Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Formates”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1996

DNA adduct formation, cell proliferation and aberrant crypt focus formation induced by PhIP in male and female rat colon with relevance to carcinogenesis.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induces colon tumors in male, but not female, F344 rats. We investigated the mechanisms leading to this difference by measuring the level of PhIP-DNA adducts, the enhancement of cell proliferation and aberrant crypt focus (ACF) formation in colon mucosa. PhIP was administered in the diet at a level of 0.04% to both male and female F344 rats for 1-8 weeks. The level of DNA adducts in the colon mucosa was measured using the 32P-postlabeling method. Four major PhIP-DNA adducts were detected in fairly constant proportions in all the animals examined. The level of PhIP-DNA adducts in male and female rats was the same, indicating no direct correlation between adduct levels and carcinogenesis. Labeling indices (LIs) were determined by measuring BrdU incorporation in rats after feeding with a PhIP diet for 4, 8 and 12 weeks. After 8 weeks administration the LI had increased 1.5-fold in the colon of the male rats, but no increase was observed in the female rats. ACF formation was examined after feeding with a PhIP diet for 14 weeks. The number of aberrant crypt foci was 6.6 +/- 1.5 per rat in males and 1.9 +/- 0.5 per rat in females. Thus differences in colon tumor development in male and female rats takes place at an early stage(s). Our results suggest that, in addition to DNA adduct formation, enhanced proliferation contributes to the formation of ACFs, which are premalignant lesions of the colon.

Animals↗
PubMed1991

Cell-type specific multiprotein complex formation over the c-fos serum response element in vivo: ternary complex formation is not required for the induction of c-fos.

At the serum response element (SRE) of the c-fos proto-oncogene a ternary complex with two proteins, ternary complex factor (p62TCF) and serum response factor (SRF) can be formed. Its formation has previously been suggested to be necessary for efficient induction of c-fos transcription by serum in mouse NIH 3T3 fibroblasts (1) and by phorbol esters, but not by serum, in mouse BALB/c 3T3 fibroblasts (2). It is shown here by genomic dimethyl sulfate (DMS) footprinting that this ternary complex is indeed formed in NIH 3T3 cells in vivo. However, cells were found, murine F9 teratocarcinoma stem cells, in which the pattern of protection and hyperreactivity is consistent with the absence of p62TCF in the protein complex in vivo, although inducibility of the endogenous c-fos gene is not impaired. Both in NIH 3T3 cells and in F9 cells a mutated c-fos promoter that binds SRF but fails to form a ternary complex, was inducible by serum and phorbol esters to the same extent as the wild-type promoter. The data suggest that ternary complex formation is not an absolute prerequisite for the transient induction of c-fos. Ternary complex formation rather appears to enhance overall promoter efficiency. A cell type specific component determines the formation of the multicomponent transcription factor complex in vivo.

Animals↗
PubMed2001

Time course of vascular remodeling, formation of neointima and formation of neoadventitia after angioplasty in a porcine model.

BACKGROUND: Vascular remodeling is the major cause of restenosis after coronary balloon angioplasty but the pathophysiology of this process is not known. OBJECTIVE: To examine the time courses of vascular remodeling, formation of neointima and adventitial changes after coronary angioplasty. DESIGN: An experimental study on pigs using coronary angiography, intravascular ultrasound (IVUS), and histology. METHODS: Deep vessel-wall injury was induced by conventional balloon angioplasty in the circumflex and right coronary arteries, and by retraction of a chain-encircled balloon in the left anterior descending artery. Angiography in all three arteries and IVUS measurements in circumflex and left anterior descending arteries were performed before and after angioplasty, and at follow-up on days 0, 1, 4, 7, 14, 28, and 56 (n = 5 in each group). Serial IVUS measurements were used to determine vascular remodeling. Formation of neointima and neoadventitia was measured by histomorphometry. RESULTS: Angiographically evident loss of lumen and ultrasonographically detectable constrictive remodeling occurred between day 7 and day 28. IVUS measurements showed that late loss of lumen (days 28 and 56) was correlated to vascular remodeling but not to the increase in wall area (neointima plus media). Histomorphometry revealed that neointima was present from day 7 and that amount of neointima increased up to day 28. Area of adventitia increased during the first 4 days and remained unchanged thereafter. Adventitial neovascularization by vasa vasorum was observed from day 4 onward. CONCLUSIONS: Formation of neoadventitia precedes late loss of lumen, constrictive remodeling, and formation of neointima. The time course of vascular remodeling coincides with growth of neointima rather than with changes in the adventitia.

