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At least 469 records · Page 26Linked to original sources
PubMed1986

Facilitation of recurrent inhibition in rat hippocampus by barbiturate and related nonbarbiturate depressant drugs.

The effects of anticonvulsant, anesthetic and convulsant barbiturates and of related depressant drugs were characterized on excitatory and inhibitory synaptic transmission in slices of rat hippocampus. The duration of recurrent GABAergic inhibition was increased by all of the drugs tested, including the convulsant barbiturate 5-ethyl-5-[1,3-dimethylbutyl]barbituric acid, anesthetic barbiturates such as pentobarbital and nonbarbiturate anesthetics such as (+)-etomidate. Several barbiturates, including phenobarbital and (+)-mephobarbital facilitated inhibition, but the maximal responses to these agents were significantly less than with pentobarbital. In general, there was a good correspondence between the potencies of these drugs in facilitating inhibition and their previously reported abilities to regulate binding at the gamma-aminobutyric acid/benzodiazepine/barbiturate receptor complex. In addition to facilitating recurrent GABAergic inhibition, at successively higher doses most of these drugs induced direct depression of the population spike response, field excitatory postsynaptic potential and presynaptic fiber spike. 5-Ethyl-5-[1,3-dimethylbutyl]barbituric acid, (+)-mephobarbital and pentobarbital facilitated excitatory synaptic transmission at the Schaffer collateral/commissural synapses on the CA1 pyramidal neurons at low doses, but caused depression at higher doses. The net effects observed with each drug tested (facilitation/depression of excitatory transmission, enhancement of GABAergic inhibition) correlated well with the behavioral effects of these agents in vivo.

Animals↗
PubMed1988

Differing actions of convulsant and nonconvulsant barbiturates: an electrophysiological study in the isolated spinal cord of the rat.

The effects of various pairs of convulsant and nonconvulsant barbiturates on mono- and polysynaptic activity were studied in the isolated spinal cord of the immature rat, using extracellular recording. The convulsant barbiturates, 5-ethyl-5-(3-methylbut-2'-enyl) barbituric acid (3M2B), 5-ethyl-5-(1,3-dimethylbut-1'-enyl) barbituric acid (1,3M1B) and (+)-5-(1,3-dimethylbutyl)-5-ethyl barbituric acid [(+) DMBB] all increased the monosynaptic reflex at concentrations between 5 and 50 microM with no change in polysynaptic activity. When the concentration was raised to between 100 and 300 microM, however, the convulsants all reduced the monosynaptic reflex, thus producing a biphasic dose-response relationship. The nonconvulsant barbiturates phenobarbital, 5-ethyl-5-(3-methylbut-1'-enyl) barbituric acid (3M1B), amylobarbital (3MB) and (-)-5-(1,3-dimethylbutyl)-5-ethyl barbituric acid [(-)DMBB] produced only a decrease in mono- and polysynaptic reflexes. At concentrations which enhanced the monosynaptic reflex, the responses of motoneurones to glycine and eledoisin-related peptide (an analogue of substance P) were reduced by (+)DMBB, while 1,3M1B and 3M2B had no significant effects upon any of the neurotransmitters tested. At concentrations which depressed the monosynaptic reflex, the convulsants all reduced the response to glycine whereas the nonconvulsant barbiturates all increased the response to GABA. With the exception of phenobarbital, both convulsant and nonconvulsant barbiturates produced a direct depolarisation of the presynaptic terminal membrane, with only the convulsants producing a depolarisation of the membrane of the motoneurone. Using another convulsant barbiturate, 5-(2-cyclohexylideneethyl)-5-ethyl barbituric acid (CHEB), this direct depolarising action was found to be calcium-dependent.

Animals↗
PubMed1980

The epoxide-diol pathway in the metabolism of vinylbital in rat and man.

1. In urine of rats given vinylbital (5-vinyl-5-(1'-methylbutyl)barbituric acid) i.p., unchanged vinylbital and its devinylated metabolite, 5-(1'-methylbutyl)barbituric acid, were identified. Rats synthetic 1',2'-epoxyvinylbital excreted the same compound as a major metabolite. No unchanged epoxide, nor 1',2'-dihydroxyvinylbital, could be identified in the urine of rats treated with vinylbital or its epoxide. 2. Attempts to synthesize 1',2'-dihydroxyvinylbital from 1',2'-epoxyvinylbital by acidic hydrolysis revealed that this possible metabolite decomposes readily to 5-(1'-methylbutyl)barbituric acid by a 'retro-aldol type' reaction. 3. In rat liver microsomal preparation 1',2'-epoxyvinylbital is readily hydrated by epoxide hydratase, but this reaction is almost completely inhibited by 0.8 mM 1,1,1-trichloropropene-2,3-oxide (TCPO). This finding and the identification of 5-(1'-methylbutyl)barbituric acid as end-product of this enzyme reaction provides further evidence for the existence of an epoxide-diol pathway in the metabolism of vinylbital. 4. Vinylbital and its devinylated metabolite are excreted in 36 h urine of rats treated with vinylbital, to an extent of 0.6 +/- 1.7% of the dose (n = 5), respectively. Upon administration of 1',2-epoxyvinylbital, 59.8 +/- 14.2% of the dose (n = 5) was excreted as 5-(1'-methylbutyl)barbituric acid. 5. In 60 h urine of three human volunteers who had taken 150 mg of vinylbital orally, 2.6 +/- 1.7% of the dose was excreted as vinylbitaland 11.0 +/- 4.1% as 5-(1'-methylbutyl) barbituric acid, illustrating that also in humans the epoxide-diol pathway plays a role in the metabolism of vinylbital.

