A preliminary study on the seasonal body temperature rhythms of the captive mountain hare (Lepus timidus)

The mountain hare (Lepus timidus) is a year-round active herbivore adapted to survive the boreal winter. Captive mountain hares (N = 4) were implanted with intraabdominal thermosensitive loggers to record their core body temperature (T_b) for a year and during food deprivation (8–48 h) in summer and winter. The average T_b was 38.7 ± 0.01 °C in summer and 38.3 ± 0.01 °C in winter. The yearly T_b correlated positively with the ambient temperature. The 24-h T_b was the highest from late scotophase to early photophase in summer and winter and the lowest during middle-late photophase in summer or during early-middle scotophase in winter. The range of the 24-h oscillations in T_b increased in three animals in winter. Food deprivation did not induce hypothermia in summer or winter. These preliminary data suggest that the mountain hare can spare a modest amount of energy with the wintertime reduction in T_b.     

Characteristics of GABA Release Induced by Free Radicals in Mouse Hippocampal Slices

The release of the inhibitory neurotransmitter GABA is generally enhanced under potentially cell-damaging conditions. The properties and regulation of preloaded [³H]GABA release from mouse hippocampal slices were now studied in free radical-containing medium in a superfusion system. Free radical production was induced by 0.01% of H₂O₂ in the medium. H₂O₂ markedly potentiated GABA release, which was further enhanced about 1.5-fold by K⁺ stimulation (50 mM). In Ca²⁺-free media this stimulation was not altered, indicating that the release was mostly Ca²⁺-independent. Moreover, omission of Na⁺ increased the release, suggesting that it is mediated by Na⁺-dependent transporters operating outwards, a conception confirmed by the enhancement with GABA homoexchange. Inhibition of the release with the ion channel inhibitors diisothiocyanostilbene-2,2′-disulphonate and 4-acetamido-4′-isothiocyanostilbene-2,2′-disulphonate indicates that Cl⁻ channels also participate in the process. This release was not modified by the adenosine receptor (A₁ and A_2a) agonists and ionotropic glutamate receptor agonists kainate, N-methy-d-aspartate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate, whereas the agonists of metabotropic glutamate receptors of group I [(S)-3,5-dihydroxyphenylglycine] and of group II [(2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate] enhanced it by receptor-mediated mechanisms, the effects being abolished by their respective antagonists. The group III agonist l(+)-2-amino-4-phosphonobutyrate reduced the evoked GABA release, but this was not affected by the antagonist. Furthermore, the release was reduced by activation of protein kinase C by 4β-phorbol 12-myristate 13-acetate and by inhibition of tyrosine kinase by genistein and of phoshoplipase by quinacrine. On the other hand, increasing cGMP levels with the phosphodiesterase inhibitor zaprinast, selective for PDE5, 6 and 9, and NO production with the NO-generating compounds hydroxylamine, sodium nitroprusside and S-nitroso-N-penicillamine enhanced the release. The regulation of GABA release induced by free radical production proved thus to be rather complex. Under potentially cell-damaging conditions, the potentiation of GABA release may be a mechanism to counteract hyperactivity and reduce the effects of excitatory amino acid release. On the other hand, reduction of GABA release could be harmful and contribute to excitotoxic damage and neuronal degeneration.     

Growth of tomato and an ABA-deficient mutant (sitiens) under saline conditions

To determine whether ABA accumulation inhibits or promotes shoot growth under stress, an ABA-deficient mutant tomato, sitiens, and its wild-type, the cultivar Rheinlands Rhum, were exposed to moderate salinity stress. Plants were grown at 75 m M NaCl for 2 weeks under conditions of moderate or high relative humidity (70% and 95% RH, respectively). At 70% RH, shoot DW and relative growth rate were reduced more in sitiens than in the cultivar, but the major difference between genotypes was in the degree of injury suffered by older leaves. Most leaves of sitiens died after 2 weeks, but those of the cultivar remained alive. When plants were grown at 95% RH, to maximize the leaf water status of both genotypes, there was no significant effect of salt on shoot DW of either genotype. However, there was still considerable leaf death in sitiens whereas no visible injury appeared in the cultivar. Cl^– accumulated to higher levels in leaf tissues than Na⁺, but to similar concentrations in both genotypes, and so could not explain the injury in the sitiens leaves. The results indicate that ABA maintains rather than inhibits new growth under stress, and has a major effect on preservation of older leaves.     

Micro‐fungi and invertebrate herbivores on birch trees: fungal mediated plant–herbivore interactions or responses to host quality?