Angioplasty, Balloon, Coronary↗
PubMed2006

Avoiding microbubbles formation during radiofrequency left atrial ablation versus continuous microbubbles formation and standard radiofrequency ablation protocols: comparison of energy profiles and chronic lesion characteristics.

BACKGROUND: Radiofrequency (RF) energy parameters and chronic lesion characteristics associated with the microbubbles formation have not been yet fully elucidated. OBJECTIVES: The objective of this study was to compare the energy profiles and chronic lesion characteristics associated with RF ablation of the pulmonary vein antrum using three different ablation protocols: (1) avoiding microbubbles; (2) continuous microbubble formation; (3) temperature-guided ablation. METHODS: A 4-mm tip ablation catheter was used for creating RF ablation lesions in 15 adult mongrel dogs. All ablation lesions were created at the posterior aspect of the PV antrum in each animal. Avoiding microbubbles (group 1, n = 5 dogs, 23 lesions), continuous microbubble formation (group 2, n = 5 dogs, 22 lesions), and temperature-guided (group 3, n = 5 dogs, 19 lesions, target temperature 60 degrees C/power limit 50 W) ablation lesions were analyzed. RESULTS: Group 1 showed significantly lower power (19 +/- 8.6 W), lower temperature (50 +/- 4.8 degrees C), higher efficiency-of-heating index (2.9 +/- 0.8 degrees C/W), and lower impedance (109 +/- 24.4 Omega) than groups 2 (38 +/- 8.4 W; 63 +/- 10 degrees C; 1.8 +/- 0.8 degrees C/W; 148 +/- 34.4 Omega) and 3 (44 +/- 12 W; 57 +/- 2.4 degrees C; 1.4 +/- 0.5 degrees C/W; 139 +/- 23.1 Omega) (P < 0.001 vs groups 2 and 3). During ablation, no significant events were detected in group 1, but 11 cases of audible pop, 11 cases of catheter tip charring, and 1 case of fatal myocardial perforation were observed in groups 2 and 3. Transmural lesions were more frequently created in group 1. CONCLUSION: RF energy delivery applying "avoiding microbubbles" protocol seems to be associated with higher degree of safety and efficacy when compared to temperature-guided and continuous microbubble-formation ablation protocols.

Animals↗
PubMed2000

Calcium-independent receptor for alpha-latrotoxin and neurexin 1alpha [corrected] facilitate toxin-induced channel formation: evidence that channel formation results from tethering of toxin to membrane.

alpha-Latrotoxin binding to the calcium-independent receptor for alpha-latrotoxin (CIRL-1), a putative G-protein-coupled receptor, stimulates secretion from chromaffin and PC12 cells. Using patch clamp techniques and microspectrofluorimetry, we demonstrate that the interaction of alpha-latrotoxin with CIRL-1 produces a high conductance channel that permits increases in cytosolic Ca(2+). alpha-Latrotoxin interaction with CIRL-1 transiently expressed in bovine chromaffin cells produced a 400-pS channel, which rarely closed under Ca(2+)-free conditions. The major effect of overexpressing CIRL-1 was to greatly increase the sensitivity of chromaffin cells to channel formation by alpha-latrotoxin. alpha-Latrotoxin interaction with CIRL-1 transiently overexpressed in non-neuronal human embryonic kidney 293 (HEK293) cells produced channels that were nearly identical with those observed in chromaffin cells. Channel currents were reduced by millimolar Ca(2+). At alpha-latrotoxin concentrations below 500 pM, channel formation occurred many seconds after binding of toxin to CIRL-1 indicating distinct steps in channel formation. In all cases there was a rapid, sequential addition of channels once the first channel appeared. An analysis of CIRL-1 mutants indicated that channel formation in HEK293 cells is unlikely to be transduced by a G-protein-dependent mechanism. alpha-Latrotoxin interaction with a fusion construct composed of the extracellular domain of CIRL-1 anchored to the membrane by the transmembrane domain of vesicular stomatitis virus glycoprotein, and with neurexin 1alpha, an alpha-latrotoxin receptor structurally unrelated to CIRL-1, produced channels virtually identical with those observed with wild-type CIRL-1. We propose that alpha-latrotoxin receptors recruit toxin to facilitate its insertion across the membrane and that alpha-latrotoxin itself controls the conductance properties of the channels it produces.

