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PubMed2000

The effects of rexinoids and rosiglitazone on body weight and uncoupling protein isoform expression in the Zucker fa/fa rat.

Agonists for the retinoid X receptor (RXR), the rexinoids, and the peroxisome proliferator-activated receptor gamma (PPARgamma), the thiazolidinediones, are effective in the treatment of insulin resistance in rodent models by enhancing insulin action and improving glycemic control. In the present study, we compared the effects of rexinoids and a thiazolidinedione on body weight and mitochondrial uncoupling protein (UCP) isoform mRNA expression in the obese Zucker fa/fa rat. Long-term (2 weeks) oral treatment with the rexinoids LG100268 and LG100324 reduced food intake and body weight gain, whereas rosiglitazone (BRL49653) tended to increase both food intake and weight gain. LG100268 and LG100324 increased brown adipose tissue (BAT) UCP-1 mRNA content by 2.7-fold (P < .002) and 3.1-fold (P < .001), respectively, while BRL49653 had no effect on BAT UCP-1 mRNA content. Neither the rexinoids nor the thiazolidinedione had any effect on the level of mRNA encoding UCP-2 and the recently described PPARgamma coactivator-1 (PGC-1). LG100324 increased UCP-3 mRNA content by 3.6-fold (P < .0005) in muscle and 4.3-fold (P < .0002) in white adipose tissue (WAT). LG100268 increased UCP-3 mRNA content in WAT by 2-fold (P < .005) but was without any effect on muscle UCP-3. BRL49653 increased UCP-3 mRNA content by 2.1-fold (P < .005) in muscle and 2.7-fold (P < .003) in WAT. Thus, the rexinoids, but not the thiazolidinedione, have an antiobesity action by reducing food intake, and the increase in UCP-1 mRNA content in BAT may reflect a stimulation of BAT UCP-1 activity.

Adipose Tissue, Brown↗

PubMed1994

Acetylcholinesterase activity in fast-twitch skeletal muscle from thyroidectomized rats.

Hypothyroidism is associated with muscle weakness and slowed movements. Hormone-deficient muscles do show changes in contractile proteins and sarcoplasmic calcium pumps, however effects on the components of the neuromuscular junction are less clear. In this study, we examined cholinesterase activity in adult fast-twitch muscle from hypothyroid and control rats. Male Holtzman rats underwent thyroidectomy and their age-matched euthyroid controls were simultaneously subjected to sham operation. Thirty days post-operative, animals were sacrificed for anterior tibialis muscles harvest. Muscle cholinesterase isoform activity was measured and compared between experimental treatment groups. Butyrylcholinesterase activities and peak I and III acetylcholinesterase (AchE) activities were similar in euthyroid and hypothyroid groups. However, hypothyroid muscles exhibited half the peak II AchE isoform (G4) activity, as compared to control muscles. Hypothyroidism specifically affects AchE isoform expression in rodent fast-twitch muscle.

Acetylcholinesterase↗

PubMedDate not supplied

Immunological relationship between the mother and the fetus.

The immunological relationship between the mother and the fetus is a bi-directional communication determined on the one hand by fetal antigen presentation and on the other hand by recognition of and reaction to these antigens by the maternal immune system. There is evidence now that immunological recognition of pregnancy is important for the maintenance of gestation, and that inadequate recognition of fetal antigens might result in failed pregnancy. In contrast to HLA-A and -B Class I genes that are downregulated in human trophoblast cells, nonpolymorphic Class I molecules, e.g., HLA-G Class Ib, are expressed in extravillous cytotrophoblast and also in endothelial cells of fetal vessels in the chorionic villi as well as in amnion cells and amniotic fluid. The trophoblast does not induce transplantation immunity and resists NK- and CTL-mediated lysis in vitro. According to our present knowledge, HLA-G presents antigens for gamma/delta T cells and at the same time defends the trophoblast from cytotoxic effector mechanisms. Since polymorphic MHC is absent from the trophoblast, presentation of fetally derived antigens is unlikely to be MHC restricted. gamma/delta T cells recognize a distinct group of ligands with a smaller receptor repertoire than alpha/beta T cells. Most gamma/delta T cells recognize unprocessed foreign antigens without MHC. In the decidua gamma/delta TCR-positive cells significantly increase in number and the majority of decidual gamma/delta T cells are in an activated form due to recognition of conserved mammalian molecules on the trophoblast. Following recognition of fetally derived antigens, the immune system reacts with the setting in of a wide range of protective mechanisms. Many observations suggest that pregnancy is associated with an altered TH1/TH2 balance. Maternal immune response is biased toward humoral immunity and away from cell-mediated immunity that could be harmful to the fetus. Cytokines of maternal origin act on placental development. On the other hand, antigen expression on the placenta determines maternal cytokine pattern. Normal human pregnancy is characterized by low peripheral NK activity, and increased NK activity seems to play a role in spontaneous abortions of unknown etiology. In early human pregnancy the majority of uterine lymphocytes are CD56(bright) granulated NK cells, which do not express CD16 or CD3. In rodents and humans, uterine NK cells are under hormonal control. In early pregnancy they are enriched at sites where fetal trophoblast infiltrates the decidua. The dynamics of the appearance of uterine NK cells suggest that one of the functions of these cells is control of placentation. Another protective mechanism operating in favor of pregnancy is progesterone-dependent immunomodulation. Due to stimulation by fetally derived antigens, pregnancy lymphocytes develop progesterone receptors and in the presence of progesterone produce a mediator (PIBF) that, through altering the cytokine balance, inhibits NK activity and exerts an antiabortive effect in mice.