We studied interactions between microfungi and herbivores sharing a host tree. In a series of experiments and field observations over a 3‐year period, we compared phenotypic and genetic correlations of fungal frequencies and performance of invertebrate herbivores growing on mature half‐sib progenies of mountain birches (Betula pubescens ssp. czerepanovii) in two environments, a forested river valley and an adjacent higher‐elevation mountain birch woodland. We found little support for direct relation between fungal frequencies and performance of herbivore species. Instead, genetic correlations, particularly between autumnal moth (Epirrita autumnata) and rust fungus (Melampsoridium betulinum), suggest that herbivore performance may be caused by (1) genetic differences in plant quality for fungi and herbivores, or (2) genetic differences in responses to environmental conditions.     

MORPHO‐FUNCTIONAL PATTERNS OF PHOTOSYNTHESIS IN THE SOUTH PACIFIC KELP LESSONIA NIGRESCENS: EFFECTS OF UV RADIATION ON 14C FIXATION AND PRIMARY PHOTOCHEMICAL REACTIONS1

The morpho‐functional patterns of photosynthesis, measured as ¹⁴C‐fixation and chl fluorescence of PSII, also as affected by different doses of UV radiation in the laboratory were examined in the South Pacific kelp Lessonia nigrescens Bory of the coast of Valdivia, Chile (40°S). The results indicated the existence of longitudinal thallus profiles in physiological performance. In general, blades exhibited higher rates of carbon fixation and pigmentation as compared with stipes and holdfasts. Light‐independent ¹⁴C fixation (LICF) was high in meristematic zones of the blades (3.5 μmol ¹⁴C·g^?1 fresh weight [FW]·h^?1), representing 2%–16% (percentage ratio) of the photosynthetic ¹⁴C fixation (20 μmol ¹⁴C·g^?1 FW·h^?1). Exposures to UV radiation indicated that biologically effective UV‐B doses (BED_{photoinhibition300}) of 200–400 kJ·m^?2 (corresponding to current daily doses measured in Valdivia on cloudless summer days) inhibit photosynthetic ¹⁴C fixation of blades by 90%, while LICF was reduced by 70%. The percentage ratio of LICF to photosynthetic ¹⁴C fixation increased under UV exposure to 45%. Primary light reactions measured as maximum quantum yield (F_v/F_m) and electron transport rate (ETR) indicated a higher UV susceptibility of blades as compared with stipes and holdfasts: after a 48 h exposure to UV‐B, the decrease in the blades was close to 30%, while in the stipes and holdfasts it was <20%. The existence of translocation of labeled carbon along the blades suggests that growth at the meristem may be powered by nonphotosynthetic processes. A possible functional role of LIFC, such as during reduction of photosynthetic carbon fixation due to enhanced UV radiation, is discussed. These results in general support the idea that the UV‐related responses in Lessonia are integrated in the suite of morpho‐functional adaptations of the alga.     

Relationship between local perfusion and FFA uptake in human skeletal muscle-no effect of increased physical activity and aerobic fitness.

We investigated heredity-independent effects of increased physical activity and aerobic fitness on skeletal muscle free fatty acid (FFA) uptake, perfusion, and their heterogeneity at rest and during exercise. Also, the relationship between local skeletal muscle FFA uptake and perfusion was studied. Nine young adult male monozygotic twin pairs with significant difference in physical activity [229 min (SD 156) average time spent for conditioning exercise per week in more and 98 min (SD 71) in less active twins, P = 0.013] and aerobic fitness [18% (SD 10) difference in maximum O2 uptake] between brothers were studied using positron emission tomography. Submaximal knee-extension exercise increased perfusion, FFA uptake, and oxygen uptake in quadriceps femoris muscles 6-10 times compared with resting values (P < 0.001). More active twins tended to utilize more oxygen, while no differences were found in muscle perfusion or FFA uptake between groups. Mean perfusion and FFA uptake correlated strongly at a whole muscle level, both at rest (r = 0.97, P = 0.03 in more and r = 0.98, P = 0.02 in less active twins) and during exercise (r = 0.99, P = 0.01 and r = 0.94, P = 0.06), but at the voxel level (87 mm3) correlation was only moderate during exercise [r = 0.73 (SD 0.08) vs. r = 0.74 (SD 0.10), P = 0.92] and weak at rest [r = 0.28 (SD 0.13) vs. r = 0.33 (SD 0.21), P = 0.58]. Exercise decreased both perfusion and FFA uptake heterogeneity within the muscles (P < 0.001) similarly in both groups. In conclusion, long-term history of moderately increased physical activity tends to enhance muscle oxidative metabolism, but it does not have any significant influence on the FFA uptake or perfusion rates or their heterogeneity in skeletal muscle. Submaximal knee-extension exercise decreases heterogeneity of muscle FFA uptake and perfusion and improves matching between local muscle perfusion and FFA uptake. Thus it seems that the genetic influence is more important to determine the heterogeneity of perfusion and FFA uptake in skeletal muscle than exercise training.     