Animals↗
PubMed1989

Receptor-mediated phagocytosis in human neutrophils is associated with increased formation of inositol phosphates and diacylglycerol. Elevation in cytosolic free calcium and formation of inositol phosphates can be dissociated from accumulation of diacylglycerol.

Phagocytosis of C3bi- or IgG-opsonized yeast particles in human neutrophils was found to be associated with an increased formation of inositol phosphates and diacylglycerol. Pertussis toxin only marginally affected phagocytosis of IgG- and C3bi-opsonized particles and the associated formation of second messengers. Forskolin, which induced a threefold rise of cellular cAMP, however, markedly inhibited both C3bi- and IgG-mediated phagocytosis as well as the particle-induced formation of inositol phosphates and diacylglycerol. These observations are in contrast to what was found to occur with chemotactic factors and indicate that chemotactic and phagocytic signaling can be regulated independently in human neutrophils. Since C3bi-mediated phagocytosis has been shown to occur at vanishingly low cytosolic free calcium levels, calcium-depleted cells were used to study the importance of the inositol cycle for the engulfment of C3bi-opsonized particles. Despite a total lack of receptor-induced formation of inositol phosphates, a significantly increased accumulation of diacylglycerol accompanied the ingestion of C3bi-opsonized particles. These data show that the engulfment of C3bi-opsonized particles can occur independently of both a calcium transient and an increased inositol phosphate production. However, the observed accumulation of diacylglycerol, not derived from phosphoinositides, suggests that this second messenger play a role in the control of the engulfment process.

Antigens, Differentiation↗
PubMed2000

Detection of p56(lck) kinase activity using scintillation proximity assay in 384-well format and imaging proximity assay in 384- and 1536-well format.

p56(lck) is a lymphocyte-specific tyrosine kinase that plays an important role in both T-cell maturation and activation. We have developed a homogeneous assay in which p56(lck) catalyzes the transfer of the gamma-phosphate group from [gamma-(33)P]ATP to a biotinylated peptide substrate. The labeled peptide is then captured on a streptavidin-coated scintillation proximity assay (SPA) bead or imaging proximity bead. The SPA is counted in a microplate scintillation counter and the imaging proximity assay is counted in a charge-coupled device-based imaging system called LEADseekertrade mark, recently launched as a homogeneous imaging system by Amersham Pharmacia Biotech. We show, via time-dependence assays and inhibitor studies, that this assay can be performed in 1536-well microplate format using imaging proximity as the method of detection. The results compare favorably with the same assay performed in 384-well microplate format using both SPA and imaging proximity as the detection methods. From this study, we conclude that a kinase assay can be performed in 384- and 1536-well format using imaging as the detection method, with significant time savings over standard scintillation counting. In addition, we show cost saving advantages of 1536- over 384-well format in terms of reagent usage, higher throughput, and waste disposal.

Amino Acid Sequence↗
PubMed2002

Morphogenetic pattern formation during ascidian notochord formation is regulative and highly robust.

The ascidian notochord forms through simultaneous invagination and convergent extension of a monolayer epithelial plate. Here we combine micromanipulation with time lapse and confocal microscopy to examine how notochord-intrinsic morphogenetic behaviors and interactions with surrounding tissues, determine these global patterns of movement. We show that notochord rudiments isolated at the 64-cell stage divide and become motile with normal timing; but, in the absence of interactions with non-notochordal tissues, they neither invaginate nor converge and extend. We find that notochord formation is robust in the sense that no particular neighboring tissue is required for notochord formation. Basal contact with either neural plate or anterior endoderm/lateral mesenchyme or posterior mesoderm are each alone sufficient to ensure that the notochord plate forms and extends a cylindrical rod. Surprisingly, the axis of convergent extension depends on the specific tissues that contact the notochord, as do other patterns of cell shape change, movement and tissue deformation that accompany notochord formation. We characterize one case in detail, namely, embryos lacking neural plates, in which a normal notochord forms but by an entirely different trajectory. Our results show ascidian notochord formation to be regulative in a fashion and to a degree never before appreciated. They suggest this regulative behavior depends on a complex interplay between morphogenetic tendencies intrinsic to the notochord plate and instructive and permissive interactions with surrounding tissues. We discuss mechanisms that could account for these data and what they imply about notochord morphogenesis and its evolution within the chordate phylum.

