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Notes: A pair potential for SiO2 proposed by Tsuneyuki, Tsukada, Aoki, and Matsui [Phys. Rev. Lett. 61, 869 (1988)] is used to calculate a range of lattice dynamical properties of α-quartz. The potential energy of the structure is minimized, and the phonon frequencies are calculated for the structural parameters corresponding to the energy minimum. Frequencies calculated throughout the Brillouin zone are used to construct a frequency distribution function and the harmonic contributions to the thermodynamic functions are calculated. The coefficients of thermal expansion perpendicular and parallel to the c axis are calculated in a perturbative approximation. The expansion coefficient parallel to the c axis is found to be negative at low temperatures, in agreement with experiment. The elastic, dielectric, and piezoelectric constants are also calculated.

Notes: Deep levels in PbI2 have been investigated by photoinduced current transient spectroscopy for the first time. By separating the signal processing from the data acquisition it was possible to analyze the transient using different methods, in particular a four-gate treatment which allows to clear the detrapping current of uncontrolled changes of the recombination lifetime of thermally released carriers. Three hole traps located at 0.30, 0.47, and 0.66 eV have been detected and the corresponding thermal capture cross sections evaluated. In addition a photomemory effect has been evidenced. The main features of the excited state of the crystal are increased photosensitivity, neutralization of hole traps, and residual conductivity. It is believed that macroscopic recombination barriers acting as minority carrier traps under optical excitation are responsible for this phenomenon. The presence of these extended defects is probably related to the layered structure of PbI2. An energy model is proposed on the basis of which the observed logarithmic time dependence of the photosensitization at room temperature can be predicted. The model allows also to give a plausible interpretation for all the characteristic features of the photomemory effect and for various results previously reported by other authors.

Notes: Abstract: This study attempts to determine if projections ascending from the guinea pig cochlear nucleus (CN) could be glutamatergic and/or aspartatergic. Multiple radio frequency lesions were made to ablate the right CN. The ablation was verified histologically. To identify the principal targets of CN efferents, silver impregnation methods were used to localize the preterminal degeneration of fibers in transverse sections of the brainstem 5 and 7 days after CN ablation. CN efferents projected heavily to the lateral superior olive (LSO) ipsilaterally, the medial superior olive (MSO) bilaterally, and contralaterally to the medial (MNTB) and ventral (VNTB) nuclei of the trapezoid body, the ventral (VNLL) and intermediate nuclei of the lateral lemniscus and the central nucleus of the inferior colliculus (ICc). There were smaller projections to the lateral nucleus of the trapezoid body ipsilaterally, the dorsal and dorsomedial periolivary nuclei bilaterally, and the dorsal nucleus of the lateral lemniscus contralaterally. There were sparse projections to the VNLL and ICc ipsilaterally and the CN contralaterally, and a very sparse projection to the contralateral LSO. To determine if CN efferents were glutamatergic and/or aspartatergic, the fresh brainstem was sectioned transversely and samples of the LSO, MSO, MNTB, VNLL, and ICc were taken to measure the electrically evoked release and the uptake of d-[3H]Asp and [14C]Gly or [14C]GABA 3–5 days after the CN ablation. The release studies suggest that only certain of the histologically identified projections ascending from the CN may be glutamatergic and/or aspartatergic. CN ablation depressed d-[3H]Asp release in the MSO bilaterally and in the contralateral MNTB and VNLL, suggesting that the CN efferents to these nuclei may use glutamate or aspartate as a transmitter. It was unclear whether a marginal depression of d-[3H]Asp release in the ipsilateral LSO reflected the presence of glutamatergic CN projections to this nucleus. d-[3H]Asp release in the ICc was unaffected, suggesting that CN efferents to this nucleus may not be glutamatergic. There were no deficits in d-[3H]Asp uptake. [14C]Gly release from the LSO and MSO was unchanged. [14C]Gly uptake was unchanged in the MSO and depressed only in the contralateral LSO, possibly reflecting subnormal uptake activity in endings contributed by contralateral MNTB cells that had lost their CN efferents. [14C]GABA uptake in the MNTB, VNLL, and ICc was unchanged. [14C]GABA release was unchanged in the VNLL and ICc. [14C]GABA release was depressed only in the contralateral MNTB, possibly reflecting the loss of a small complement of GABAergic CN efferents and the reaction of GABAergic projections from the contralateral VNTB to their loss of CN efferents.

Notes: Abstract: This study attempts to determine if the medial (MSO) and lateral superior olive (LSO), medial nucleus of the trapezoid body (MNTB), ventral nucleus of the lateral lemniscus (VNLL), and central nucleus of the inferior colliculus (ICc) contain glutamatergic synaptic endings. Micropunch and microdissection procedures provided fresh samples of these auditory nuclei for the measurement of the high-affinity uptake and electrically evoked release of exogenous d-[3H]ASP. The study also determined if the LSO and MSO contain glycinergic synaptic endings by measuring uptake and release of [14C]-Gly in these nuclei, and whether the MNTB, VNLL, and ICc contain GABAergic endings by assessing the uptake and release of [14C]GABA in these structures. Several strategies optimized the evoked Ca2+-dependent release of the labeled amino acids. These included the enhancement of high-affinity uptake during loading of the markers into the tissues, inhibition of uptake during the subsequent measurement of release, and use of an electrical stimulus current that evoked maximal Ca2+-dependent release. Each of these nuclei manifested the high-affinity uptake and the evoked Ca2+-dependent release of d-[3H]Asp, suggesting the presence of synaptic endings that may use Glu or Asp as a transmitter. Similar findings suggest the presence of glycinergic synaptic endings in the LSO and MSO, and of GABAergic synaptic endings in the MNTB, VNLL, and ICc.

