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Timing and function of chitin synthesis in yeast.

A temperature-sensitive mutant of Saccharomyces cerevisiae, L-2-42, is blocked at 37 C at a stage of the cell cycle prior to septum formation. When single cells of the mutant are allowed to bud at 37 C in a medium containing tritiated glucose, a large incorporation of radioactivity into chitin takes place. Thus, the synthesis of chitin, the major component of the primary septum, is initiated in a phase of the cell cycle which precedes septum closure. This early period of chitin synthesis is not required for emergence and growth of buds because, in the wild type, budding takes place normally in the presence of concentrations of polyoxin D that effectively and specifically prevent chitin formation. However, at a later time a majority of these cells lyse, presumably because of the inability to form a septum. Polyoxin D also prevents the appearance of enhanced fluorescence at the junction between mother cell and bud, as observed in the presence of a brightener. Therefore, the fluorescence is due to chitin and its presence at the base of very early buds indicates that chitin synthesis begins at or shortly after bud emergence. A scheme for chitin synthesis and primary septum formation which embodies these and other results is presented.

Anti-Bacterial Agents↗

Rates of glucose utilization and glucogenesis in rats in the basal state induced by halothane anaesthesia.

1. Rates and rate coefficients of glucose utilization and replacement were determined with [5-3H]- and [U-14C]-glucose in rats starved for 24h, either conscious or under halothane anaesthesia, in a thermoneutral environment. Plasma insulin concentrations were also measured. 2. Halothane anaesthesia decreased the turnover rate by 20%, which was similar to previously reported decreases in metabolic rates caused by natural sleep. 3. Fractional recycling of glucose carbon was little affected by halothane. 4. Comparison of values in one rat with those in another, among both conscious rats and those under halothane anaesthesia, showed that rate coefficients were inversely correlated with plasma glucose concentrations. 5. These findings indicated that halothane, in the concentration used (1.25%, v/v), had little specific effect on glucose metabolism. 6. Although equilibrium plasma glucose concentrations in different rats under halothane were widely different (4-8 mmol/l) the rates of utilization were very similar (2.5-3.1 micronmol/min per 100 g), indicating that these rates were determined by the production of glucose from gluconeogenic precursors released by basal metabolism, the rate of which is necessarily similar in different rats. 7. Among rats under halothane anaesthesia plasma insulin concentrations were negatively correlated with rate coefficients, showing that the differences between rate coefficients were mostly accounted for by differences between rats in tissue sensitivities to insulin. Thus in each 24h-starved rat, sleeping or resting, the main regulators of the plasma glucose concentrations were the rate of supply of gluconeogenic substrates from energy metabolism and the intrinsic sensitivity of the tissues to insulin. 8. We found that a commonly used deionization method of purifying glucose for determination of its specific radioactivity was inadequate.

Anesthesia, Inhalation↗

Membrane lesions in cultured mouse neuroblastoma cells exposed to metal compounds.

Tritiated 2-deoxy-D-glucose (dGlc) was rapidly taken up into cultured mouse neuroblastoma C1300 cells (clone 41A3). Upon perfusion the preloaded cultures slowly released radioactivity as [3H] 2-deoxy-D-glucose-6-phosphate ([3H]dGlc-6-P) (rate const. = 0.017 min-1) from a pool corresponding to 74% (t1/2 = 41 min) of the total radioactivity incorporated. Destruction of the plasma membrane of the cells by means of Triton X-100 (1.0%) resulted in a rapid and total release of the radioactivity. CH3HgCl, HgCl2, (C2H5)3SnCl and K2Cr2O7 all caused an increase in the passive cell membrane permeability to [3H]dGlc-6-P. A membrane toxic concentration (MTC) was defined as the concentration of the tested metal compound giving rise to an increase in the relative efflux from 1.0 to 1.2 during 60 min perfusion. Using this MTC-value, the membrane toxicity of the compounds could be ranked in the following order: CH3HgCl (MTC = 9 x 10(-7) M) greater than HgCl2 (MTC = 6 x 10(-6) M) greater than (C2H5)3SnCl (MTC = 3 x 10(-4) M) greater than K2Cr2O7 (MTC = 7 x 10(-4) M). Since this differential toxicity is in accordance with other reports it is concluded that 2-deoxy-D-glucose (dGlc) may be used together with 41A3 cells to screen metal compounds for their membrane toxicity.

Animals↗

Cerebral glucose and energy utilization during the evolution of hypoxic-ischemic brain damage in the immature rat.

