, which had characteristics of the delayed-rectifier and voltage-dependent, barium- and 4-aminopyridine-sensitive inward currents, which had characteristics of the inward rectifier. Differences between RPE cells from RCS rats and normal rats were as follows. (a) Cultured RCS rat RPE cells showed a resting potential and an activation threshold for the voltage-dependent outward current significantly more positive than that found in cells from non-dystrophic rats. (b) In the presence of 10 mM barium, the voltage-dependent outward current was reduced in both types of cells; in cells from RCS rats, an additional voltage-dependent inward current was observed. (c) This additional inward current had characteristics of L-type calcium channels and was reduced by verapamil (30 microM) and diltiazem (30 microM). In summary, we conclude that the membrane conductances of RPE cells from normal and RCS rats are dominated by potassium conductances. In contrast to cells from non-dystrophic rats, cells of RCS rats expressed an increased membrane conductance for calcium.

4-Aminopyridine↗

PubMed1991

Bone histomorphometric analysis for the cause of osteopenia in vitamin C-deficient rat (ODS rat).

A particular strain of rat, the osteogenic disorder rat (ODS rat), was established in 1973. Phenotypic expression of od/od in ODS rat develops signs characteristics of a vitamin C-deficient animal, with bleeding tendencies and limb fractures. We investigated the bone histomorphometry to clarify the pathogenesis of osteopathy found in ODS rat. Bone histomorphometry revealed that static parameters reflecting bone formation were found to be remarkably decreased in od/od rats. These observations were more prominent in the metaphysis of distal femurs of od/od rats than those in the tail vertebrae. Parameters reflecting bone resorption in od/od rats were reduced in the distal femoral metaphysis, but were similar to those of controls in the tail vertebrae. These parameters were restored to control levels after ascorbic acid supplementation to pair-fed od/od rats. The mineral appositional rate in od/od rats was not significantly different from that in controls. Although body weight gain in pair-fed controls was significantly reduced compared to those fed ad libitum, histomorphometric parameters, on the contrary, were unaltered between these groups. Our present study provides evidence that the cause of osteopenia found in od/od rat is attributable to an imbalance between the total amounts of resorption and formation, and the pathogenesis of osteopathy could be due to ascorbic acid deficiency itself rather than malnutrition.

Alkaline Phosphatase↗

PubMed1986

Specific saturable binding of rat high-density lipoproteins to rat kidney membranes.

The binding of rat 125I-labelled high-density lipoprotein (HDL) to rat kidney membranes was studied using HDL fractions varying in their apolipoprotein E content. The apolipoprotein E/apolipoprotein A-I ratio (g/g) in the HDL fractions ranged from essentially 0 to 1.5. All these HDL preparations showed the same binding characteristics. The saturation curves, measured at 0 degrees C in the presence of 2% bovine serum albumin, consisted of two components: low-affinity non-saturable binding and high-affinity binding (Kd about 40 micrograms of HDL protein/ml). Scatchard analyses of the high-affinity binding suggest a single class of non-interacting binding sites. These sites could be purified together with the plasma membrane marker enzyme 5'-nucleotidase. The binding of rat HDL to rat kidney membranes was not sensitive to high concentrations of EDTA, relatively insensitive to pronase treatment and influenced by temperature. The specific binding of rat HDL was highest at acid pH and showed an additional optimum at pH 7.5. On a total protein basis unlabelled rat VLDL competed as effectively as unlabelled rat HDL for binding of 125I-labelled rat HDL to partially purified kidney membranes. Rat LDL, purified by chromatography on concanavalin A columns and human LDL did not compete. Unlabelled human HDL was a much weaker competitor than unlabelled rat HDL and the maximal specific binding of 125I-labelled human HDL was only 10% of the value for 125I-labelled rat HDL.

Animals↗