Animals↗

PubMed1992

Epidemiologic classics of Carter, Maxcy, Trudeau, and Smith.

Four great epidemiologists whose work so concisely linked clinical observations, epidemiologic clues, and logical preventive measures are discussed. Henry Rose Carter set the stage for the Walter Reed successes in Cuba by showing that 9-16 days must elapse after contact before yellow fever develops. This provided the link for the Reed group to allow the "virus" to incubate in the mosquito before becoming infectious. Kenneth Maxcy clarified the controversy between endemic typhus fever and Brill's disease in the southeastern United States. His clinical, epidemiologic, and laboratory findings led him to propose that the causative organism (Rickettsia typhi) was in rodents and the probable vector, fleas. When confirmed, effective control measures were applied. Two other American investigators, Edward L. Trudeau and Theobald Smith, helped prove Robert Koch wrong on three counts: (1) Tuberculin is not an effective therapeutic agent for tuberculosis; (2) there are two distinct types of tubercle bacillus, human and bovine; and (3) the bovine form of Mycobacterium tuberculosis is remarkably pathogenic for humans. The significance of these findings is unlimited.

History, 19th Century↗

PubMed1989

Interactions between vitamin A deficiency and Plasmodium berghei infection in the rat.

It has been claimed that vitamin A deficiency increases the severity of malarial infection in rats. We measured parasitemia, mortality, serum retinol, liver retinol, spleen weight, and degree of xerophthalmia in vitamin A-deficient rats (A-), pair-fed control rats (A+PF), and ad libitum-fed control rats (A+AL) infected with Plasmodium berghei, a rodent malarial parasite. In experiments 1 and 2 vitamin A deprivation began at weaning. Parasitemia and mortality among mildly deficient (expt. 1, mean serum retinol 19 micrograms/dl) or acutely deficient rats (expt. 2, mean serum retinol less than 5 micrograms/dl) infected with P. berghei were not significantly different from those of infected A+AL or A+PF rats. Furthermore, when the mildly deficient rats were given a second, larger dose of P. berghei, all demonstrated complete immunity to the parasite. However, when vitamin A was withdrawn midway through pregnancy (expt. 3), the A- rats experienced significantly higher parasitemia and mortality during infection with P. berghei. Malaria caused a significant decrease in the serum retinol but not liver retinol of the A+PF and A+AL rats. Among the acutely deficient rats, xerophthalmia was significantly more prevalent and more severe among those infected with malaria than among those not infected with malaria. Malaria and vitamin A deficiency acted synergistically to increase spleen weight, and this interaction was highly significant. In these experiments, vitamin A deficiency decreased the rats' ability to recover from malaria, but only when the deficiency began early in life, was very severe, and the rats were young when infected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Up-regulation of telomerase in primary cultured rat hepatocytes.