The cerebral metabolic rate for glucose (CMRg1) and cerebral energy utilization (CEU) were assessed in immature rats during recovery from cerebral hypoxia-ischemia. CMRg1 was determined using a modification of the Sokoloff technique with 2-deoxy-[14C]glucose (2-DG) as the radioactive tracer. CEU was determined using the Lowry decapitation technique. Seven-day postnatal rats underwent unilateral common carotid artery ligation, followed 4 h thereafter by exposure to 8% oxygen at 37 degrees C for 3 h. At 1, 4, or 24 h of recovery, the rat pups underwent those procedures necessary for the measurement of either CMRg1 or CEU. At 1 h of recovery, the CMRg1 of the cerebral hemisphere ipsilateral to the carotid artery occlusion was 97% of the control rate (8.7 mumol 100 g-1 min-1) but was only 48% of the control in the contralateral hemisphere. At 4 h of recovery, the CMRg1 was increased 49% above baseline in the ipsilateral hemisphere, decreasing thereafter to 84% of the control at 24 h. The CMRg1 of the contralateral hemisphere normalized by 4 h of recovery. An inverse correlation between endogenous concentrations of ATP or phosphocreatine and CMRg1 in the ipsilateral hemisphere was apparent at 4 h of recovery. CEU in the ipsilateral cerebral hemisphere was 64 and 46% of the control (3.47 mmol approximately P/kg/min) at 1 and 24 h, respectively (p < 0.05) and 77% of the control at 4 h of recovery. CEU in the contralateral hemisphere was unchanged from the control at all measured intervals. Correlation of the alterations in CMRg1 with those in CEU at the same intervals indicated that substrate supply exceeds energy utilization during early recovery from hypoxia-ischemia. The discrepancy combined with a persistent disruption of the cerebral energy state implies the existence of an uncoupling of mitochondrial oxidative phosphorylation as one mechanism for the occurrence of perinatal hypoxic-ischemic brain damage.

3-Hydroxybutyric Acid↗

Evidence for biochemical and physiological differences between enzyme genotypes in Drosophila melanogaster.

The in vivo flux of carbon through the pentose shunt is investigated as a function of different 6-phosphogluconate dehydrogenase (6Pgd) and glucose-6-phosphate dehydrogenase (G6pd) genotypes by using differential radioactive labeling of the C-1 and C-6 positions of glucose. Alternative 6Pgd-G6pd genotypes are shown to differ in relative in vivo carbon flux through the pentose shunt. The relative in vitro specific activity differences between the 6PgdSS and 6PgdFF genotypes appear to be primarily responsible for these differences. In addition, the pentose-shunt activity is correlated with the rate of lipid synthesis. This correlation is consistent with the major metabolic function of the pathway, which is to produce NADPH for lipid synthesis. Taken together, the results of these experiments show that different genotypes of 6Pgd are associated with measurable biochemical and physiological differences. Higher order phenotypic differences of this kind must be demonstrated to support the hypothesis that natural selection can discriminate among allozymes of a given genetic locus.

Animals↗

Pathways of acetate, propionate, and butyrate formation by the human fecal microbial flora.

The pathways of short-chain fatty acid (SCFA; acetate, propionate, and butyrate) formation from glucose were determined for the human fecal microbial communities of two subjects. The pathways were identified by radioisotope analysis of the SCFA and CO2 obtained after incubation of fecal suspensions with glucose under 20% CO2 with [1-14C]glucose, [3,4-14C]glucose, or 14CO2. Acetate was chemically degraded to learn the labeling of the methyl and carboxyl carbons. The labeling of CO2 and acetate showed that the major route of glucose catabolism was the Embden-Meyerhof-Parnas pathway, with production of CO2 from pyruvate carboxyl carbon. Labeling of the methyl and carboxyl carbons of acetate by 14CO2 or [3,4-14C]glucose proved that acetate was formed from CO2 by the Wood-Ljungdahl pathway. CO2 reduction accounted for about one-third of the acetate formed by suspensions from subject 1 and about one-fourth of the acetate formed by suspensions from subject 2. Propionate was formed by a CO2 fixation pathway, and butyrate was formed by classical routes of acetyl-S coenzyme A condensation. The amount of CO2 formed from [1-14C] glucose and acetate labeling patterns obtained with the other 14C precursors indicated that the Entner-Doudoroff, transketolase-transaldolase, and heterolactic pathways were not significant. Fermentation of cabbage cellulose by subject 1 followed the same pathways as were used for glucose. The results with suspensions from subject 2 suggested that some radioactive acetate was formed from the C-3 of glucose by the Bifidobacterium pathway.

