Protein secretion in suspensions of isolated rat hepatocytes: no influence of acute ethanol administration

The effect of ethanol on the secretion of proteins was studied in hepatocytes isolated from 24-h fasted rats and from fed rats. Hepatocytes were isolated after collagenase disruption of the liver and incubated in a standard medium containing amino acids, bovine albumin, glucose, penicillin and streptomycin in HEPES buffer. Cell viability was determined by urea production and trypan blue exclusion. When studying protein export, a model had to be chosen in which the labeling is accomplished before the addition of the test agents. Cells were incubated with [3H]valine for 2.5 and 7.5 min followed by a 15-mM valine chase and the incubates were adjusted to final concentrations of ethanol of 50 mM, 100 mM, colchicine 5-50 microM or cycloheximide 18 microM. Cells and media were harvested at various times, and counts incorporated into medium and cell protein were determined. Cycloheximide inhibited protein synthesis by 99%, decreased protein secretion by 10-20%, but did not further inihibit protein labeling when given after the chase confirming the chase's effectiveness. Colchicine inhibited protein release by 27-54% depending on the dose. With control cells labeled protein and specifically albumin appeared in the medium 20 min from the start of the pulse and this release of protein was not inhibited by 50 mM or 100 mM ethanol incubated with cells from the same animal whether the donor has been fed or fasted. The values for the ethanol-treated cells ranged from 94.0 to 113% of the control values from 30 to 120 min after the addition of the pulse. Lactate levels were markedly elevated, and urea synthesis decreased in the presence of either 50 mM EtOH or 100 mM EtOH. Thus using a method that can distinguish the effect of ethanol on synthesis from secretion, it is concluded that acute exposure to EtOH does not interfere with protein secretion.     

Rates of lysine catabolism are inversely related to rates of protein synthesis when measured concurrently in adult female rats induced to grow at different rates

To test the effect of changes in the rate of protein synthesis on amino acid oxidation, both were studied concurrently in individual 200-g female Sprague-Dawley rats. In a growth trial (Experiment 1), recombinant bovine somatotropin (rbST) was injected subcutaneously (0, 2 or 12 mg/d) over 6 d (n = 4 rats per rbST level). Weight gain increased with rbST level (P < 0.01); 1.96 +/- 0.8, 4.24 +/- 0.8 and 8.67 +/- 0.8 g/d, respectively. After treatment with rbST (0 or 12 mg/d) for 4 d (Experiment 2), rats were injected via a tail vein catheter with valine (400 mmol, 4.07 mBq L-[3,4(n)-3H]valine) at 0, 4, 10, 13 or 16 h after the daily rbST injection and killed 20 min later. This flooding dose was 5 to 6 times, not 10 times, the free pool as hoped. Protein synthesis in rbST-treated rats increased 46% in muscle (P < 0.001) and 36% in liver (P < 0.01). The ks was unaltered with time after rbST injection (0-16 h, P > 0.05). When 600 mmol valine (4.4 mBq L-[3,4(n)-3H]valine) was used in Experiment 3, specific activity (SA) of free valine was constant over 20 min and was 94 +/- 4% of that injected. Finally, in Experiment 4, protein synthesis and amino acid oxidation rates measured in the same rat revealed a 35% increase (P < 0.01) in protein synthesis in hind leg muscle and a 29% increase in liver (P < 0.05) from rbST-injected (12 mg/d) rats (n = 6). Lysine oxidation was estimated by continuous (12 h) infusion of L-[1-14C]lysine via the opposite tail vein catheter. Expired CO2 was collected over 20-min intervals and SA at plateau was estimated by fitting an exponential model. Lysine oxidation was reduced (P < 0.05) by 44% in rbST-treated rats. The idea that an increase in protein synthesis results in decreased amino acid oxidation remains tenable.     

Arterial elastin synthesis in the young chick

In the growing chick a marked stimulation in soluble and mature arterial elastin synthesis occurs 2 and 5 weeks after hatching. Measurement of [3H]valine and [3H]proline incorporation into arterial soluble protein during this period indicated that most of the label is found in a 70 000 dalton protein subunit. The labeled soluble subunit had the characteristics of native soluble elastin or tropoelastin. During the period in which the greatest percentage increase in mature elastin occurs, the highest specific activities of soluble [3H]valine-labeled protein were observed. These changes were striking and suggest a developmental period for the growing chick in which factors related to elastin metabolism may be more easily studied.     

Dissociation of place and cue learning by telencephalic ablation in goldfish.