Telomerase is a unique reverse transcriptase involved in the maintenance of telomeric DNA, which is generally undetectable in normal human somatic cells. However, it has been found in organs of normal adult rodents including the liver. In order to elucidate relevant control mechanisms operating in normal somatic cells, we examined telomerase activity in primary cultured rat hepatocytes. During culture under serum-free conditions, rat hepatocytes rapidly lose the ability of organ-specific expression of serum albumin, apolipoprotein A-I, and hepatocyte nuclear factor 4, and the capacity for cytochrome P-450 induction by xenobiotics. The telomerase activity was found to be concomitantly increased about 2. 5-fold at 48 h and 3-fold at 72 h. Northern blot and RT-PCR analyses with primary cultured hepatocytes revealed the associated accumulation of rat telomerase RNA subunits (TR), and the mRNAs for a telomerase reverse transcriptase (TERT) and a telomerase-associated protein (TEP1). The activity of hepatocyte telomerase, which was elevated during the primary culture, increased further when the cells were stimulated with hepatocyte growth factor. In this case, however, the levels of TR, TERT, and TEP1 mRNA did not show any detectable changes.

Animals↗

PubMed1991

Hypercarbic acidosis reduces cardiac resuscitability.

BACKGROUND AND METHODS: Marked increases in myocardial hypercarbia and acidosis accompany cardiac arrest and resuscitation. To investigate whether hypercarbic acidosis independent of oxygenation is of itself detrimental to cardiac resuscitation, three groups of six Sprague-Dawley rats were ventilated with gas mixtures containing concentrations of inspired CO2 (FICO2) of 0.0, 0.3, or 0.5, with oxygen fractions held constant at 0.5. After 4 mins of ventricular fibrillation, mechanical chest compressions were initiated with a pneumatic thumper; 2 mins later, transthoracic defibrillation was attempted. RESULTS: Each animal ventilated with FICO2 of 0.0 or 0.3 was successfully resuscitated. However, none of the animals ventilated with FICO2 of 0.5, in which aortic pH was less than 6.67 and aortic PCO2 was greater than 200 torr (greater than 26.7 kPa), was resuscitated (p less than .001). This finding contrasted with a second control group of seven identically treated animals which, in the absence of cardiac arrest, demonstrated no adverse effects after ventilation with an FICO2 of 0.5. CONCLUSIONS: Increases in FICO2 to levels of 0.5 under conditions of constant arterial oxygenation and controlled coronary perfusion pressure preclude successful resuscitation in this rodent model of CPR.

Acidosis, Respiratory↗

PubMed1995

Outgroup heteroduplex analysis using temperature gradient gel electrophoresis: high resolution, large scale, screening of DNA variation in the mitochondrial control region.

The ability of DNA screening techniques such as Temperature Gradient Gel Electrophoresis (TGGE) and Heteroduplex Analysis to provide resolution approaching that provided by DNA sequencing for a fraction of the time, effort and expense point to them as the logical successor to allozyme electrophoresis for population genetics. Here we present a novel alternative to the standard TGGE/Heteroduplex Analysis protocol - Outgroup Heteroduplex Analysis (OHA). We assess this technique's sensitivity in comparison to previous screening approaches using a known hierarchy of sequence differences. Our data show that Outgroup Heteroduplex Analysis has greatly increased sensitivity for screening DNA variants from that of TGGE used alone and is easily applicable to large numbers of samples. Using this technique we can consistently detect differences of as small as one base change in a 433-base-pair fragment of Control Region mitochondrial DNA from Melomys cervinipes (an Australian rodent). The approach should easily be extendable to nuclear loci and is not necessarily dependent on the use of a denaturing gradient. When combined with a targeted sequencing effort, OHA provides a sensitive and simple means of obtaining allele/haplotype frequencies and their phylogenies for population and phylogeographic studies in molecular ecology.

Animals↗

PubMed1999

Lifelong treatment with oral DHEA sulfate does not preserve immune function, prevent disease, or improve survival in genetically heterogeneous mice.