Animals↗
PubMed2005

What makes a good format: frameworks for evaluating the effect of graphic risk formats on consumers' risk-related behavior.

The format in which risk information is presented has a fundamental influence on the quality of risk communication with health consumers. Graphic formats might enhance the risk communication process, but we know little about how these formats affect risk-related behavior. Based on a review of literature within and outside the medical domain, we present four useful frameworks for evaluating the effects of graphic format on risk-related behavior.

Audiovisual Aids↗
PubMed1989

[Study on the uremic protein binding inhibitors as uremic toxin: toxic effect on erythroid colony formation, lymphocyte blast formation and renal function].

Certain uremic metabolites are recognized to have high affinity to serum protein and some of them have been identified as hippuric acid (HA), quinolinic acid (QA) and indoxyl sulfate (IS). Cell toxicity and effect on renal function of these substances were examined by means of erythroid colony formation, lymphocyte blast formation and isolated perfused rat kidney. These substances inhibited the binding of diphenylhydantoin to albumin, depending on the concentration of the substances. At the same concentration of 10 mg/dl, IS was most potent and QA was the second. QA and IS suppressed the erythroid colony formation, depending on the concentration of QA and IS. On the other hand, HA had no suppressive effect even at the higher concentration. The suppressive effect of QA and IS were attenuated by increasing erythropoietin concentration. QA and IS had strong suppressive effect of lymphocyte blast formation and interleukin 2 production at the concentration of uremic serum. However, they did not suppress the increase of intracellular calcium concentration of lymphocytes after stimulation by mitogen. This might indicate the possibility that these substances act not only on cell surface but on intracellular protein. HA and IS inhibited para-aminohippurate secretion and QA suppressed tubular reabsorption of sodium in isolated perfused rat kidney. These results show that the uremic protein binding inhibitors may influence renal regulation of fluid and electrolyte homeostasis. It is concluded that some of the protein binding inhibitors have toxic effects on cell function of various tissues and play a role in pathophysiology of uremia.

Animals↗
PubMed1988

Vitamin K-dependent carboxylase. Stoichiometry of vitamin K epoxide formation, gamma-carboxyglutamyl formation, and gamma-glutamyl-3H cleavage.

The rat liver microsomal vitamin K-dependent carboxylase catalyzes the carboxylation of peptide-bound glutamyl residues to gamma-carboxyglutamyl (Gla) residues with the concomitant formation of vitamin K 2,3-epoxide (KO). These studies have demonstrated that the half-reaction, formation of KO, occurs in the absence of carboxylation at low glutamyl substrate concentration but that the ratio of KO/Gla approaches unity as the glutamyl substrate concentration is increased. Utilization of the carboxylase substrate Phe-Leu-[gamma-3H] Glu-Glu-Leu has demonstrated that the ratios of KO/gamma-C-H bonds cleaved and Gla/gamma-C-H bonds cleaved are equivalent at high substrate concentrations and that these ratios approach unity. At low substrate concentrations, KO formation occurs at a higher rate than gamma-H bond cleavage. These data are consistent with a mechanism involving the formation of an oxygenated intermediate from vitamin KH2 and O2 that is converted to KO during hydrogen abstraction from the gamma-position of the Glu substrate. In the absence of a Glu substrate, the intermediate is converted to KO by a mechanism not coupled to glutamyl activation.

1-Carboxyglutamic Acid↗
PubMed1987

Interchain disulfide bond formation in types I and II procollagen. Evidence for a protein disulfide isomerase catalyzing bond formation.

The assembly of reduced pro-alpha chains of type I and type II procollagen into the native triple-helical molecule was examined in vitro in the presence and absence of pure protein disulfide isomerase. The data clearly indicates that protein disulfide isomerase is able to accelerate the formation of native interchain disulfide bonds in these procollagens. It takes about 6 min after disulfide bonding before triple-helical molecules exist, while the time required to produce triple-helical type I procollagen in the presence of protein disulfide isomerase is 9.4 min and that for type II procollagen 17.2 min. These values agree with those obtained for type I and II procollagen in vivo suggesting that protein disulfide isomerase is also an enzyme catalyzing interchain disulfide bond formation in procollagen in vivo. The formation of native disulfide bonds can proceed without any enzyme catalysis but then requires the presence of reduced and oxidized glutathione. Bonding is rather slow in such a case, however, resulting in a delay in the formation of the triple helix.

