bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Timing and Nitrogen Fertilizer Application on Winter Oilseed Rape (Brassica napus L.). II. Nitrogen Uptake Dynamics and Fertilizer Efficiency
Authors: Barłóg P. , Grzebisz W. 
Published: September 2004

AbstractField experiments were carried out on grey‐brown podzolic soil in the four consecutive growing seasons (1998–2001) at Krzeslice Farm, central‐western Poland. The effect of seven N fertilization treatments (in kg N ha−1): 80NF + 80CAN; 80NF + 50CAN + 30CN; 80CAN + 80CAN; 80CAN + 80CAN + 30CN; 80AN + 80AN; 80AN + 50AN + 30CN, where, NF – nitrofos NPK, CAN – calcium‐ammonium nitrate, AN – ammonium nitrate, CN – calcium nitrate and control (without N) on N uptake dynamics and N efficiency was studied. Mineral fertilizers were applied at the start of spring regrowth, beginning of stem elongation and at the flower‐bud‐visibility stage. The study revealed two distinct strategies of oilseed rape plants’ adaptation to timing and N fertilizer application sequences. Both strategies based on nitrogen uptake rate (NUR), were analysed at different plant growth stages. Ammonium nitrate (AN) applied in the two‐split system gave the highest NUR (387 mg m−2 day−1) during stem elongation (for comparison, a value of 166 mg m−2 day−1 was obtained in the control). In the case of calcium‐ammonium nitrate (CAN), a moderate level of NUR was obtained (304 mg m−2 day−1) but N uptake lasted 12 days longer compared with the AN treatment. Hence, N accumulation in leaves at the end of flowering explained about 81 % of yield variability. The second adaptation strategy was attributed to the three‐split N treatment. Plants fertilized with AN and CAN fertilizers showed an inconsistent pattern of NUR with time. Nitrogen accumulation in stems at the beginning of maturity, explained 69 % of yield variability. Nitrogen‐use efficiency did not show any response to N treatments.
Chronic stress attenuates GABAergic inhibition and alters gene expression of parvocellular neurons in rat hypothalamus
Authors: Verkuyl J. Martin , Hemby Scott E. , Joëls Marian 
Published: September 2004

AbstractChronic stress causes disinhibition of the hypothalamus–pituitary–adrenal axis. Consequently, the brain is overexposed to glucocorticoids which in humans may precipitate stress‐related disorders, e.g. depression. The hypothalamus–pituitary–adrenal activity is strongly regulated by GABAergic input to parvocellular neurons in the hypothalamic paraventricular nucleus. We here report a reduced frequency of miniature inhibitory postsynaptic currents (mIPSCs) in parvocellular neurons of rats exposed to 3 weeks of unpredictable stress. The mIPSC amplitude and kinetic properties were unchanged, pointing to a presynaptic change caused by chronic stress. Because paired‐pulse inhibition was unaffected by chronic stress, the number of functional GABAergic synaptic contacts rather than the release probability seems to be reduced after chronic stress. Linearly amplified RNA from postsynaptic cells was hybridized with multiple cDNA clones of interest, including most GABAA receptor subunits. In agreement with the electrophysiological observations, relative expression of the prevalent GABAAα1, α3, γ1 and γ2 receptor subunits, which largely contribute to the recorded responses, was not altered after chronic stress. However, expression of the extra‐synaptic GABAAα5 subunit, earlier linked to depression in humans, and of the δ receptor subunit were found to be significantly changed. In conclusion, chronic stress leads to presynaptic functional alterations in GABAergic input to the paraventricular nucleus which could contribute to the observed disinhibition of the hypothalamus–pituitary–adrenal axis; additionally other aspects of GABAergic transmission may also be changed due to transcriptional regulation of specific receptor subunits in the parvocellular neurons.
Axon behaviour at Schwann cell – astrocyte boundaries: manipulation of axon signalling pathways and the neural adhesion molecule L1 can enable axons to cross
Authors: Adcock Kathryn H. , Brown David J. , Shearer Morven C. , Shewan Derryck , Schachner Melitta , Smith George M. , Geller Herbert M. , Fawcett James W. 
Published: September 2004

