SEARCH · PubMed Health

Results for “VALERIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 325 records · Page 18Linked to original sources

PubMed2002

A rapid selective extraction procedure for the outer membrane protein (OmpF) from Escherichia coli.

Porins are essential pore-forming proteins found in the outer membrane of several gram-negative bacteria. Investigating the relationships between molecular structure and function involves an extremely time-consuming and labor-intensive purification procedure. We report a method for rapid extraction of the outer membrane protein, OmpF, from freeze-dried Escherichia coli cells using valeric acid, alleviating the effort and time in sample preparation. Extraction results in a highly enriched fraction containing OmpF as 76% of the total protein content. The apparent molecular mass determined by SDS-PAGE mobility was 38,900, similar to that of the monomeric form of OmpF. N-terminal sequencing yielded 23 amino acids with 100% identity to the published OmpF sequence. The trimeric form of OmpF was observed in unheated samples run on SDS-PAGE and analysis of these samples by periodic acid/silver staining revealed the presence of unbound lipopolysaccharides. Furthermore, this method should prove useful for isolating other outer membrane proteins.

Amino Acid Sequence↗

PubMed1986

The role of the anterior intralaminar nuclei and N-methyl D-aspartate receptors in the generation of spontaneous bursts in rat neocortical neurones.

The nature of spontaneous unitary activity of rat neocortex was investigated during slow wave sleep and urethane anaesthesia. Neurones in layer IV and V locations fired in a burst-pause pattern at a low burst repetition rate (0.5-4 per second) during both stage 3/4 sleep and urethane anaesthesia. Occasionally an alternative mode of firing (spindle clusters), associated with focal spindle wave activity, was also found to occur in both states. Using dual microelectrode implants it was found that the onset times of bursts (but not spindle clusters), coincided in the same and opposing cortices, whether in functionally similar or disparate areas. The highest probability was that burst onsets occurred simultaneously (resolution = 2.56 ms, interquartile range = 40 ms). Spontaneous unitary activity was investigated in the thalamus for temporal correlation with spontaneous unitary activity in neocortex under urethane anaesthesia. Neurones of the anterior intralaminar group (aIL) consistently fired in a burst-pause pattern such that each aIL burst showed a strong tendency to precede a cortical burst. Unilateral electrical stimulation of the aIL nuclei evoked widespread bilateral entrainment of cortical bursts. In contrast stimulation of VPl, or cutaneous sites, evoked only short duration spike responses together with burst abolition in the appropriate restricted Sml area. Ionophoresis of NMDA (N-Methyl D-Aspartate) onto Sm1 neurones increased the probability of cortical burst responses to aIL stimulation in addition to decreasing the latency by 20-40 ms (n = 11). Ionophoresis of 2APV (2-amino 5-phosphono valeric acid) caused simultaneous abolition of spontaneous cortical bursts and bursts evoked by aIL stimulation. Short latency responses to cutaneous and VPl stimulation were unaffected by ionophoresis of 2APV sufficient to cause burst elimination, suggesting that this pathway does not operate via a 2APV sensitive receptor mechanism. Anatomical features of the aIL nuclei and their overall cortical projection pattern are discussed in relationship to these findings. The activation of cortical NMDA/APV sensitive receptors by aIL afferents in the "spontaneous" generation of bursts in cortical cells is discussed.

Action Potentials↗

PubMed1981

The coordinating properties of d-biotin.

The coenzyme d-biotin offers in its anionic form to metal ions 3 possible binding sites: the carboxylate group of the valerate side chain, the ureido residue of the 2-imidazolidone ring, and the thioether sulfur of the tetrahydrothiophene ring; the coordinating properties of these groups are summarized and compared. Hydrogen bond formation of the ureido group has also been observed, and hydrogen bonding may possibly be important in biotin-bicarbonate recognition. The aliphatic part of the valeric acid side chain can undergo hydrophobic interactions. Such interactions and/or the stereoselective sulfur-metal ion coordination could be the means for a correct 'fixation' of the biotinyl moiety at the surface of a protein, thus creating the active enzyme-substrate complex.

Binding Sites↗

PubMed2006

Production of polyhydroxyalkanoates from methanol by a new methylotrophic bacterium Methylobacterium sp. GW2.