This study examined the spatial strategies used by goldfish (Carassius auratus) to find a goal in a 4-arm maze and the involvement of the telencephalon in this spatial learning. Intact and telencephalon-ablated goldfish were trained to find food in an arm placed in a constant room location and signaled by a local visual cue (mixed place-cue procedure). Both groups learned the task, but they used different learning strategies. Telencephalon-ablated goldfish learned the task more quickly and made fewer errors to criterion than controls. Probe trials revealed that intact goldfish could use either a place or a cue strategy, whereas telencephalon-ablated goldfish learned only a cue strategy. The results offer additional evidence that place and cue learning in fish are subserved by different neural substrates and that the telencephalon of the teleost fish, or some unspecified structure within it, is important for spatial learning and memory in a manner similar to the hippocampus of mammals and birds. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

125I] beta-CIT-FE and [125I] beta-CIT-FP are superior to [125I] beta-CIT for dopamine transporter visualization: autoradiographic evaluation in the human brain

The binding of the three dopamine transporter radioligands ([125I] beta-CIT, [125I] beta-CIT-FE, and [125I] beta-CIT-FP) was studied using whole-hemisphere autoradiography on postmortem human brains. The autoradiograms revealed an intense and homogeneous labeling of the nucleus caudatus and putamen but also to varying extent to serotonergic and noradrenergic transporters of neocortex and thalamus. The order of specificity estimated (striatum over neocortex ratios) was beta-CIT-FP > beta-CIT-FE > > beta-CIT, suggesting that beta-CIT-FE and beta-CIT-FP should be preferred for in vivo studies of the dopamine transporter in the human brain.     

Tricarboxylic acid cycle in rat brain synaptosomes. Fluxes and interactions with aspartate aminotransferase and malate/aspartate shuttle

The flux through different segments of the tricarboxylic acid cycle was measured in rat brain synaptosomes with gas chromatography-mass spectrometry using either deuterated glutamine or [13C]aspartate. The flux between 2-oxoglutarate and oxaloacetate was estimated to be 3.14 and 4.97 nmol/min/mg protein with and without glucose, respectively. These values were 3-5-fold faster than the flux between oxaloacetate and 2-oxoglutarate (0.92 nmol/min per mg protein) measured in the presence of glucose. The pattern of intermediates labeling suggests that the overall rate-controlling reaction involves either citrate synthase or pyruvate dehydrogenase but not 2-oxoglutarate or isocitrate dehydrogenase. The enrichment in [3,3,4,4-2H4]glutamate from [2,3,3,4,4-2H5]glutamine was as rapid as in [2,3,3,4,4-2H5]glutamate, which indicates that the aspartate aminotransferase reaction is severalfold faster than the flux through the tricarboxylic acid cycle. [13C]Aspartate was rapidly converted to [13C]malate, suggesting that in intact synaptosomes aspartate entry into the mitochondrion is very slow. The finding that aspartate is taken up by mitochondria as malate, along with the observed high enrichment in [3-2H]malate (from [2,3,3,4,4-2H5]glutamine), is consistent with the substantial synaptosomal activity of the malate/aspartate shuttle.     

Infusion of soy and casein protein meals affects interorgan amino acid metabolism and urea kinetics differently in pigs

For routine evaluation of the quality of dietary protein, amino acid scoring patterns were used. Evaluation of this pattern for soy and casein revealed that these proteins are of almost equal quality. However, in vivo studies showed a large difference. To study the biological effects of meals with casein and soy protein, the contributions of individual amino acids to net protein retention and amino acid kinetics in gut, liver and muscle in healthy pigs were investigated. Isonitrogenous enteral nutrition, infused at a rate of 10 mL. kg body wt-1. h-1 and consisting of maltodextrin (137 g/L) with added casein (53 g/L) or soy protein (68 g/L), was given to conscious, healthy female multicathetized pigs (20-22 kg, n = 12). A primed-constant infusion protocol with L-[ring-2,6-3H]phenylalanine, L-[3,4-3H]valine and [15N-15N]urea was used to measure amino acid and urea kinetics in gut, liver and muscle. Measurements were done postabsorptively and 2-6 h after initiation of the enteral nutrition. During the meal, appearance of amino acids into the portal vein and the uptake by the liver was lower with casein infusion. Muscle uptake did not differ. Gut protein synthesis tended to be lower with soy infusion (P = 0.1). Liver protein synthesis and degradation were higher with casein infusion (P < 0.05), while in muscle, soy infusion stimulated protein turnover (P < 0.05). In comparison to the postabsorptive condition, liver urea production was unchanged after casein infusion, while it was significantly increased after soy infusion. These results suggest that the quality of soy protein is inferior to that of casein protein.     