OBJECTIVES: To determine whether lifelong exposure to dehydroepiandrosterone sulfate extends the lifespan or retards immune senescence in mice. DESIGN: Double-blind, placebo-controlled intervention trial. SETTING: A specific pathogen-free rodent vivarium. PARTICIPANTS: 120 mice bred as a cross between CB6F1 females and C3D2F1 males. INTERVENTION: DHEAS at 100 microg/mL in drinking water from weaning until death. MEASUREMENT: Age at death, cause of death, antibody production after erythrocyte immunization, and T cell subset profiles in peripheral blood at ages 8 and 18 months. RESULTS: DHEAS ingestion did not lead to a significant increase in mean or maximal longevity: the 95% confidence interval for DHEAS effect on mean lifespan ranged from +35 days to -80 days. There were no significant effects of DHEAS on incidence of lethal illnesses, except for a trend toward higher levels of mammary adenocarcinoma in DHEAS-treated females and mouse urinary syndrome in DHEAS-treated males. DHEAS treatment did not improve the ability of middle-aged mice to produce antibody to a foreign particulate antigen, and it did not alter the proportions of age-sensitive T cell subsets in middle-aged animals. CONCLUSION: Although differences among species in pharmacokinetics complicate interpretation of studies in which DHEA or DHEAS is administered to rodents, our data provide no support for the idea that chronic exposure to this steroid retards immune senescence or prevents late life illness.

Adenocarcinoma↗

PubMed1981

Release of somatostatin from rodent antral mucosae maintained in organ culture.

Somatostatin secretion was investigated from rodent antral mucosal biopsies maintained in organ culture. Under control conditions, the somatostatin secretory output was fairly constant, with each biopsy releasing a mean value of 29.1 +/- 7.5 pg of hormone over a 15-min period. Incubation of the mucosa in medium containing 5% peptone directly induced a 20-fold increase in medium somatostatin levels to 622.5 +/- 15.5 pg/ml. In contrast, a peptone dialysate was a weaker stimulant of hormone release, inducing a three- to fourfold increase in medium somatostatin concentration. Additionally, it was determined that a peptic hydrolysate of bovine serum albumin was a significantly more potent in vitro stimulant of somatostatin secretion than the intact undigested molecule. These results suggest that the amino acid and peptide constituents of these proteinaceous substances are the major stimulants of somatostatin release in vitro. It is presently uncertain whether this direct peptone-induced release of somatostatin from antral mucosal explants can account for the previously reported [Am. J. Physiol. 235 (Endocrinol. Metab. Gastrointest. Physiol. 4): E410-E415, 1978] gastrin secretory "off response" to the same agent, because addition of exogenous somatostatin to the medium failed to block this peptone-induced gastrin secretory response.

Animals↗

PubMed2000

Leptin regulates pulsatile luteinizing hormone and growth hormone secretion in the sheep.

Administration of leptin during reduced nutrition improves reproductive activity in several monogastric species and reverses GH suppression in rodents. Whether leptin is a nutritional signal regulating neuroendocrine control of pituitary function in ruminant species is unclear. The present study examined the control of pulsatile LH and GH secretion in sheep. We determined whether exogenous leptin could prevent either the suppression of pulsatile LH secretion or the enhancement of GH secretion that occur during fasting. Recombinant human met-leptin (rhmet-leptin; 50 microg/kg BW; n = 8) or vehicle (n = 7) was administered s.c. every 8 h during a 78-h fast to estrogen-treated, castrated yearling males. LH and GH were measured in blood samples collected every 15 min for 6 h before fasting and during the last 6 h of fasting. Leptin was measured both by a universal leptin assay and by an assay specific for ovine leptin. During the fast, endogenous plasma leptin fell from 1.49 +/- 0.16 to 1.03 +/- 0.13 ng/ml. The average concentration of rhmet-leptin 8 h after leptin administration was 18.0 ng/ml. During fasting, plasma insulin, glucose, and insulin-like growth factor I levels declined, and nonesterified fatty acid concentrations increased similarly in vehicle-treated and leptin-treated animals. In vehicle-treated animals, LH pulse frequency declined markedly during fasting (5.6 +/- 0.5 vs. 1.1 +/- 0.5 pulses/6 h; fed vs. fasting; P < 0.0001). Leptin treatment prevented the fall in LH pulse frequency (5.0 +/- 0.4 vs. 4.9 +/- 0.4 pulses/6 h; P = 0.6). Neither fasting nor leptin administration altered GH pulse frequency. Fasting produced a modest increase in mean concentrations of circulating GH in control animals (2.4 +/- 0.5 vs. 3.4 +/- 0.6 ng/ml; P = 0.04), whereas there was a much greater increase in GH during leptin treatment (2.7 +/- 0.6 vs. 8.6 +/- 1.6 ng/ml; P = 0.0001). GH pulse amplitudes were also increased by fasting in control (P = 0.04) and leptin-treated sheep (P = 0.007). The finding that exogenous rhmet-leptin regulates LH and GH secretion in sheep indicates that this fat-derived hormone conveys information about nutrition to mechanisms controlling neuroendocrine function in ruminants.