Animals↗
PubMed1981

Colony formation by bone marrow cells after incubation with neuraminidase. II. Sensitivity of erythroid progenitor cells for burst promoting activity and erythropoietin and restoration of reduced spleen colony formation in mice pretreated with desialated erythrocyte membrane fragments.

Incubation of bone marrow cells (BMC) with neuraminidase (NA) reduces their ability to form colonies in the spleen of lethally irradiated mice. In vivo the largest reduction was observed in the erythrocytic colonies, whereas in vitro an inhibiting effect of NA incubation was observed on the plating efficiency of erythrocyte precursors (CFUE and day 7 BFUE). Masking of the receptors for neuraminidase-treated cell surface determinants in the recipient's body by infection of desialated erythrocytes (NA-Ery) or erythrocyte membrane fragments (NA-Efr) did largely restore the reduced colony formation of NA-BMC with respect to both the total number of spleen colonies and their type. Pretreatment of irradiated host with NA-Ery, but with NA-Efr, led to a slight polycythemia as judged by the number of erythrocytic and undifferentiated colonies as well as by the surface colony diameter. The reduced erythrocytic colony formation of NA-BMC was considerably enhanced in anemic irradiated recipients (from 25-70% of respective controls). Under all experimental circumstances the erythrocytic colony formation of NA-BMC never exceeded that of normal BMC (N-BMC). Further, in normal or anemic recipients whether or not treated with NA-Efr, the diameters of the spleen surface colonies in NA-BMC injected animals were smaller than in recipients of control-incubated BMC. In vitro experimentation indicated that the reduced plating efficiency of CFUE and BFUE following incubation could not be attributed to a decreased sensitivity to erythropoietin. However, day 7 BFUE with deficient cell surface sialic acid residues had a decreased sensitivity to burst promoting activity. Among several other explanations, our data support the possibility that the desialated colony forming cells that give rise to erythrocytic colonies in vivo have higher requirements for early regulatory factors than granulocytic precursor cells. In contrast to the normal postirradiation situation the level of these factors could be increased in recipients, which are bled subsequently to irradiation. Evidence is presented in support of our concept that neuraminidase-treated CFU are fully capable to exhibit normal, although delayed, colony formation in vivo in animals with covered receptors for galactosyl residues.

Animals↗
PubMed1994

Amyloid fibril formation in gelsolin-derived amyloidosis. Definition of the amyloidogenic region and evidence of accelerated amyloid formation of mutant Asn-187 and Tyr-187 gelsolin peptides.

BACKGROUND: We have recently shown that the actin-modulating cytoskeletal and plasma protein gelsolin is involved in the pathogenesis of familial amyloidosis of Finnish type. To define the amyloidogenic region(s) in gelsolin and clarify the mechanisms involved in amyloid formation, we tested the amyloidogenicity of synthetic gelsolin peptide analogues. EXPERIMENTAL DESIGN: The in vitro amyloid fibril formation was studied using 22 synthetic peptides 7 to 30 residues long having sequence homology with wild-type or mutant gelsolins. Amyloid formation was monitored by Congo-red staining and polarization microscopy of the peptide aggregates, by negative staining electron microscopy, and by quantitative fluorometry with thioflavine T. RESULTS: Ultrastructurally, amyloid-like fibrils were formed from the mutant Asn-187 and Tyr-187 gelsolin peptides corresponding to the naturally occurring missense mutations found in familial gelsolin amyloidosis syndromes, as well as from a gelsolin peptide having a Val-187 substitution. The shortest peptide tested that was capable of forming amyloid-like fibrils was 9-residue mutant Asn-187 peptide. The corresponding wild-type peptide did not form amyloid. Quantitative fluorometry at the emission maximum 482 nm revealed highly accelerated amyloid fibril formation of the mutant Asn-187, Tyr-187 and Val-187 peptides as compared with the corresponding wild-type peptides. CONCLUSIONS: We have defined the amyloidogenic region of gelsolin to a 9-residue sequence in the highly conserved repetitive motif B and showed that residue 187 represents a critical site where a substitution of an amino acid with a charged side chain (Asp) with an amino acid with an uncharged (Asn) or hydrophobic side chain (Tyr, Val) creates a conformation that is highly amyloidogenic thus providing an explanation for the amyloidogenicity of the Asn-187 and Tyr-187 gelsolin variants.

