Effect of different labio-lingual spaces in tray designs on the displacement of and pressure against a mobile tooth.

The present study aimed to examine the effect of custom tray designs on the displacement of mobile tooth and local impression pressures during the impression procedure, using partially edentulous simulation models with six anterior teeth containing a mobile tooth prepared in previous studies. The custom trays were designed by altering the thickness of the respective spaces on the labial and lingual sides of the remaining tooth arch. In previous studies, the mobile tooth was displaced in the labial direction and local impression pressures of the mobile tooth were greater against the lingual side than the labial side for all custom tray designs. Furthermore, the custom trays perforated with holes on the lingual side were effective to reduce mobile tooth displacement, labial and lingual impression pressures against the mobile tooth, and the differences between them. Therefore, the present study was performed focusing on the labial and lingual thickness of spaces in custom tray designs. It was found that mobile tooth displacement, labial and lingual impression pressures against the mobile teeth and their differences were less in trays with spaces>3.0 mm thick on both the labial and lingual sides, but markedly greater in trays with a 1.5 mm-thick space on the labial side. These results indicate that the thickness of spaces on the labial side in the tray should not be reduced to prevent mobile tooth displacement.

Impression pressures against teeth in a partially edentulous model with a mobile tooth: influence of impression tray design.

The purpose of the present study was to examine the effect of custom tray designs on local pressures against teeth during the impression procedure. In a previous study, a partially edentulous simulation model with a mobile tooth was used, and the effect of custom tray designs on the displacement of the mobile tooth was examined during the impression procedure. Based on that study's results, we have assumed that the differences in impression pressures between the labial and the lingual sides of a mobile tooth could either cause or affect displacement. The present study was undertaken to determine the local impression pressures against each side of three anterior teeth, including one mobile tooth, using the same simulation model and the same custom trays as in the previous study. It was found that the local pressures exerted against teeth during the impression procedure were affected by the custom tray designs and varied according to the coronal shape, axis inclination and location of the teeth.

[The correlation between concentrations of anticonvulsive drugs in the brain and various parameters of maximal electroshock seizures in mice].

The relationship between concentrations of anticonvulsive drugs in the brain and various parameters of maximal electroshock seizures was investigated in mice. Maximal electroshock seizures were elicited with a current intensity (60 Hz, 50 mA for 0.2 sec) through corneal electrodes. Convulsive movements were detected by an accelerometer, amplified and recorded by a polygraph. Concentrations of anticonvulsive drugs in the whole brain were determined by the method of enzyme immunoassay. With various doses of phenobarbital (PB: 5-35 mg/kg, i.p.), duration of tonic flexion (TF) was prolonged, whereas duration of tonic extension (TE) and clonic convulsion (CL) was shortened in a dose-dependent manner. The correlation coefficient between the PB concentration and the duration of TF, TE or CL was 0.680, -0.882 or 0.409, respectively. The correlation coefficient between the PB concentration and the intensity of TE or CL, measured by the integrated curve of the accelerometer, was -0.847 or 0.440. The correlation coefficient between the PB concentration and the ratio of TE-duration/TF-duration (TE/TF ratio) was -0.901. After administration of phenytoin (PNT), carbamazepine (CBZ) or valproic acid (VPA), a highly negative correlation between the drug level in the brain and the TE/TF ratio was also obtained. In the case of diazepam, clonazepam, ethosuximide or trimethadione, the TE/TF ratio was decreased dose-dependently, but the slope of the dose-response regression line was less steep than that obtained by the administration of PB, PNT, CBZ, VPA or primidone. These results suggest that the TE/TF ratio may be the most reliable parameter for drug evaluation of the anticonvulsive efficacy against tonic-clonic seizures in human patients.

Modification of the antiepileptic actions of phenobarbital and phenytoin by the taurine transport inhibitor, guanidinoethane sulfonate.

We investigated whether chronic administration of guanidinoethane sulfonate, an inhibitor of taurine uptake, could modify the antiepileptic actions of phenobarbital and phenytoin on maximal electroshock seizures in mice. Treatment with 1% guanidinoethane sulfonate decreased the taurine concentration in the brain to 76% of the control value. Under these conditions, neither the severity of tonic convulsions of maximal electroshock seizures nor the threshold for tonic extension caused by electroshock was altered. However, treatment with guanidinoethane sulfonate lessened the antiepileptic actions of phenobarbital and phenytoin on electroshock seizures. The brain concentrations of phenobarbital and phenytoin were unaltered by administration of guanidinoethane sulfonate. The brain concentrations of guanidinoethane sulfonate and total guanidino compounds were unchanged by the injection of either phenobarbital or phenytoin. It is suggested that the observed loss of anticonvulsive potency of phenobarbital and phenytoin may have been related to the decrease in taurine concentration produced by guanidinoethane sulfonate.

Reduced taurine contents and modification of anticonvulsive effects of phenobarbital and phenytoin by guanidinoethane sulfonate in mice.

In the present study, we investigated whether administration of guanidinoethane sulfonate, and inhibitor of taurine uptake, worsens electroshock-induced convulsions or modifies the antiepileptic actions of phenobarbital or phenytoin against maximal electroshock seizures in mice. Treatment with 1% guanidinoethane sulfonate in drinking water for 9 days decreased taurine concentration in the brain to 76% of control value. Under these conditions, neither the severity of tonic convulsions of maximal electroshock seizures nor the threshold for tonic extension caused by electroshock was altered. On the other hand, the antiepileptic potency of phenobarbital and phenytoin against tonic convulsions of maximal electroshock seizures in mice was significantly lessened by chronic administration of guanidinoethane sulfonate. This decrease in potency was not due to an alteration in pharmacokinetics, as the brain levels of these drugs were unchanged. Furthermore, administration of the anticonvulsive drugs did not change brain concentrations of guanidinoethane sulfonate and total guanidino compounds. It is suggested that the observed loss of anticonvulsive potency of phenobarbital and phenytoin may be related to the decreased concentration of taurine produced by administration of guanidinoethane sulfonate.

Phenytoin potentiates methamphetamine-induced behavior in mice.

We demonstrated that stereotyped behavior and tremor induced by methamphetamine (MA) were potentiated by pretreatment with phenytoin (PNT) in mice. Similar enhancing effects were obtained by pretreatment with carbamazepine. Gas chromatographic study demonstrated that pretreatment with PNT increased MA concentrations in the brain to approximately 2.5 times of control level. The increased MA concentrations were thought to be a major factor for the observed potentiation of MA-induced behavior by PNT. However, all MA-induced behavior were not equally potentiated; tremor was enhanced more than stereotypy. These results suggest that central neuronal mechanisms may also be involved in PNT-potentiated MA-induced behavior in mice.