Notes: Abstract: Hypoxia induces alterations of central mono-aminergic transmission and of behavior. We studied the effect of hypoxia on adult and newborn rats to obtain more information about long-lasting changes of dopamine (DA) transmission caused by neonatal hypoxia. One single exposure of adult rats to hypoxia leads to short-term alterations of DA uptake: decreased affinity of the uptake carrier to DA (Km, 269.5% versus control) and a sharp increase of Vmax up to 301.4% resulting in an increase of total uptake of DA into the striatum synaptosomes. The K+-evoked DA release decreased to 69.5%. After 1 week of recovery all parameters are normalized. Chronic postnatal hypoxia (postnatal day 2–11) caused long-lasting changes of DA release and uptake opposite to those observed in adult rats. Three months after hypoxia, the K+-stimulated DA release was enhanced (132% of control), and the uptake was reduced due to decreased affinity of the uptake carrier system for the substrate (Km, 187% of control value). In conclusion, the alterations observed after chronic postnatal hypoxia reflect special adaptive processes that are related to the high plasticity of the immature neonatal brain and contribute to an increased DA function in the nigrostriatal system.

Notes: Abstract: Arachidonic acid is transiently accumulated in the brain as a result of a variety of pathological conditions. The synthesis and release of some of its metabolites, namely, prostaglandin E2 (PGE2), thromboxane B2 (TXB2), and 6-keto-prostaglandin F1α (6-keto-PGF1α) from cortical slices of mice were studied following exposure to 6 min of hypoxia (7% O2), 45 s of anoxia, and 5 min-4 h of reoxygenation following anoxia. Hypoxia induced a slight increase in the rate of TXB2 release and a slight decrease in the rate of PGE2 release, whereas 6-keto-PGF1α was unaffected. Anoxia (45 s) followed by reoxygenation induced a transient increase in the release of PGE2 and of 6-keto-PGF1α with a return to the normal rate at 30 min and 2 h of recovery, respectively. However, the rate of TXB2 synthesis and release reached its peak (twofold increase) after I h and remained significantly higher than the control rate even after 4 h of normal air breathing. Our results demonstrate that hypoxia and anoxia, even of short duration, selectively trigger the activity of thromboxane synthetase and that this elevated rate of synthesis and release persists long after normal oxygen supply is restored. We suggest that enhanced thromboxane synthesis, with normal prostacyclin levels, might have a role in the pathophysiology of ischemic cell damage.

Notes: SYNOPSIS. Several substrains of Euglena gracilis var. bacillaris made chlorotic by treatment with pyribenzamine or streptomycin, or by growth at high temperature (35–36°C.), have been examined for their carotenoid content. They differ from the normal green strain both qualitatively and quantitatively. Some strains produce no detectable carotenoids while the carotenoid concentration in the strains producing most is at best only one-fifth that of the normal strain. In all substrains producing carotenoids, the carotene fraction consists of β-carotene accompanied by some members of the phytofluene series. In only two of these substrains, HB-G and PBZ-G3, are xanthophylls produced in significant amounts. In HB-G, the main pigment is echinenone, and in PBZ-G3 it is zeaxanthin. The significance of these findings is briefly discussed.

Notes: SYNOPSIS. Euglena and Chlamydomonas were cultured in an organic medium in the dark and at several light intensities (15, 60 and 150 ft-c) at temperatures from 20d̀ to 35d̀C. Below 32.5d̀, growth of Euglena was independent of light. Chlamydomonas was light dependent at all temperatures where growth occurred; there was no growth in the dark, at 15 ft-c, or at temperatures above 32.5d̀. At 35d̀, growth of Euglena became inversely light dependent; the higher the illumination, the poorer the growth. Multinucleated, giant euglenas were found at 35d̀, a greater percent of abnormal cells appearing at the higher light intensities. Monsters were not observed in Chlamydomonas.To explain the growth-inhibiting, monster-inducing effect of elevated temperatures on Euglena, it is postulated that a dark-formed thermosensitive protein, essential for normal cell division, is denatured. Light may increase the effect of heat on chlorophyll and the chloroplast, possibly by being converted to intraplastidic heat through the plastid carotenoids, thus having some indirect synergistic role in the phenomenon.

Notes: SYNOPSIS. Three chlorotic Euglena substrains, PBZ-G4, SM-L1, and HB-G, were cultured in light and dark at 25° and 33–35°C. These permanently chlorophyll-less flagellates with different carotenoid distributions were originally derived from a photosynthetic stock culture. Astasia longa, a naturally pigmentless flagellate, and the ciliate Tetrahymena were also employed.None of the organisms were light-dependent at 25°C. At high temperatures only the Euglena substrains showed an effect of light on growth: PBZ-G4 was inhibited, as was the photosynthetic parent strain, whereas SM-L1 and HB-G were stimulated. In all three substrains, monster forms were produced at elevated temperatures; SM-L1 and HB-G were multinucleated, while PBZ-G4 had an enlarged, single nucleus. A small percentage of astasias became multinucleated and almost all the tetrahymenas became giants when cultured at high temperature but neither was affected by light.Light-temperature interactions in the nonphotosynthetic substrains of Euglena are, at present, unexplained. The results are discussed in relation to the carotenoid content and the possible site of interaction. The major factor inducing abnormality is thermal stress.