A new bacterial strain, isolated from groundwater contaminated with explosives, was characterized as a pink-pigmented facultative methylotroph, affiliated to the genus Methylobacterium. The bacterial isolate designated as strain GW2 was found capable of producing the homopolymer poly-3-hydroxybutyrate (PHB) from various carbon sources such as methanol, ethanol, and succinate. Methanol acted as the best substrate for the production of PHB reaching 40 % w/w dry biomass. PHB accumulation was observed to be a growth-associated process, so that there was no need for two-step fermentation. Optimal growth occurred at 0.5 % (v/v) methanol concentration, and growth was strongly inhibited at alpha concentration above 2 % (v/v). Methylobacterium sp. strain GW2 was also able to accumulate the copolyester poly-3-hydroxybutyrate-poly-3-hydroxyvalerate (PHB/HV) when valeric acid was supplied as an auxiliary carbon source to methanol. After 66 h, a copolymer content of 30 % (w/w) was achieved with a PHB to PHV ratio of 1:2. Biopolymers produced by strain GW2 had an average molecular weight ranging from 229,350 to 233,050 Da for homopolymer PHB and from 362,430 to 411,300 Da for the copolymer PHB/HV.

Biopolymers↗

PubMed1984

Induction of phencyclidine metabolism by phencyclidine, ketamine, ethanol, phenobarbital and isosafrole.

The in vitro metabolism of phencyclidine (PCP) was investigated in 9000 g supernatant fractions of both control and PCP-, ketamine-, ethanol-, phenobarbital- or isosafrole-pretreated rats. Levels of PCP, trans-4-phenyl-4-piperidinocyclohexanol (I), 1-(1-phenylcyclohexyl)-4-hydroxypiperidine (II), N-(5-hydroxypentyl)-1-phenylcyclohexylamine (IX), and 5-(1-phenylcyclohexylamino)-valeric acid (X) were monitored by gas chromatographic analysis in all cases. The inhibition of metabolism by N2, CO, SKF-525A or 2,4-dichloro-6-phenylphenoxyethylamine (DPEA), or deletion of NADPH or protein, implied the involvement of cytochrome P-450 in the reactions. The various inducing agents affected the metabolism of PCP in different ways, implying that at least several isozymes of cytochrome P-450 were involved in the total metabolism. The majority of the consumed PCP was not accounted for by the measured metabolites so that some other metabolic pathways of major quantitative importance must be operative.

Animals↗

PubMed1993

Extracellular potassium, glial and neuronal potentials in the solitary complex of rat brainstem slices.

Extracellular K+ activities (aKe) and neuronal and glial membrane potentials were recorded in the nucleus tractus solitarius (NTS) and in the dorsal vagal motor nucleus (DVMN) of rat brainstem slices after orthodromic stimulation of the tractus solitarius (TS). In glial cells, repetitive stimulation of the TS induced depolarizations of up to 30 mV followed by repolarizations which were fitted by exponential curves with a time constant of 1.6-5 s. Similar stimulations induced elevations of aKe of up to 8 mM, the recovery of which was fitted by single exponential curves with a time constant ranging between 1.6 and 4 s. These elevations in aKe were reduced by 75% during blockage of synaptic transmission in low Ca2+, high Mg2+ solution, and by 24% with application of 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX, 50 microM). Perfusion with a low Mg2+ solution increased the aKe response to stimulation of the TS, an effect that was reduced by the addition of 2-amino-5-phosphono-valeric acid (AP7, 50 microM) to the bath. No significant change in aKe and glial potential was seen when superfusing high concentrations of the C-terminal octapeptide of cholecystokinin (CCK8, 1-5 microM) and C-terminal tetrapeptide (CCK4, 50-100 microM). The effect of TS stimulations on solitary complex neurons suggests that extracellular K+ concentration is increased during synaptic activation of non-NMDA or NMDA ionotropic receptors. Conversely, slow depolarizations elicited by repetitive afferent activity or excitation by CCK agonists develop in neurons in the absence of measurable extracellular K+ fluctuations or glial depolarization.

Animals↗

PubMed1986

Uterine arginase inhibition affect the rat embryonic development.

