Stress-Induced Alterations in Metabolism of Γ-Aminobutyric Acid in Rat Brain

The effect of a stressful manipulation on the metabolism of gamma-aminobutyric acid (GABA) in the rat brain was studied. Application of an immobilized stress to animals induced a significant increase in the striatal and hypothalamic GABA contents without affecting those in other central structures examined. It was also found that the increase in striatal GABA level preceded that in the hypothalamus. This increase in steady-state levels of GABA in the striatum and hypothalamus disappeared at 12 h after the termination of the application of stress for 3 h, which exhibited a maximal stimulatory action on the GABA contents in both central areas. The activity of L-glutamic acid decarboxylase was found to be significantly elevated in the striatum and hypothalamus following the stress application with a concomitant decrease in the content of L-glutamic acid, which is converted to GABA by the catalytic action of the latter enzyme. The in vivo turnover of GABA in the brain was estimated by taking advantages of the postmortem accumulation of GABA following decapitation and of the selective inhibitory action of a low dose of aminooxyacetic acid on the GABA degrading system, respectively. Analysis using these two different methods revealed that the cerebral turnover of GABA in vivo was not significantly altered under stressful situations despite of the increase in its steady-state level. These results suggest that central GABA system may respond to the input of painful stimuli resulting from the application of a severe physical and psychological stressor, in addition to the well-known functional alterations in catecholamine neurons. The functional significance of these alterations in the central GABA neurons is also discussed.     

Chain conformation of copoly(γ-methyl D,L-glutamate)

Copolymers of γ-methyl D - and L -glutamates with various D /L ratios were prepared. Infrared absorption spectra of solid films were measured and sums of right- and left-handed helix contents were determined from intensities of amide V bands. Farultraviolet absorption spectra and optical rotatory dispersion of these copolymers in solutions are used to ascertain their helical character. Chain conformations of DL -copolypeptides are discussed.     

Relative Activities of NAD- and NADP-Isocitric Dehydrogenases in Bean Mitochondria Modified by Glycerol or NADP

Mitochondria from cotyledons of Vigna sesquipedalis (L.) Fruwirth (starchy seed) showed no NAD-isocitric dehydrogenase (NAD-IDH) activity by the methods which have been known to be useful for the detection of NAD-IDH in mitochondria of plants including castor bean and alaska pea. When the Vigna cotyledon mitochondria were treated with glycerol, NAD-IDH activity appeared and NADP-isocitric dehydrogenase (NADP-IDH) activity was inhibited. The inhibition of mitochondrial NADP-IDH by glycerol was overcome by the addition of excess NADP.On the other hand, NADP-IDH activity in the soluble fraction of cell components was only slightly inhibited by glycerol and no NAD-IDH activity was elicited.It was postulated that NADP-IDH in mitochondria is converted to NAD-IDH by glycerol and back to NADP-IDH with NADP by the alteration in the spatial configuration of the enzyme. However, there could be 2 proteins as the other possibility.The NADP-IDH in the soluble fraction which is not subject to such alteration is different from the mitochondrial NADP-IDH.     

Studies on Auxin Protectors. IV. The Effect of Manganese on Auxin Protector-I of the Japanese Morning Glory

Auxin protector-I of the Japanese morning glory is inactivated by manganese. Experiments carried out in vitro indicate that in the absence of oxygen the manganic, but not the manganous, ion rapidly inactivates the protector. It is clear from these, and other data described in this report, and the results of other workers, that in the presence of oxygen, manganese accelerates auxin inactivation by means of 2 separate and distinct mechanisms: 1) manganese catalyzes the oxidation of auxin protectors, and 2) following the inactivation of the protectors, or in the absence of protectors, accelerates the oxidation of indoleacetic acid by endogenous peroxidases.     

Distribution of Three Auxin Protector Substances in Seeds and Shoots of the Japanese Morning Glory (Pharbitis nil)

The existence of substances which inhibit the enzymatic destruction of auxin in shoots of the Japanese morning glory (Pharbitis nil Choisy) has been confirmed, as has the fact that these substances are distributed in a gradient diminishing from apex to base in a manner indicating a regulatory role in internode elongation and tissue maturation. In addition to the 2 auxin protector substances reported previously (protectors I and II) which appear to account for most of the inhibition of the enzymatic destruction of auxin in young, elongating stem tissue, a third substance, designated as protector A, has been found to be highly active in seeds, and shoot tips of mature plants: In germinating seeds, no protector I or II activity was observed; in stem tips, no protector II and only slight protector I activity was observed. In contrast, old tissue contained no detectable amounts of protector A, but did contain protectors I and II. Between these extremes along the shoot axis, mixtures of the 3 substances were found. The evidence can be interpreted to mean that protector A is degraded into protectors I and II and perhaps translocated in this form. Gel filtration studies indicate that protector A has a molecular weight exceeding 200,000 gm/mole.     

Changes in body temperature of rats acclimated to heat with different acclimation schedules

Male Wistar rats, initially maintained at an ambient temperature (Ta) of 23.8 degrees C, were subjected to one of seven different heat acclimation schedules under a 12:12-h light-dark cycle (lights on at 0600 h). Two groups of rats were exposed to Ta of 32.4 degrees C all day for 5 (HC5) or 10 (HC10) days. The other four groups were exposed to Ta of 32.8 degrees C for 5 h/day during the last half of the dark phase for 5 (NI5) or 10 (NI10) consecutive days or during the last half of the light phase for 5 (DI5) or 10 (DI10) consecutive days. Control rats (C) were kept at 23.8 degrees C throughout the experiment. Hypothalamic temperature (Thy) was measured every 5 min with a chronically implanted thermocouple from 1 day before the beginning to 2 days after the end of the heat acclimation periods. During the heat acclimation periods, daily mean Thy rose significantly in HC5 and HC10 rats but decreased significantly in NI5 and NI10 rats. Daily mean Thy did not change in C, DI5, and DI10 rats. Thy in HC10 rats sharply decreased at the end of the heat acclimation periods and remained at low levels for approximately 3 h. On the 2nd postacclimation day, however, mean Thy returned and remained at a significantly higher level. In NI10 rats, the mean Thy in the postacclimation period was significantly lower than the preacclimation values. No such changes in mean Thy were observed in DI10 rats. Five-days of heat exposure had little effect on the postacclimation Thy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alteration of opioid receptors in seizure-susceptible El mouse brain

The distribution density of opioid receptors in the brain of El mice (seizure-susceptible strain) was examined to determine the relation between seizures and the opioid system. Saturation curves and Scatchard plots of [³H]2-d-alamine-5-d-leucine enkephalin binding revealed that the opioid delta receptor density in adult El mice during interictal periods was significantly increased in the cerebral cortex, hippocampus, and septal area. It was further shown that the concentration of such receptors in 25-day-old El mice that had no seizures was also significantly increased in the hippocampus and septal area, with no changes in apparent affinities, as compared with in the corresponding regions in ddY mice (seizure-nonsusceptible strain; the mother strain of El). Such up-regulation of opioid receptors in the El mouse brain could result from deficits in endogenous opioid peptides, which could be associated with the pathogenesis of seizure diathesis in the El mouse.