Animals↗

PubMed2001

Apoptotic cell death in the porcine endometrium during the oestrous cycle.

It has been reported that apoptosis plays an essential role in controlling the physiological cell kinetics in the human and rodent endometrium but this type of death has never been studied in the porcine endometrium. The aim of this study was to investigate the apoptotic cell death in the porcine endometrium during the middle (Days 9-11) and late (Day 13) luteal phase, during the luteolysis (Day 15) and early follicular phase (Days 17-19) of the oestrous cycle. Apoptotic cells were identified by in situ DNA 3'-end labelling method. It was revealed that the greatest number of apoptotic cells in the luminal and glandular epithelium was found on Days 17-19 and on Day 15 of the oestrous cycle, respectively. In the stroma, the greatest number of these cells was found on Days 9-11. Our data have shown that in the porcine endometrium, both epithelial and stromal cells undergo apoptosis and that the number of apoptotic cells varies depending on the phase of the oestrous cycle.

Animals↗

PubMed1988

Biochemical characterization of brown adipose tissue beta-adrenergic receptor.

The beta-adrenergic receptor of rodent brown fat plays a key role in the control of energy dissipation by this tissue. The aim of the present study was to further characterize the biochemical properties of this receptor. The beta-receptor of rat interscapular brown adipose tissue plasma membranes was found to bind the beta-adrenergic antagonist [125I]cyanopindolol with a high affinity (KD 67 pM). The [125I]cyanopindolol receptor complex could be solubilized by digitonin and the isoelectric point of the solubilized receptor was found to be 5.8. Brown adipose tissue plasma membranes were labeled with the photoaffinity ligand [125I] cyanopindolol diazirine and labeled membrane proteins were separated by sodium dodecylsulfate polyacrylamide gel electrophoresis and analyzed by autoradiography. Autoradiograms revealed a peptide of 62 kDa whose labeling was stereoselectively displaced by alprenolol and isoproterenol. The beta 1-selective antagonist betaxolol was about 100 times more potent in displacing the labeling of this 62 kDa peptide than the beta 2-selective antagonist ICI 118,551. Based upon these data, it appears that the beta-receptor in brown adipose tissue is a beta 1 subtype with molecular weight of 62 kDa.

Adipose Tissue, Brown↗

PubMed1990

Effects of Fusarium moniliforme and corn associated with equine leukoencephalomalacia on rat neurotransmitters and metabolites.

Fusarium moniliforme (FM) is associated with equine leukoencephalomalacia (ELEM) and hepatotoxicities in horses and rats. The neurochemical effects of ELEM-associated corn naturally infected with FM and FM strain MRC 826 were studied in rats. Increases in brain 5-hydroxyindoleacetic acid (5-HIAA, major metabolite of serotonin, 5-HT) and 5-HIAA/5-HT ratios were observed in rats fed the ELEM-FM corn. These rats had reduced body weights (17%, P less than 0.01) and increased brain weight/body weight ratios (14%, P less than 0.01) as compared with controls that were fed commercial corn. Rats fed a rodent chow supplemented (16%, w/w) with corn cultures of FM (MRC 826) had brain 5-HT and 5-HIAA increased (11% and 60%, P less than 0.01, respectively). At 20% FM (MRC 826)-chow diet, the 5-HIAA levels were increased (18%, P less than 0.01). In both the 16% and 20% diets, brain 5-HIAA/5-HT ratios were increased (45%, P less than 0.01 and 10%, P less than 0.05), body weights reduced (30% and 18%, P less than 0.01) and brain weight/body weight ratios increased (40% and 16%, P less than 0.01), respectively. The incidences of microscopic liver lesions (particularly bile duct proliferations, hepatocellular hyperplasia, and focal necrosis) were consistent with rats fed the FM contaminated and FM-fortified diets. These results suggest a possible FM (ELEM-associated)-induced dysfunction in either 5-HT metabolism or 5-HIAA elimination in rat brains.