The presence of polyamines (putrescine, spermidine and spermine) and the enzymatic activity of extrahepatic arginase (E.C. 3.5.3.1) which catalizes the hydrolysis of L-arginine into L-ornithine and urea have been related with cellular growth and development in several tissues. The enzymatic activity of arginase in rat implantation sites and its participation in reproductive process is demonstrated. Long-Evans adult rats during the 4th or 5th days of pregnancy were utilized. Arginase activity is higher in non-decidualized tissue (86.1 +/- 33 nmoles of urea/mg protein/min-1) when was compared with implantation sites (61.7 +/- 17). Intrauterine administration of several concentrations of a new synthetic L-ornithine analogue, AIAVA (2-amine-5-iodoacetamide valeric acid), produced embryonic growth arrest concomitant with arginase inhibition but not ornithine decarboxylase. From our results it is possible to stress the metabolic importance of uterine arginase in reproductive process.

Animals↗

PubMed1991

Riluzole prevents hyperexcitability produced by the mast cell degranulating peptide and dendrotoxin I in the rat.

Using electroencephalographic (EEG) recordings in freely moving rats and extracellular neuronal firing-rate recordings in hippocampal slices, we examined the effects of riluzole (RP 54274), a compound with anti-glutamate properties, against the convulsive seizures and the cellular hyperexcitability produced by the mast-cell degranulating peptide (MCD), dendrotoxin I (DTXi) and 4-aminopyridine (4-AP). I.c.v. administration of riluzole (10 nmol) prevented the seizures induced by MCD, and to a lesser extent those due to DIXi, whilst leaving 4-AP seizures unaffected. This effect was also present after oral administration of the compound (4 mg kg-1) and lasted for approximately 6 h. Electrophysiological recordings in vitro confirmed that riluzole dose dependently and reversibly abolished the sustained increase in firing rate induced by both MCD and DTXi in the hippocampus. These results indicate that the anti-epileptic spectrum of riluzole in this model has similarities with, but is not identical to, that of classical potassium channel openers, and differs from that of calcium channel blockers or other glutamate antagonists such as D(-)-2-amino-5-phosphono-valeric acid. However, since MCD releases glutamate, the preventive effect of riluzole in this model may involve direct or indirect interaction with glutamatergic processes.

4-Aminopyridine↗

PubMed1991

Effects of chlordiazepoxide and putative anxiogenics on conditioned suppression in rats.

This paper reports two experiments. In Experiment 1, the effects of chlordiazepoxide alone and in combination with a series of putative antagonists at various sites on the GABA/benzodiazepine receptor complex on conditioned suppression of operant behavior in rats were assessed. Response rates during presentation of a stimulus associated with shock (CS responding) and when only positive reinforcement is effective (pre-CS responding) were analysed. Chlordiazepoxide (10 mg/kg) significantly increased CS responding. This effect was significantly antagonised by Ro15-1788 (10 mg/kg) and by picrotoxin (1.5 mg/kg), but not by bicuculline (1.5 mg/kg) or by delta-amino-n-valeric acid (10 or 20 mg/kg). Chlordiazepoxide also significantly, albeit more slightly, increased pre-CS responding and none of the other drugs tested significantly antagonised this action, though Ro15-1788 plus chlordiazepoxide resulted in pre-CS response rates not significantly different from either chlordiazepoxide alone or control. These interactions are discussed in the context of the proposed GABA/benzodiazepine receptor complex with the conclusion that drug effects at the benzodiazepine- and picrotoxin-sensitive channel sites have an important role in mediating anxiolytic action. However, behavioral evidence of an important role for GABAa or GABAb receptors remains very limited. The second experiment studied the intrinsic actions of bicuculline, picrotoxin, and Ro15-1788 on conditioned suppression. Responding during a conditioned stimulus associated with a mild (0.125 to 0.15 mA) electric shock (CS responding) and a control rate of responding (pre-CS responding) were recorded. Bicuculline (1.5 mg/kg) and Ro15-1788 (10 mg/kg) did not significantly affect either response rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

PubMed1992

ONO-4057, a novel, orally active leukotriene B4 antagonist: effects on LTB4-induced neutrophil functions.