Amino Acid Sequence↗
PubMed2006

Formate-reduced E. coli formate dehydrogenase H: The reinterpretation of the crystal structure suggests a new reaction mechanism.

Re-evaluation of the crystallographic data of the molybdenum-containing E. coli formate dehydrogenase H (Boyington et al. Science 275:1305-1308, 1997), reported in two redox states, reveals important structural differences for the formate-reduced form, with large implications for the reaction mechanism proposed in that work. We have re-refined the reduced structure with revised protocols and found substantial rearrangement in some parts of it. The original model is essentially correct but an important loop close to the molybdenum active site was mistraced, and, therefore, catalytic relevant residues were located in wrong positions. In particular selenocysteine-140, a ligand of molybdenum in the original work, and essential for catalysis, is no longer bound to the metal after reduction of the enzyme with formate. These results are incompatible with the originally proposed reaction mechanism. On the basis of our new interpretation, we have revised and proposed a new reaction mechanism, which reconciles the new X-ray model with previous biochemical and extended X-ray absorption fine structure data.

Crystallography, X-Ray↗
PubMed1989

Characterization of a cis regulatory DNA element necessary for formate induction of the formate dehydrogenase gene (fdhF) of Escherichia coli.

The fdhF gene, encoding the selenopolypeptide of formate dehydrogenase (FDHH), has a -12/-24 nif-type consensus promoter. A cis-acting DNA element, which is required for the regulation of the promoter by formate under anaerobic conditions, has been identified. This regulatory sequence of about 25 bp in length is located 110 bp upstream of the transcription start site. By analysing a variety of mutant constructs in this region (5' deletions, internal deletions and point mutations) we were able to identify a hexanucleotide sequence -GTCACG-, which is important for the formate regulation of the fdhF promoter. The data also indicate that this element has many of the properties characteristic of eukaryotic enhancers.

Aldehyde Oxidoreductases↗
PubMed1990

Identification and expression of the Escherichia coli fdhD and fdhE genes, which are involved in the formation of respiratory formate dehydrogenase.

The two closely linked fdhD and fdhE genes of Escherichia coli are required for the formation of active membrane-bound phenazine methosulfate-linked formate dehydrogenase (FDH-PMS). Both genes were isolated from a cosmid library. Restriction endonuclease analysis associated with Mu dII1734 insertion mutagenesis indicated that the two genes were separated by at least 4 kilobases and transcribed in opposite orientations. Initial experiments indicate that the region between the two genes seems not to be essential to FDH-PMS activity. fdhD and fdhE were expressed either in maxicells or from the T7 promoter-polymerase system. They were shown to encode proteins with approximate Mr 30,500 and 32,000, respectively. Both proteins appeared in the soluble fraction and were not recognized by an FDH-PMS-specific antiserum. Therefore, neither fdhD nor fdhE plays a structural role in the formation of FDH-PMS. Expression of a phi(fdhD-lacZ) operon fusion was decreased about threefold by aerobiosis but was indifferent to other effectors tested. It was unaffected by pfl, chlA, selA, and fnr mutations. Expression of a phi(fdhE-lacZ) operon fusion was slightly induced by nitrate. This induction, requiring the presence of functional chl and fnr alleles, was mediated via nitrate metabolism. Transcription of phi(fdhE-lacZ) fusion was fully dependent on wild-type sel alleles. This might suggest the participation of fdhE in the synthesis of the selenopolypeptide of FDH-PMS.

Cloning, Molecular↗
PubMedDate not supplied

[Correlation between bioelectrical processes of the cortex, thalamus, midbrain reticular formation during formation of a defensive conditioned reflex in rabbits].

EEG power spectra of the sensorimotor area of the neocortex, the dorsal hippocampus, midbrain reticular formation and anteroventral thalamic nucleus, as well as corresponding coherence functions and phase spectra, undergo changes during formation and performance of defensive conditioned reflex in rabbit. The conclusion is draen that in the process of conditioning a morphofunctional system of brain structures is established including the above mentioned formations. Their functional integration occurs on the basis of theta-rhythm. The execution of a conditioned act requires isorhythmicity of electrical processes within the theta-range in the studied structures and an adequate level of their excitability, which is manifested in the dominance of 6,0 c/s frequency.

Animals↗