Animals↗
PubMed1990

Calcium-dependent actions of the convulsant barbiturate, CHEB, on transmitter release at the rat neuromuscular junction.

1. The effect of convulsant barbiturates on spontaneous and evoked acetylcholine release was studied at the rat neuromuscular junction in vitro. 2. The convulsant barbiturates (+)-5-(1,3-dimethylbutyl)-5-ethyl barbituric acid [(+)-DMBB], 5-(2-cyclohexylideneethyl)-5-ethyl barbituric acid (CHEB), 5-ethyl-5-(3-methylbut-2'-enyl) barbituric acid (3M2B) and 5-ethyl-5-(1,3-dimethylbut-1'-enyl) barbituric acid (1,3M1B) all produced a concentration-dependent increase in miniature end-plate potential (MEPP) frequency. 3. With CHEB (100 microM) this increase in MEPP frequency was found to be dependent on the [Ca2+]o. CHEB in 0.5 mM [Ca2+]o did not alter MEPP amplitude, but in 1.3 and 2.5 mM [Ca2+]o CHEB significantly reduced the amplitude. 4. At a [Ca2+]o of 0.5 mM, CHEB produced an increase in both EPP amplitude and quantal content, while at 1.3 mM [Ca2+]o CHEB did not alter EPP amplitude or quantal content. 5. The plot of log quantal content vs log [Ca2+]o showed a parallel shift to the left in the presence of 100 microM CHEB. This change occurred without any alteration in the maximum quantal content. This suggests that the enhancement of transmitter release may be mediated by an effect on calcium fluxes in the pre-junctional nerve terminal.

Acetylcholine↗
PubMed1980

Phenobarbital specific antibody production: preparation of 5-phenyl-5-(4-aminobutyl) barbituric acid-bovine serum albumin conjugate.

The aminobutyl derivative of phenobarbital, 5-phenyl-5-(4-aminobutyl)barbituric acid hydrochloride, was synthesized through two synthetic pathways for the preparation of immunogen in production of phenobarbital specific antibody. The produced antiserum had high titer, specificity, affinity and sensitivity (0.5ng/ml), when examined by radioimmunoassay.

Animals↗
PubMed1990

Influence of liver tumor promoters and structurally related chemicals on survival of normal adult rat hepatocytes in primary culture.

The influence of four liver tumor promoters and two structurally related chemicals (non-promoters) on survival of normal adult rat hepatocytes was examined in primary culture. Of the four promoters, butylated hydroxytoluene (BHT), dichlorodiphenyltrichloroethane (DDT), barbital sodium and phenobarbital sodium, only phenobarbital efficiently prolonged the hepatocyte survival and maintained the morphological features of the cells. Both BHT and DDT were toxic to hepatocytes within the dose ranges tested. Barbital was also ineffective for maintenance of primary cultured hepatocytes but not toxic to the cells. Of the two non-promoters, barbituric acid and amobarbital, barbituric acid also showed no maintenance effect on hepatocytes. However, amobarbital resembled phenobarbital in its effect on the maintenance of hepatocytes in primary culture. DNA synthesis of primary cultured hepatocytes was severely suppressed by phenobarbital in a dose-dependent manner. The results clearly show that the ability to support long-term survival of primary cultured hepatocytes is a common property of some barbiturates but not of liver tumor promoters, and that the maintenance of hepatocytes by phenobarbital is not due to a counterbalance of stimulated proliferation and death of the cells.

Animals↗
PubMed1975

Metabolism of quinalbarbitone.

The human metabolism of (+/-)-5-allyl-5-(1'-methylbutyl) barbituric acid (I), quinalbarbitone, taken orally, has been studied. Comparison of g.c. and g.c.-m.s. data from derivatized extracts of urine with similar data from synthetic samples confirmed the presence of the two diastereoisomeric forms of 5-allyl-5-(3'hydroxy-1'-methylbutyl)barbituric acid (II), 5-allyl-5-(3'-oxo-1'-methylbutyl)barbituric acid (III), 5-allyl-5-(1'-methyl-3'-carboxypropyl)barbituric acid (IV), and 5-(2',3'-dihydroxypropyl)-5-(1'-methylbutyl)barbituric acid (V) in the urine. There was no evidence for the urinary excretion of unchanged drug. The rate of excretion of these metabolites has been examined in some detail, and rate-limited kinetics shown to apply for excretion of the acid (IV) and the diol (V).

Chromatography, Gas↗