ONO-4057(5-[2-(2-Carboxyethyl)-3-[6-(4-methoxyphenyl)-5E- hexenyl]oxyphenoxy]valeric acid), an orally active leukotriene B4(LTB4) antagonist, displaced the binding of [3H] LTB4 to the LTB4 receptor in human neutrophil (Ki = 3.7 +/- 0.9 nM). ONO-4057 inhibited the LTB4-induced rise in cytosolic free calcium (the concentration causing 50% inhibition (IC50) = 0.7 +/- 0.3 microM) and inhibited human neutrophil aggregation, chemotaxis or degranulation induced by LTB4 (IC50 = 3.0 +/- 0.1, 0.9 +/- 0.1 and 1.6 +/- 0.1 microM) without showing any agonist activity at concentration up to 30 microM. ONO-4057 did not inhibit fMLP or C5a-induced neutrophil activation at concentrations up to 30 microM. In the in vivo study, ONO-4057 given orally, prevented LTB4-induced transient neutropenia or intradermal neutrophil migration in guinea pig (the dose causing 50% efficacy (ED50) = 25.6mg/kg or 5.3mg/kg). Furthermore, ONO-4057 given topically, suppressed phorbol-12-myristate-13-acetate (PMA)-induced neutrophil infiltration in guinea pig ear (the effective dose = 1 mg/ear). These results indicate that ONO-4057 is a selective and orally active LTB4 antagonist and may be a potential candidate for the treatment of various inflammatory diseases.

Animals↗

PubMed1986

Comparison of anticonvulsant effect of pentobarbital and phenobarbital against seizures induced by maximal electroshock and picrotoxin in rats.

Pentobarbital and phenobarbital exhibited anticonvulsant effect against maximal electroshock (MES) and picrotoxin-induced seizures in rats. Bicuculline, a GABAA receptor antagonist, reversed the anticonvulsant effect of pentobarbital, but not of phenobarbital, at a dose having no effect per se. Although picrotoxin (2 mg/kg, IP) potentiated MES seizures, it did not reverse the anticonvulsant effect due to either pentobarbital or phenobarbital. GABAB receptor antagonists such as delta-amino-n-valeric acid and homotaurine failed to modify the anticonvulsant effect due to pentobarbital or phenobarbital. Furthermore, GABAA agonist muscimol but not baclofen, a GABAB receptor agonist, exhibited the anticonvulsant effect against MES-induced seizures. However, baclofen when combined with sub-effective dose of pentobarbital or phenobarbital offered protection against MES seizures. Pentobarbital and phenobarbital were effective in almost equivalent doses against MES, as well as against picrotoxin-induced seizures. These observations indicated that pentobarbital exhibits anticonvulsant effect against MES seizures through the involvement of GABAA receptors, and activation of GABAB receptors alone does not seem to play any significant role in MES seizures and in the anticonvulsant effect of pentobarbital. However, activation of GABAB receptor does potentiate the facilitatory effect of barbiturates on GABAAergic transmission and in their anti-MES effect. Moreover, these results also suggest that the anticonvulsant effect of barbiturates against MES-seizures may involve other mechanisms in addition to GABAAergic transmission.

Amino Acids↗

PubMed1990

Effects of agonists and antagonists at the GABA/benzodiazepine receptor on conditioned suppression in rats.

Certain drugs generally regarded as GABA agonists, such as valproate and combinations of muscimol and baclofen, have been reported to produce apparent anxiolytic effects in various animal behavioral tests. The present paper reports two experiments on the effects of these agents on conditioned suppression in rats. In the first study, muscimol (0, 1.25 micrograms/kg or 1 mg/kg), baclofen (0, 1 mg/kg) and combinations of these treatments failed to alleviate conditioned suppression. Experiment Two showed that valproate (200 mg/kg) did attenuate conditioned suppression, and that its effects were antagonised by picrotoxin (1.5 mg/kg), but not by bicuculline (1.5 mg/kg), Ro 15-1788 (10 mg/kg) or by delta-amino-n-valeric acid (10 mg/kg). The findings are discussed in the context of the proposed GABA/benzodiazepine receptor complex, with the conclusion that there is little evidence for a mediating role of GABAa or GABAb receptors in such drug actions, and that the site of valproate action is probably the chloride ion channel associated with the receptor complex.