Acetates↗

Increased insulin sensitivity and responsiveness of glucose metabolism in adipocytes from female versus male rats.

This study was undertaken to examine whether there were sex-associated differences in the action of insulin on glucose metabolism in adipocytes. Insulin binding and the dose-response curves for glucose transport (assessed by measuring the cell-associated radioactivity after 15-s incubation with 50 microM [6-14C]glucose) and [U-14C]glucose (5 mM) metabolism into CO2 and lipids were compared in retroperitoneal adipocytes from age-matched (84 d) male and female rats. In addition, the activity of fatty acid synthetase, one of the key lipogenic enzymes, was determined. Fat cell size was not significantly larger in females than in males (0.238 vs. 0.209 microgram lipid per cell). At insulin concentrations less than or equal to 1.6 nM, adipocytes from females bound significantly more insulin than did adipocytes from males, due to an increased apparent affinity of the receptors for insulin. Accordingly, the sensitivity of glucose transport to insulin was greater in females than in males: insulin concentration eliciting half-maximal stimulation (ED50) = 0.19 nM vs. 0.41 nM. At maximal insulin stimulation the rates of glucose transport (12 times the basal values) were similar in the two sexes. In contrast, the maximal effect of insulin on glucose conversion to CO2 plus lipids was much greater in the adipocytes from females than males (increment over basal: 472 vs. 249 nmol/10(6) cells per 2 h). Fatty acid synthesis contributed approximately 40% of the incremental difference between the two types of adipocytes, while glyceride-glycerol synthesis contributed less than 10%. The insulin dose-response curves for adipocytes from females were shifted to the left for all the metabolic pathways investigated. The mean ED50 for total glucose metabolism in females was 50% of that in males (0.07 nM vs. 0.15 nM). Marked sex-associated differences in the action of insulin on glucose metabolism were also observed in subcutaneous inguinal adipocytes (increment over basal: 137 and 56 nmol/10(6) cells per 2 h, ED50 = 0.13 nM and 0.30 nM in females and males, respectively). The intracellular capacity to metabolize glucose through the fatty acid synthesis pathway, as assessed by FAS activity, was higher in adipocytes from females than in those from males and was greater in retroperitoneal than in inguinal adipocytes. Furthermore, by plotting the individual data, a highly significant correlation (r = 0.92, P less than 0.001) was found between the absolute effect of insulin on glucose metabolism at maximal stimulation and the fatty acid synthetase activity of the cells. These results indicate that the response of glucose metabolism to insulin in adipocytes from female as compared with male rats is characterized by two main features: (a) an increased sensitivity primarily due to an increase in insulin binding, and (b) an increased responsiveness closely associated with a postreceptor increase in the lipogenic capacity of the cell. These findings might be relevant to the differential disposition of male and female rats to develop fatness.

Adipose Tissue↗

Contribution of intermuscular fat to lipogenesis from dietary glucose carbon in mice.

We assessed the contribution of various tissues to the synthesis of fat from glucose carbon in mice during rapid lipogenic activation induced by a glucose test meal. Nibbling and gorging mice were maintained on a 58% glucose, fat-free diet. The mice were fasted 22 h and refed 5-10 muCi [U-14C]glucose (120 mg/20 g body weight) either by gastric intubation or as a test meal (58% glucose diet). The muscular carcass in both nibblers an gorgers contained more than 75% of the total radioactivity in the fatty acids derived from glucose; liver and epididymal fat pad accounted for only a small percentage. Mort than half the carcass activity was in the "muscular" tissue as neutral lipid acids. We could isolate a discrete fat body in the popliteal region of the leg muscle ("muscle fat", "intermuscular fat"). The popliteal fat converted glucose carbon to fatty acids an order of magnitude faster, per unit weight, than the epididymal fat pad or skeletal muscle. The fatty acid moiety of the triacylglycerols had the major portion of the label in the popliteal fat 2 and 6 h after ingestion of the glucose test meals. The diacylglycerol pool was active at 2 h and its activity faded at 6 h implicating its intermediary role in lipid metabolism similar to published findings in epididymal fat pad. These results indicate that fat cells associated with the muscular carcass may play a major role in the de novo synthesis of fat from dietary carbohydrate in mice.

Adipose Tissue↗

INFLUENCE OF BIOLOGICAL METHYLATION ON THE BIOSYNTHESIS OF MITOMYCIN A.