Alphavirus Replicase Protein NSP1 Induces Filopodia and Rearrangement of Actin Filaments

Expression of the NSP1 protein of Semliki Forest virus and Sindbis virus in cultured cells induced filopodia-like extensions containing NSP1 but not F actin. The actin stress fibers disappeared, whereas vimentin, keratin, and tubulin networks remained intact. The effects of NSP1 were dependent on its palmitoylation but not on its enzymatic activities and were also observed in virus-infected cells.     

Interference of S-Alkyl Derivatives of Glutathione with Brain Ionotropic Glutamate Receptors

The effects of glutathione, glutathione sulfonate and S-alkyl derivatives of glutathione on the binding of glutamate and selective ligands of ionotropic N-methyl-D-aspartate (NMDA) and non-NMDA receptors were studied with mouse synaptic membranes. The effects of glutathione and its analogues on ⁴⁵Ca²⁺ influx were also estimated in cultured rat cerebellar granule cells. Reduced and oxidized glutathione, glutathione sulfonate, S-methyl-, -ethyl-, -propyl-, -butyl- and -pentylglutathione inhibited the Na⁺-independent binding of L-[³H]glutamate. They strongly inhibited also the binding of (S)-2-amino-3-hydroxy-5-[³H]methyl-4-isoxazolepropionate [³H]AMPA (IC₅₀ values: 0.8–15.9 M). S-Alkylation of glutathione rendered the derivatives unable to inhibit [³H]kainate binding. The NMDA-sensitive binding of L-[³H]glutamate and the binding of 3-[(R)-2-carboxypiperazin-4-yl][1,2-³H]propyl-1-phosphonate ([³H]CPP, a competitive antagonist at NMDA sites) were inhibited by the peptides at micromolar concentrations. The strychnine-insensitive binding of the NMDA coagonist [³H]glycine was attenuated only by oxidized glutathione and glutathione sulfonate. All peptides slightly enhanced the use-dependent binding of [³H]dizocilpine (MK-801) to the NMDA-gated ionophores. This effect was additive with the effect of glycine but not with that of saturating concentrations of glutamate or glutamate plus glycine. The glutamate- and NMDA-evoked influx of ⁴⁵Ca²⁺ into cerebellar granule cells was inhibited by the S-alkyl derivatives of glutathione. We conclude that besides glutathione the endogenous S-methylglutathione and glutathione sulfonate and the synthetic S-alkyl derivatives of glutathione act as ligands of the AMPA and NMDA receptors. In the NMDA receptor-ionophore these glutathione analogues bind preferably to the glutamate recognition site via their -glutamyl moieties.     

Release of Endogenous Glutamate,Aspartate, GABA,and Taurine from Hippocampal Slices from Adult and Developing Mice under Cell-Damaging Conditions

The releases of endogenous glutamate, aspartate, GABA and taurine from hippocampal slices from 7-day-, 3-, 12-, and 18-month-old mice were investigated under cell-damaging conditions using a superfusion system. The slices were superfused under hypoxic conditions in the presence and absence of glucose and exposed to hydrogen peroxide. In the adult hippocampus under normal conditions the basal release of taurine was highest, with a response only about 2-fold to potassium stimulation (50 mM). The low basal releases of glutamate, aspartate, and GABA were markedly potentiated by K⁺ ions. In general, the release of the four amino acids was enhanced under all above cell-damaging conditions. In hypoxia and ischemia (i.e., hypoxia in the absence of glucose) the release of glutamate, aspartate and GABA increased relatively more than that of taurine, and membrane depolarization by K⁺ markedly potentiated the release processes. Taurine release was doubled in hypoxia and tripled in ischemia but K⁺ stimulation was abolished. In both the mature and immature hippocampus the release of glutamate and aspartate was greatly enhanced in the presence of H₂O₂, that of aspartate particularly in developing mice. In the immature hippocampus the increase in taurine release was 10-fold in hypoxia and 30-fold in ischemia, and potassium stimulation was partly preserved. The release processes of the four amino acids in ischemia were all partially Ca²⁺-dependent. High concentrations of excitatory amino acids released under cell-damaging conditions are neurotoxic and contribute to neuronal death during ischemia. The substantial amounts of the inhibitory amino acids GABA and taurine released simultaneously may constitute an important protective mechanism against excitatory amino acids in excess, counteracting their harmful effects. In the immature hippocampus in particular, the massive release of taurine under cell-damaging conditions may have a significant function in protecting neural cells and aiding in preserving their viability.