Animals↗

PubMed1991

An investigation of the involvement of GABA in certain pharmacological effects of delta-9-tetrahydrocannabinol.

Experiments were performed with mice to determine whether doses of the benzodiazepine, flurazepam, or the GABA uptake inhibitor, NO-328, known to potentiate catalepsy induced by delta-9-tetrahydrocannabinol (THC), would also interact synergistically with THC in the production of certain other effects. No synergism was detected either in the production of antinociception (tail flick test) or in a test in which the ability of flurazepam to delay onset of clonic convulsions induced by intravenous infusion of pentylenetetrazole was compared in the presence and absence of THC or cannabidiol. The hypothermic effect of THC was unaffected by NO-328 but enhanced by flurazepam, albeit only at doses higher than those needed to potentiate THC-induced catalepsy. In vitro experiments with guinea pig ileum showed that the ability of THC to inhibit electrically evoked contractions was unaffected by delta-amino-n-valeric acid, a GABA(B) receptor antagonist, and that preparations rendered tolerant to GABA responded normally to THC. Contractions induced by GABA in unstimulated ileal longitudinal muscle were attenuated by THC. We conclude that there is little evidence from our data that any of the THC effects studied were GABA mediated.

Amino Acids↗

PubMed1992

Direct evidence for mediation of an anticonflict effect of baclofen by GABAb receptors.

The present article reports an experiment on the effects of baclofen (0, 0.5, 1.0, and 2.0 mg/kg) on punished drinking in rats and the modification of these by delta-amino-n-valeric acid (DANVA) (0 and 10.0 mg/kg). Baclofen significantly enhanced punished drinking and this increase was abolished by DANVA, which had no intrinsic anxiogenic activity. It is concluded that GABAb receptors probably mediate this effect of baclofen and that such receptors may be a potential site of anxiolytic drug action.

Amino Acids↗

PubMed1991

Accumulation of a poly(hydroxyalkanoate) copolymer containing primarily 3-hydroxyvalerate from simple carbohydrate substrates by Rhodococcus sp. NCIMB 40126.

A number of taxonomically-related bacteria have been identified which accumulate poly(hydroxyalkanoate) (PHA) copolymers containing primarily 3-hydroxyvalerate (3HV) monomer units from a range of unrelated single carbon sources. One of these, Rhodococcus sp. NCIMB 40126, was further investigated and shown to produce a copolymer containing 75 mol% 3HV and 25 mol% 3-hydroxybutyrate (3HB) from glucose as sole carbon source. Polyesters containing both 3HV and 3HB monomer units, together with 4-hydroxybutyrate (4HB), 5-hydroxyvalerate (5HV) or 3-hydroxyhexanoate (3HHx), were also produced by this organism from certain accumulation substrates. With valeric acid as substrate, almost pure (99 mol% 3HV) poly(3-hydroxyvalerate) was produced. N.m.r. analysis confirmed the composition of these polyesters. The thermal properties and molecular weight of the copolymer produced from glucose were comparable to those of PHB produced by Alcaligenes eutrophus.

Glucose↗

PubMed1990

N-methyl-D-aspartate, kainate and quisqualate release endogenous adenosine from rat cortical slices.