Kirsch, E. J. (Lederle Laboratories, Pearl River, N.Y.), and J. D. Korshalla. Influence of biological methylation on the biosynthesis of mitomycin A. J. Bacteriol. 87:247-255. 1964.-Methionine-methyl-C(14) was shown to contribute radioactive carbon to the mitomycin antibiotic complex synthesized by Streptomyces verticillatus in a simple synthetic medium containing glucose and inorganic salts. The position of radioactivity in mitomycin A was determined by selective hydrolysis of the 7 and 9a methoxyl functions. Essentially all of the radioactivity incorporated was distributed evenly between these two substituent groups. Mitomycin A, synthesized by washed resting cells of S. verticillatus at the expense of internal metabolites, also incorporated methyl label. When the methionine antagonist, d,l-ethionine, was added to resting cells at a concentration causing 65% inhibition of antibiotic synthesis, incorporation of radioactive methyl groups was reduced to the same extent. Synthetic medium supplemented with d,l-ethionine supported about 90% maximal growth of the culture, but antibiotic biosynthesis was markedly inhibited. The addition of the inhibitor during the period of rapid antibiotic synthesis resulted in cessation of further increases in antibiotic titer. l-Methionine was shown to be capable of reversing ethionine inhibition; the extent of reversal was dependent on the concentration, as well as on the time of addition of amino acid. The data suggest the critical nature of a methyl transfer system in the biogenesis of biologically active mitomycins.

Amino Acids↗

Formation of dolichol monophosphate 2-deoxy-D-glucose and its interference with the glycosylation of mannoproteins in yeast.

A crude membrane fraction from Saccharomyces cerevisiae has been found to catalyze 2-deoxy-D-glucose transfer from GDP-2-deoxy-D-glucose to endogeneous lipid and glycoprotein acceptor. Evidence will be represented that the glycolipid formed has properties characteristic dolichol monophosphate 2-deoxy-D-glucose. The 2-deoxy-D-glucosyl group can further be transferred from the glycolipid into a membrane-bound polymer fraction. More than 95% of the radioactivity incorporated can be released by beta-elimination, indicating an O-glycosidic linkage to serine or threonine. The only radioactive product obtained is 2-deoxy-D-glucose. When dolichol monophosphate 2-deoxy-[14C]glucose is incubated together with non-radioactive GDP-mannose subsequent beta-elimination yields no higher oligosaccharides in contrast to an experiment where dolichol monophosphate [14C]mannose and GDP-mannose are used as donors. The results are consistent with the assumption that the non-physiological nucleotide sugar interferes with GDP-mannose for mannosylation and terminates further elongation of the serine/threonine-bound oligomannose side chains. UDP-2-deoxy-D-glucose, used as donor, results also in the formation of a glycolipid. In this case, however, no polyprenol derivative is formed. Instead, the glycolipid displays properties characteristic of sphingolipid or a sterol glucoside.

Cell Membrane↗

Secretagogue-responsive and -unresponsive pools of phosphatidylinositol in pancreatic islets.

The effect of glucose on phosphatidylinositol turnover was studied. Phosphatidylinositol of rat pancreatic islets was labeled with myo[2-3H]inositol in the presence of various secretagogues (16.7 mM D-glucose, 22 mM D-mannose, 20 mM D-glyceraldehyde) and nonsecretagogues (3.3 mM D-glucose, 20 mM pyruvate, 16.7 mM D-galactose, 16.7 mM L-glucose). Upon subsequent stimulation with 16.7 mM D-glucose, only the islets that were labeled in the presence of secretagogues showed a loss of radioactivity from phosphatidylinositol. No loss of radioactivity from phosphatidylinositol occurred in the presence of 3.3 mM D-glucose even after labeling in the presence of secretagogues. A comparison of the subcellular distribution of labeled phosphatidylinositol in islets before and after stimulation with insulinotropic glucose revealed a loss of radioactivity from the plasma membrane fraction as judged by subcellular fractionation with a sucrose gradient. These results support a hypothesis advanced previously that pancreatic islets contain a unique pool of phosphatidylinositol that undergoes rapid turnover only in the presence of insulinotropic concentrations of D-glucose or other secretagogues [R. S. Rana, R. J. Mertz, A. Kowlura, J. F. Dixon, L. E. Hokin, and M. J. MacDonald (1985) J. Biol. Chem. 260, 7861-7867]. On the basis of the subcellular fractionation studies reported here, the secretagogue-responsive phosphatidylinositol pool appears to be located primarily in the plasma membrane of pancreatic islets.