Animal Feed↗

PubMed2000

Loss of p27Kip1 from cyclin E/cyclin-dependent kinase (CDK) 2 but not from cyclin D1/CDK4 complexes in cells transformed by polyamine biosynthetic enzymes.

Cancer cells are known to display up-regulation of ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (AdoMetDC), the key enzymes in the biosynthesis of polyamines that are essential for cellular proliferation. We have shown previously that overexpression of ODC or AdoMetDC alone can induce tumorigenic transformation of rodent fibroblasts. Because the subversion of normal cell cycle control is thought to be a crucial event in cancer development, we examined ODC- and AdoMetDC-transformed fibroblasts for alterations in the cell cycle components. The level of cyclin D1 and cyclin D1-dependent kinase and total cyclin-dependent kinase (CDK) 4 activities were elevated in the ODC transformants and particularly in the AdoMetDC transformants. Cyclin E content was not elevated, but a moderate increase in cyclin E-dependent kinase activity was seen in both cells. Total CDK2 activity was increased only in the ODC-transformed cells. The amount of the p27Kip1 CDK inhibitor was greatly decreased in both transformants. Nevertheless, p27Kip1 was present in the active cyclin D1/CDK4 complexes in the cells but absent from the cyclin E/CDK2 complexes. Restoration of p27Kip1 expression in the ODC- and AdoMetDC-transformed cells by transfection resulted in growth inhibition, but not in morphological reversion. An elevation in the level of hyperphosphorylated retinoblastoma protein was observed mainly in the ODC-transformed cells. These results suggest that the expression of ODC or AdoMetDC may affect cell cycle regulation in many ways. However, the largest common effect, which is therefore potentially relevant to some aspects of transformation, appears to be the constitutive down-regulation of p27Kip1 and its loss from the cyclin/CDK2 complexes.

3T3 Cells↗

PubMed2002

The insertions of the cruropedal muscles and implications for the locomotor evolution in primates.

We examined gross-anatomically the cruropedal muscles, which control the toe movements, in some species of insectivores, rodents and primates including humans, with a focus on the phylogenetic developments of these muscles including the distribution patterns of the tendons to the toes. Morphological changes corresponding to the phylogenetic advancement from primitive terrestrial mammals to arboreal primates were found in the short extensors and flexors, presumably in association with the enhancement of independent digital mobility. In contrast, the changes which correspond to the acquisition of terrestrial bipedality in humans were identified in the development of extensors and flexors which govern the first toe, as well as in establishment of the peroneus tertius that dorsi-flexes the talocrural joint.

Animals↗

PubMed2004

Range of retinal diseases potentially treatable by AAV-vectored gene therapy.

Viable strategies for retinal gene therapy must be designed to cope with the genetic nature of the disease and/or the primary pathologic process responsible for retinal malfunction. For dominant gene defects the aim must be to destroy the presumably toxic gene product, for recessive gene defects the direct approach aims to provide a wild-type copy of the gene to the affected retinal cell type, and for diseases of either complex or unknown genetic origin, more general cell survival strategies that deal with preserving affected retinal cells are often the best and only option. Hence examples of each type of therapy will be briefly discussed in several animal models, including ribozyme therapy for autosomal dominant retinitis pigmentosa in the transgenic P23H opsin rat, beta-PDE gene augmentation therapy for autosomal recessive retinitis pigmentosa in the rd mouse, glial cell-derived neurotrophic factor (GDNF) gene therapy for autosomal dominant RP in the transgenic S334ter opsin rat and pigment epithelial cell-derived neurotrophic factor (PEDF) gene therapy for neovascular retinal disease in rodents. Each employs a recombinant AAV vectored passenger gene controlled by one of several promoters supporting either photoreceptor-specific expression or more general retinal cell expression depending on the therapeutic requirements.

Animals↗

PubMedDate not supplied

Alpha-linolenic acid, long-chain n-3 fatty acids, and neonatal brain development.

There appear to be mechanisms that enable the developing brain to regulate its concentration of 22:6n-3 in response to both dietary deficiencies and excesses. This appears to be true whether the n-3 fatty acids are supplied as 18:3n-3 or the long-chain derivatives, suggesting that the presence of 22:6n-3 during development may be of functional consequence to the operation of the nervous system. Although there is experimental support for specific effects of n-3 fatty acids on retinal function, further studies with better methodological controls are needed before effects on cognitive function in rodents can be considered unequivocal.

Animals↗