N-Methyl-D-aspartate, kainate, and quisqualate released endogenous adenosine from superfused slices of rat parietal cortex. N-Methyl-D-aspartate-evoked adenosine release was blocked by D,L-2-amino-5-phosphono-valeric acid and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801), indicating that it was receptor-mediated, although it did not show the expected potentiation in the absence of Mg2+. In contrast, N-methyl-D-aspartate-evoked release of [3H]noradrenaline from the same slices was markedly potentiated in Mg2(+)-free medium. Therefore, the lack of Mg2+ modulation of N-methyl-D-aspartate-evoked adenosine release was not due to depolarization-induced alleviation of the Mg2+ block in the slices. Kainate-evoked adenosine release was diminished by the non-specific excitatory amino acid antagonist, gamma-D-glutamyl-glycine, and kainate- and quisqualate-evoked adenosine release was diminished by 6,7-dinitroquinoxaline-2,3-dione, indicating that these agonists release adenosine by acting at non-N-methyl-D-aspartate receptors. Tetrodotoxin decreased N-methyl-D-aspartate- and kainate-evoked adenosine release by 40% and 19% respectively, indicating that release was mediated in part by propagated action potentials in the slices. Total release of adenosine by N-methyl-D-aspartate, kainate or quisqualate was not diminished in the absence of Ca2+. A second exposure to kainate following restoration of Ca2+ to slices previously depolarized in the absence of Ca2+ resulted in an amount of adenosine release equal to an initial release by slices in the presence of Ca2+, a result suggesting the presence of separate Ca2(+)-dependent and Ca2(+)-independent pools of adenosine. The present experiments demonstrate that activation of all three major subtypes of excitatory amino acid receptors in the cortex releases adenosine, possibly from separate Ca2(+)-dependent and -independent pools. Adenosine released from the cortex following excitatory amino acid stimulation may, by acting at inhibitory P1 purinoceptors, diminish excitatory neurotransmission and protect against excitotoxicity.

2-Amino-5-phosphonovalerate↗

PubMedDate not supplied

Induction of delayed synchronized bursts in hippocampal slices by weak sine-wave stimulation; role of the NMDA receptor.

Weak (20-50 microA) sine-wave stimulation at 60 Hz (SWS) of either the mossy fibers or the Schaffer collaterals promoted epileptiform synchronized bursts in the CA2/3 area of rat hippocampal slices in the absence of epileptogenic agents. Following brief SWSs (2-10 sec every 5 min), delayed synchronized bursts (DSBs) were triggered by weak test pulses in either pathway and transmitted to CA1. The long (2-10 sec) refractory periods which followed synchronized bursts in CA2/3 limited their rate of occurrence. Furthermore, SWS decreased the activity for several minutes in slices that exhibited frequent bursts. DSBs were reversibly blocked by perfusion with the N-methyl-D-aspartate (NMDA) specific antagonist DL-2-amino-5-phosphono-valeric acid (APV). The involvement of NMDA receptors was further suggested by the facilitation of CA2/3 synchronized bursts in medium with NMDA (5 microM) or lacking magnesium, and by iontophoresis of NMDA in the CA2/3 stratum radiatum. The findings that SWS-induced DSBs persisted for hours in undisturbed slices, and that bursts abolished by APV reappeared during washout in control solution, suggest long-term changes in the CA2/3 synaptic region.

2-Amino-5-phosphonovalerate↗

PubMed1991

Transition from normal to epileptiform activity in kindled rat hippocampal slices.

We previously demonstrated kindling of synchronized bursts (ISs) by repeated sine-wave stimulation (SW: 2-5 sec, 60 Hz, 20-50 microA, every 5 min) in the CA2/3 area of rat hippocampal slices. Here we report the behavior of individual CA2/3 neurons during the kindling procedure. Intra- and extracellular recordings were obtained concurrently before, during and following SW. Test pulses and SWs were applied in CA2/3 or CA1 stratum radiatum. Neuronal response to to intracellular stimulation was tested by 100 msec depolarizing dc pulses or by 2-20 sec sinusoidal currents. The role of the N-methyl-D-aspartate (NMDA) receptor in the transition from normal responses to ISs was assessed by perfusing the slices with a specific antogonist (DL-2-amino-5-phosphono-valeric acid, APV, 50-200 microM). Our results show that kindling of ISs occurred in two steps: (1) via NMDA-dependent depolarizations during SW, or during SW-induced afterdischarges, and (2) through the recruitment of secondary, late EPSPs (1EPSPs), between consecutive SWs. ISs developed from the 1EPSPs, while the early responses (action potentials, EPSPs, and population spikes) remained unchanged. Kindling of ISs occurred with no changes in resting membrane potential, membrane resistance, or threshold of action potentials. APV did not block kindled ISs, but considerably reduced their amplitude and duration, and increased their frequency. These latter findings suggest that APV-insensitive mechanisms, activated through NMDA-dependent processes, were responsible for the triggering of ISs, and that NMDA receptor systems participated in the control of their rate of occurrence.

2-Amino-5-phosphonovalerate↗