Animals↗

Anomeric specificity of human liver and B-cell glucokinase: modulation by the glucokinase regulatory protein.

The anomeric specificity of the wild-type recombinant forms of human liver and B-cell glucokinase was investigated using radioactive anomers of d-glucose as tracers. With d-glucose at anomeric equilibrium and at 30 degrees C, the maximal velocity, Hill number, and K(s) amounted, respectively, to 16 micromol min(-1) mg(-1), 1.8 and 6.9 mM in the case of liver glucokinase, and 7.3 micromol min(-1) mg(-1), 2.0 and 7.1 mM in the case of B-cell glucokinase. Whether at 20-22 or 30 degrees C, the maximal velocity, Hill number, and K(m) were significantly lower with alpha-d-glucose than with beta-d-glucose in both liver and B-cell glucokinase. As a result of these differences, the reaction velocity was higher with alpha-d-glucose at low hexose concentrations, while the opposite situation prevailed at high hexose concentrations. In the presence of 0.2 mM d-fructose 6-phosphate, the glucokinase regulatory protein caused a concentration-related inhibition of d-glucose phosphorylation, such an effect fading out at high concentrations of either d-glucose or glucokinase relative to that of its regulatory protein. The phosphorylation of alpha-d-glucose by liver glucokinase appeared more resistant than that of beta-d-glucose to the inhibitory action of d-fructose 6-phosphate, as mediated by the glucokinase regulatory protein. Such a phenomenon failed to achieve statistical significance in the case of the B-cell glucokinase. It is proposed that this information, especially the novel findings concerning the anomeric difference in both Hill number and sensitivity to the glucokinase regulatory protein, should be taken into account when considering the respective contributions of alpha- and beta-d-glucose to the overall phosphorylation of equilibrated d-glucose by glucokinase.

Adaptor Proteins, Signal Transducing↗

Plant glucosidase II catalyzes a transglucosylation reaction in addition to the hydrolytic reaction.

When the purified plant glucosidase II was incubated with [3H]Glc2Man9GlcNAc in the presence of glycerol and the products were analyzed by gel filtration, a large peak of radioactivity emerged just before the glucose standard. The formation of this peak was dependent on both the presence of Glc2Man9GlcNAc and the presence of glycerol, and the amount of this product increased with time of incubation and amount of glucosidase II in the incubation. When the incubation was performed with [3H]Glc2Man9GlcNAc plus [14C]glycerol, the product contained both 14C and 3H. Strong acid hydrolysis of the purified product gave rise to [14C]glycerol and [3H]glucose. Various other chemical treatments and chromatographic techniques showed that the product was glucosyl----glycerol. Since the glucose was released by alpha-glucosidase, the product must be glucosyl-alpha-glycerol. This study demonstrates that the processing glucosidase II catalyzes a trans-glycosylation reaction in the presence of acceptors like glycerol. Since this transglycosylation reaction may give rise to unexpected products, investigators should be aware of its possible occurrence.

Fabaceae↗

The assay of glucocerebrosidase activity using the natural substrata.

We examined eight published methods for the assay of glucocerebrosidase using the natural substrate glucocerebroside and tabulated the variable components and conditions while comparing these methods to ours. In each case assays were performed using our 8000-fold, partially purified human placental enzyme, having a pH optimum of 5.4-5.6 and a Km of approximately 0.60 mmol per liter. Results were obtained by following the release of radioactive ceramide or of unlabelled glucose. In many cases published results had been based on a one- or two-hour incubation time. Apparent specific activities varied over a 70-fold difference between the various procedures. When we measured activities from the linear (15-30 min) portion of rate curves the values increased by 1.4 to 3 times but still ranged from 6 X 10(3) - 180 X 10(3) nmol . mg-1 protein . h-1. We obtained maximum velocity using 1.2 mmol glucocerebroside, 0.5% (w/v)crude taurocholate and 2 microgram enzyme protein/ml. Specific activities reported from different laboratories are not directly comparable. Conditions for assay should be optimized for the enzyme preparation to be studied.

Cerebrosides↗

Effect of 6-aminonicotinamide on pentose cycle activity in isolated hepatocytes.