Synthesis of deoxyglucose-1-phosphate, deoxyglucose-1,6-bisphosphate, and other metabolites of 2-deoxy-D-[14C]glucose in rat brain in vivo: influence of time and tissue glucose level

When the kinetics of interconversion of deoxy[14C]glucose ([14C]DG) and [14C]DG-6-phosphate ([14C]DG-6-P) in brain in vivo are estimated by direct chemical measurement of precursor and products in acid extracts of brain, the predicted rate of product formation exceeds the experimentally measured rate. This discrepancy is due, in part, to the fact that acid extraction regenerates [14C]DG from unidentified labeled metabolites in vitro. In the present study, we have attempted to identify the 14C-labeled compounds in ethanol extracts of brains of rats given [14C]DG. Six 14C-labeled metabolites, in addition to [14C]DG-6-P, were detected and separated. The major acid-labile derivatives, DG-1-phosphate (DG-1-P) and DG-1,6-bisphosphate (DG-1,6-P2), comprised approximately 5 and approximately 10-15%, respectively, of the total 14C in the brain 45 min after a pulse or square-wave infusion of [14C]DG, and their levels were influenced by tissue glucose concentration. Both of these acid-labile compounds could be synthesized from DG-6-P by phosphoglucomutase in vitro. DG-6-P, DG-1-P, DG-1,6-P2, and ethanol-insoluble compounds were rapidly labeled after a pulse of [14C]DG, whereas there was a 10-30-min lag before there was significant labeling of minor labeled derivatives. During the time when there was net loss of [14C]DG-6-P from the brain (i.e., between 60 and 180 min after the pulse), there was also further metabolism of [14C]DG-6-P into other ethanol-soluble and ethanol-insoluble 14C-labeled compounds. These results demonstrate that DG is more extensively metabolized in rat brain than commonly recognized and that hydrolysis of [14C]DG-1-P can explain the overestimation of the [14C]DG content and underestimation of the metabolite pools of acid extracts of brain. Further metabolism of DG does not interfere with the autoradiographic DG method.     

Modulation by magnesium of N-methyl-D-aspartate receptors in developing human brain

AIM: To investigate age related alterations in glutamate N-methyl-D-aspartate (NMDA) receptor binding produced by the modulatory compounds glutamate, glycine, and magnesium (Mg2+) sulphate. METHODS: The effects produced by glutamate plus glycine, and Mg2+ on the binding of [3H]MK-801, a ligand for the N-methyl-D-aspartate ion channel phencyclidine site, were measured in membrane preparations made from prefrontal cortex from human neonate (n = 5), infant (n = 6), and adult (n = 6) necropsy brains. RESULTS: Neonatal brains had the least [3H]MK-801 binding, suggesting either a low density of NMDA receptors or a more restricted access of [3H]MK-801 to cation channel sites. Infant brains had the most [3H]MK-801 binding which was stimulated to a greater extent by L-glutamate (100 microM) and glycine (10 microM) than in neonatal and adult brains. MG2+ invariably inhibited [3H]MK-801 binding. However, the Mg2+ IC50 value was higher in neonatal brain (3.6 mM) than infant (1.4 mM) and adult (0.87 mM) brains. CONCLUSION: Infant brain may have excess NMDA receptors which are hyper responsive to glutamate and glycine. The lower potency of Mg2+ to inhibit [3H]MK-801 binding in neonatal cortex may be because newborn babies have NMDA receptors without the normal complement of Mg2+ sites. The findings suggest that therapeutic NMDA receptor block in neonates requires higher concentrations of magnesium sulphate in brain tissue.     

Determination of low isotopic enrichment of L-[1-13C]valine by gas chromatography/combustion/isotope ratio mass spectrometry: a robust method for measuring protein fractional synthetic rates in vivo

A method was developed for measuring protein fractional synthetic rates using the N-methoxycarbonylmethyl ester (MCM) derivative of L-[1-13C]valine and on-line gas chromatography/combustion/isotope ratio mass spectrometry (GC/C/IRMS). The derivatization procedure can be performed rapidly and GC separation of valine from the other branched-chain amino acids, leucine and isoleucine, is easily obtained. A good linear relationship was observed between the increment of the 13C/12C isotope ratio in CO2 gas derived from the combustion of derivatized valine and the tracer mole ratio of L-[1-13C]valine to unlabelled valine. The limit of quantitation was at an L-[1-13C]valine tracer mole ratio of 0.0002. The method was used to measure the isotopic enrichment of L-[1-13C]valine in standard mixtures and in skeletal muscle of six growing piglets infused with L-[1-13C]valine (2 mg kg-1 h-1 for 6 h). After infusion of L-[1-13C]valine the mean tracer mole ratio in plasma of L-[1-13C]valine at the isotopic steady state was 0.0740 +/- 0.0056 (GC/MS, mean +/- SEM) and the mean tracer mole ratio of valine in muscle protein fraction at 6 h was 0.000236 +/- 0.000038 (GC/C/IRMS). The resulting mean protein fractional synthetic rate in piglet skeletal muscle was 0.052 +/- 0.007% h-1, which is in good agreement with literature data obtained with alternative, more elaborate techniques. By this method protein fractional synthetic rates can be measured at low isotopic enrichment levels using L-[1-13C]valine, the MCM derivative and on-line GC/C/IRMS.     

Nitric oxide involvement in regulating the dopamine transport in the striatal region of rat brain

Spontaneous [3H]dopamine ([3H]DA) overflow was measured from striatal slices in the presence of different glutamate (Glu) receptor agonists such as N-methyl-D-aspartate (NMDA), kainate (KA) and quisqualate (QA) and their corresponding antagonists, Dizocilpine maleate (MK-801), D-gamma-glutamyl-aminomethanesulfonic acid (GAMS) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), respectively. [3H]DA uptake and release in the presence of L-Arginine (L-Arg) and NG-nitro-arginine (L-N-Arg), an inhibitor of nitric oxide (NO) synthesis were also evaluated. L-N-Arg alone or combined with L-Arg significantly reduced [3H]DA uptake at 10 and 100 microM from 33% to 44% from striatal slices. Whereas, in brain synaptosomal fractions L-Arg induced a biphasic effect on that [3H]DA uptake in a dose dependent manner, and L-N-Arg showed an absolute inhibition in 80-90% of this [3H]DA uptake at 1-500 microM. The amino acids, lysine, valine and histidine (100 microM) had a little effect inhibitory on [3H]DA uptake from synaptosomal fractions. Glu agonists, NMDA (10 microM) and KA (10 microM) importantly increased the spontaneous [3H]DA overflow, which was blocked by MK-801 (10 microM) and GAMS (10 microM), respectively. QA had no effect on [3H]DA release. L-Arg (10-200 microM) potentiated the spontaneous [3H]DA overflow in a dose dependent fashion from striatal slices, being reverted by 10 microM L-N-Arg alone or in combination with all other compounds; whereas, lysine, histidine and valine did not modify that spontaneous [3H]DA overflow. Results support the hypothesis related to the participation of NO on DA transport possibly synthesized at the dopaminergic (DAergic) terminals in the striatum; also that L-Arg concentration may determine alternative mechanisms to regulate the DAergic activity at the striatum.     

The zebrafish brain: a neuroanatomical comparison with the goldfish

The zebrafish Danio rerio is an important model system for genetic and developmental studies of the vertebrate central nervous system. Considerable knowledge concerning the embryonic development of the central nervous system of the zebrafish has accumulated in recent years. However, there is an apparent lack of information on the organization of the adult zebrafish brain. We have therefore recently studied in detail the neuroanatomy of the adult zebrafish. Here we compare the brains of the zebrafish and of the closely related and neurobiologically well-investigated goldfish, Carassius auratus. Two sensory systems, the visual and the gustatory systems, were identified as differing on the gross morphological and histological levels in the two species. The goldfish shows the simple (evolutionarily reduced) pattern of pretectal organization, and its gustatory system is massively enlarged. The pretectum of the zebrafish conforms to this simplified visual pretectal pattern, although the retention of some ancestral pretectal characters indicates a lesser degree of reduction of the visual system compared to the goldfish. The gustatory system shows many similarities with the evolutionarily derived and functionally specialized gustatory system of the goldfish. However, some peripheral and central gustatory characters are missing in the zebrafish, indicating a less specialized gustatory system.     