1. 6-aminonicotinamide (6AN), a purported inhibitor of 6-phosphogluconate (6PG) dehydrogenase, has been regarded as an inhibitor of the pentose cycle. 2. Incubation of isolated hepatocytes with 6AN caused a time- and concentration-dependent accumulation of 6PG. 3. At 5 mM, 6AN increased the 6PG level 1000-times to values comparable to those observed in the livers of rats injected with this niacin antagonist. 4. Despite the accumulation of 6PG, neither the total rate of lipogenesis, nor the incorporation of radioactivity from [3-3H]glucose, used to estimate the activity of the pentose cycle, were impaired to a large extent. 5. The evidence presented suggests that the accumulation of 6PG is not a sufficient criterion to establish blockade of the pentose cycle.

6-Aminonicotinamide↗

Effects of oral and parenteral quinine on rats with ventromedial hypothalamic knife-cut obesity.

The addition of quinine to the food reversed the obesity in rats with hypothalamic hyperphagia induced by knife cuts. Similarly, the injection of quinine into rats with hypothalamic knife cuts reduced food intake and body weight but the effects were smaller than those observed when quinine was added to the diet. Urinary quinine excretion was similar by the oral and parenteral routes. The food intake of the knife-cut animals receiving quinine gradually fell to the same level as in the sham-operated animals receiving quinine by either route. The weights of retroperitoneal fat pads were related to the weights of the animals and were reduced in the quinine-treated groups. Plasma insulin concentrations were significantly higher in the knife-cut animals and were reduced toward control levels by quinine treatment. Gluconeogenesis, measured by incorporation of radioactivity from labeled bicarbonate into glucose, was unaffected by treatment with quinine or by knife cuts. Lipogenesis from tritiated water in vivo was not different between treatment groups in the liver or retroperitoneal fat pads. However, in vivo lipogenesis was reduced in knife-cut rats fed ad libitum compared with quinine-treated rats. The response of lipogenesis to insulin in vitro was also not different between treatment groups. These data suggest that a major part of the reduction in food intake in hyperphagic rats eating a quinine-adulterated diet is due to postingestional events.

Adipose Tissue↗

High level arsenite resistance in Leishmania tarentolae is mediated by an active extrusion system.

Leishmania tarentolae cells selected for resistance to the oxyanions pentavalent or trivalent antimonials or to trivalent arsenicals exhibited cross-resistance to the other oxyanions. The basis for resistance in these mutants was studied by transport experiments using radioactive arsenite. All mutants exhibiting high level resistance to arsenite showed a marked decrease in the steady-state accumulation of arsenite. Decreased accumulation was also observed in antimonials-resistant mutants cross-resistant to various concentrations of arsenite. Cells depleted of endogenous energy reserves with metabolic inhibitors were loaded with radioactive arsenite; following addition of glucose, rapid efflux of arsenite was observed from arsenite mutant cells. Mutants resistant to high levels of arsenicals exhibited amplification of the P-glycoprotein related gene ltpgpA or of a linear amplicon of unknown function. However, the efflux-mediated arsenite resistance did not correlate with the amplification of the ltpgpA gene or with the presence of the linear amplicon. The calcium channel blocker verapamil and arsenite act in synergy in cells exhibiting the efflux system. Overall the oxyanion efflux system in Leishmania shares several properties with other resistance efflux systems mediated by transporters.

Animals↗

Radioactive 2-DG incorporation patterns in the mesial frontal cortex of task-performing monkeys.

The pattern of radioactive 2-deoxy-D-glucose (2-DG) uptake in the rostral mesial cortex was investigated in seven hemispheres of four task-performing monkeys (a delayed-response task performed with a forelimb). A two-dimensional 2-DG map was constructed from frontal sections. Blob-like 2-DG incorporation sites (2-DG active sites) were observed in single frontal sections, e.g., in the anterior cingulate gyrus (CiG) and supplementary and primary motor cortices in the mesial surface, and around the superior precentral sulcus in the premotor area. Blob-like 2-DG incorporation sites were also observed in the medial part of the dorsal frontal cortex near the midline. However, most of these blob-like 2-DG active sites were revealed in fact not to be blobs. They formed rostrocaudally continuous streaks when they were constructed in a two-dimensional map. Streaks fused with one another in some areas, and gave off branches in other areas. These 2-DG uptake patterns were similar between the paired left and right hemispheres of three brains. It is highly probable that these 2-DG active streaks (or blobs) reflected neuronal activity related to somatomotor and/or eye movements, because the 2-DG-labeled areas included motor, premotor, supplementary motor, and possibly part of the supplementary eye fields. It is also probable that this 2-DG incorporation was related to cognitive or memory functions, because neuronal activity related to performance of a delayed-response was reported in the rostral mesial cortex and in the CiG.

Animals↗