Effects of the trichothecene mycotoxin T-2 toxin on neurotransmitters and metabolites in discrete areas of the rat brain

Systemic exposure to T-2 toxin disrupts brain biogenic monoamine metabolism. Although the mechanisms underlying these neurochemical perturbations are unclear, we have suggested that they are a reflection of increased blood-brain barrier (BBB) permeability, or altered protein synthesis that affects brain enzyme activities. Accordingly, BBB permeability, in vitro protein synthesis and in vitro monoamine oxidase (MAO) activity were examined in rats after either acute, or 7-day exposure to T-2. Membrane permeability was assessed from the recovery of systemically administered [14C]mannitol and [14C]dextran with [3H]water as the diffusible reference, either 2 hr post-intraperitoneal (i.p.) injections of 0, 0.2 and 1 mg T-2/kg body weight or following a 7-day exposure to diets containing 0 and 10 ppm T-2. Protein synthesis, determined by [14C]leucine incorporation, and MAO activity, determined by H2O2 production, were observed either 2 hr post-ip injection of 0 and 1 mg T-2/kg body weight or following a 7-day exposure to diets containing 0, 2.5 and 10 ppm T-2. Permeability increases were observed in all brain regions examined for mannitol, but not for dextran following T-2 i.p. The effect of dietary T-2 was more modest, affecting mannitol uptake in two brain regions, the cerebellum and pons plus medulla regions. Protein synthesis was significantly decreased by i.p. administration of T-2, while dietary treatment significantly reduced MAO enzyme activity. Collectively, the effect of T-2 toxin on BBB permeability, protein synthesis and MAO enzyme activity may account for the neurochemical imbalance observed in T-2 intoxication.     

Reaction of the type III iodothyronine deiodinase with the affinity label N-bromoacetyl-triiodothyronine

The type III iodothyronine deiodinase (ID-III) catalyzes the inner ring deiodination and, thus, the inactivation of the thyroid hormones T4 and T3. ID-III activity in rat brain, rat placenta and embryonic chicken liver is inhibited by the affinity label N-bromoacetyl-T3 (BrAcT3) with an affinity similar to that of T3. Reaction of rat brain and placenta microsomes with BrAc[125I]T3 resulted in the extensive labeling of a 32 kDa protein (p32). However, p32 was also prominently labeled in fetal rat liver microsomes which have no ID-III activity. Labeling of p32 was not influenced by 100 microM substrate analogs or inhibitors of ID-III, some of which completely inhibit ID-III activity at 1 microM. BrAc[125I]T3 labeling of embryonic chicken liver microsomes did not reveal p32 or another protein possibly related to ID-III. In contrast to previous suggestions, it is unlikely that p32 represents ID-III or a subunit thereof.     

Age-related changes of sodium-dependent D-[3H]aspartate and [3H]FK506 binding in rat brain

We investigated age-related changes in excitatory amino acid transport sites and FK506 binding protein (FKBP) in 3-week-, and 6-, 12-, 18- and 24-month-old Fischer 344 rat brains using receptor autoradiography. Sodium-dependent D-[3H]aspartate and [3H]FK506 were used to label excitatory amino acid transport sites and immunophilin (FKBP), respectively. In immature rats (3-week-old), sodium-dependent D-[3H]aspartate binding was lower in the frontal cortex, parietal cortex, striatum, nucleus accumbens, whole hippocampus, thalamus and cerebellum as compared to adult animals (6-month-old), whereas [3H]FK506 binding was significantly lower in only the hippocampus, thalamus and cerebellum. 3[H]FK506 binding exhibited no significant change in the brain regions examined during aging. However, sodium-dependent D-[3H]aspartate binding showed a conspicuous reduction in the substantia nigra in 18-month-old rats. Thereafter, a significant reduction in sodium-dependent D-[3H]aspartate binding was found in the thalamus, substantia nigra and cerebellum in 24-month-old rats. Other regions also showed about 10-25% reduction in sodium-dependent D-[3H]aspartate binding. The results indicate that excitatory amino acid transport sites are more susceptible to aging process than immunophilin. Further, our findings demonstrate the conspicuous differences in the developmental pattern between excitatory amino acid transport sites and immunophilin in immature rat brain.     

Opposite effects of CCK(B) agonists in grooming behaviour in rats: further evidence for two CCK(B) subsites

Opioid receptor binding properties of [3H]Tyr-D-Ala-Phe-Phe-NH2 (TAPP) were characterized in rat brain and Chinese hamster ovary (CHO) cells expressing the rat mu-receptor. In rat brain, [3H]TAPP labeled a single class of opioid sites with a dissociation constant (Kd) of 0.31 nM and maximal number of binding sites (Bmax) of 119 fmol/mg protein. In CHO-mu/1 cell membranes, the Kd and Bmax values were 0.78 nM and 1806 fmol/mg protein, respectively. Binding to rat brain was demonstrated to be pharmacologically identical to that obtained with CHO-mu/1 cell membranes and modulated by Na+ ions and guanine nucleotides. The high affinity and selectivity of [3H]TAPP together with its low non-specific binding make this radioligand a useful tool for labeling the native and cloned mu-opioid receptor.     

Characterisation of the gene encoding adenylosuccinate lyase of Plasmodium falciparum

Pregnant Wistar rats were exposed to a single 1.0 Gy dose of gamma-irradiation on gestational day 13, 15, 17 or 19. Thirty-day-old male offspring received a mechanical lesion in the left cerebral hemisphere. One, 2 or 4 days after the injury the rats were injected with [3H]thymidine and sacrificed 4 h after the injection. Thereafter, brain sections were immunostained for GFAP or S100 beta protein, subjected to autoradiography and examined microscopically to record immunopositive astrocytes labelled with [3H]thymidine. Statistically significant elevation of the reactive astrocyte proliferation was revealed on the 2nd day following injury in brains irradiated on gestational day 15. The results represent the first in vivo evidence that a low-dose prenatal gamma-irradiation can induce a long-term increase in the ability of astroglia to proliferate in response to injury.     

Metabolism of glycine in primary astroglial cells: synthesis of creatine, serine, and glutathione

The metabolism of [2-13C]glycine in astroglia-rich primary cultures obtained from brains of neonatal Wistar rats was investigated using 13C NMR spectroscopy. After a 24-h incubation of the cells in a medium containing glucose, glutamate, cysteine, and [2-13C]glycine, cell extracts and incubation media were analyzed for 13C-labeled compounds. Labeled creatine, serine, and glutathione were identified in the cell extracts. If arginine and methionine were present during the incubation with [2-13C]glycine, the amount of de novo synthesized [2-13C]creatine was two-fold increased, and in addition, 13C-labeled guanidinoacetate was found in cell extracts and in the media after 24 h of incubation. A major part of the [2-13C]glycine was utilized for the synthesis of glutathione in astroglial cells. 13C-labeled glutathione was found in the cell extracts as well as in the incubation medium. The presence of newly synthesized [2-13C] serine, [3-13C]serine, and [2,3-13C]serine in the cell extracts and the incubation medium proves the capability of astroglial cells to synthesize serine out of glycine and to release serine. Therefore, astroglial cells are able to utilize glycine as a precursor for the synthesis of creatine and serine. This proves that at least one cell type of the brain is able to synthesize creatine. In addition, guanidinoacetate, the intermediate of creatine synthesis, is released by astrocytes and may be used for creatine synthesis by other cells, i.e., neurons.     

Decreases in peripheral-type benzodiazepine receptors in postmortem brains of chronic schizophrenics

We measured the peripheral-type benzodiazepine receptors (PBRs), a marker of gliosis, in 26 brain areas (cerebral cortex, thalamus and extrapyramidal system) of the postmortem brains of 13 chronic schizophrenics and 10 controls, using [3H] PK 11195 as a ligand for the receptor assay. The specific [3H] PK 11195 binding was significantly decreased in three brain areas (superior parietal cortex, primary visual area and putamen) of schizophrenics, although there were no changes in the binding in the other brain areas. Scatchard analysis revealed that there were decreases in both the Bmax and Kd of [3H] PK 11195 binding in the brain areas. These results were almost in accordance with a number of neuropathological studies reporting that there was no change or reduction in glial cells in the brain regions of schizophrenics and suggested that the decreased density of PBRs in the brain may be involved in the pathophysiology of schizophrenia, associated with reduced production of neurosteroids coupled to PBRs.     

Encoding of Geometric and Featural Spatial Information by Goldfish (Carassius auratus).

Goldfish (Carassius auratus) were trained in different place-finding tasks as a means of analyzing their ability to encode the geometric and the featural properties of the environment. Results showed that goldfish could encode and use both geometric and featural information to navigate. Goldfish trained in a maplike, or relational, procedure encoded both types of information in a single representation. In contrast, fish trained in a directly cued procedure developed 2 independent and competing strategies. These results suggest that the geometric properties of the spatial arrangement and discrete landmarks are sensitive to encoding in a maplike or relational system, whereas different sources of spatial information are encoded in a single and flexible representation of the environment. (PsycINFO Database Record (c) 2010 APA, all rights reserved)