AbstractAxon regeneration in vivo is blocked at boundaries between Schwann cells and astrocytes, such as occur at the dorsal root entry zone and around peripheral nerve or Schwann cell grafts. We have created a tissue culture model of these boundaries in Schwann cell – astrocyte monolayer co‐cultures. Axon behaviour resembles that in vivo, with axons showing a strong preference for Schwann cells over astrocytes. At boundaries between the two cell types, axons growing on astrocytes cross readily onto Schwann cells, but only 15% of axons growing on Schwann cells are able to cross onto astrocytes. Treatment with chondroitinase or chlorate to reduce inhibition by proteoglycans did not change this behaviour. The neural adhesion molecule L1 is present on Schwann cells and not astrocytes, and manipulation of L1 by application of an antibody, L1‐Fc in solution, or adenoviral transduction of L1 into astrocytes increased the proportion of axons able to cross onto astrocytes to 40–50%. Elevating cAMP levels increased crossing from Schwann cells onto astrocytes in live and fixed cultures, and had a co‐operative effect with NT‐3 but not with NGF. Inactivation of Rho with a cell‐permeant form of C3 exoenzyme also increased crossing from Schwann cells to astrocytes. Our experiments indicate that the preference of axons for Schwann cells is largely mediated by the presence of L1 on Schwann cells but not astrocytes, and that manipulation of growth cone signalling pathways can allow axons to disregard boundaries between the two cell types.
Mu‐opioid receptor knockout mice show diminished food‐anticipatory activity
Authors: Kas Martien J. H. , Van Den Bos Ruud , Baars Annemarie M. , Lubbers Marianne , Lesscher Heidi M. B. , Hillebrand Jacquelien J. G. , Schuller Alwin G. , Pintar John E. , Spruijt Berry M. 
Published: September 2004

AbstractWe have previously suggested that during or prior to activation of anticipatory behaviour to a coming reward, µ‐opioid receptors are activated. To test this hypothesis schedule induced food‐anticipatory activity in µ‐opioid receptor knockout mice was measured using running wheels. We hypothesized that µ‐knockout mice show little food‐anticipatory activity. In wildtype mice we observed that food‐anticipatory activity increased proportional to reduced food intake levels during daily scheduled food access, and thus reflects the animal's physiological need for food. µ‐Knockout mice do not adjust their schedule induced running wheel behaviour prior to and during feeding time in the same way as wildtype mice; rather than showing more running wheel activity before than during feeding, they showed an equal amount of activity before and during feeding. As food‐anticipatory activity is dependent on the mesolimbic dopamine system and µ‐opioid receptors regulate dopaminergic activity, these data suggest a change in the dopamine system's activity in µ‐knockout mice. As we observed that µ‐knockout mice tended to show a stronger locomotor activity response than wildtype mice to the indirect dopamine agonistd‐amphetamine, it appears that the dopaminergic systemper seis intact and sensitive to activation. We found no differences in the expression of pro‐opiomelanocortin, a precursor of endogenous endorphin, in the arcuate nucleus between µ‐knockout mice and wildtype mice during restricted feeding, showing that the µ‐opioid receptor does not regulate endogenous endorphin levels. These data overall suggest a role for µ‐opioid receptors in adapting reward related behaviour to the requirements of the environment.
Lesions of the Edinger–Westphal nucleus in C57BL/6J mice disrupt ethanol‐induced hypothermia and ethanol consumption
Authors: Bachtell Ryan K. , Weitemier Adam Z. , Ryabinin Andrey E. 
Published: September 2004

AbstractThe Edinger–Westphal nucleus (EW) is a brain region that has recently been implicated as an important novel neural target for ethanol. Thus, the EW is the only brain region consistently showing elevated c‐Fos expression following both voluntary and involuntary ethanol administration. Ethanol‐induced c‐Fos expression in the EW has been shown to occur in urocortin I‐positive neurons. Moreover, previous reports using several genetic models have demonstrated that differences in the EW urocortin I system are correlated with ethanol‐mediated behaviours such as ethanol‐induced hypothermia and ethanol consumption. The aim of this study was to confirm these relationships using a more direct strategy. Thus, ethanol responses were measured following electrolytic lesions of the EW in male C57BL/6J mice. Both EW‐lesioned and sham‐operated animals were tested for several ethanol sensitivity measures and ethanol consumption in a two‐bottle choice test. The results show that lesions of the EW significantly disrupted ethanol‐induced hypothermia, while having no effect on pupillary dilation, locomotor activity or ethanol‐induced sedation. In addition, EW‐lesioned animals showed significantly lower ethanol preference and total ethanol dose consumed in the two‐bottle choice test. EW‐lesioned animals also consumed less sucrose than sham‐operated animals, but did not have altered preferences for sucrose or quinine in a two‐bottle choice test. These data support previously observed genetic correlations between EW urocortin I expression and both ethanol‐induced hypothermia and ethanol consumption. Taken together, the findings suggest that the EW may function as a sensor for ethanol, which can influence ethanol consumption and preference.
Beneficial effects of enriched environment on adolescent rats from stressed pregnancies
Authors: Laviola Giovanni , Rea Monica , Morley‐Fletcher Sara , Di Carlo Simonetta , Bacosi Antonella , De Simone Roberta , Bertini Mario , Pacifici Roberta 
Published: September 2004

AbstractThe capacity of an early environmental intervention to normalize the behavioural and immunological dysfunctions produced by a stressed pregnancy was investigated. Pregnant Sprague‐Dawley rats underwent three 45‐min sessions per day of prenatal restraint stress (PS) on gestation days 11–21, and their offspring were assigned to either an enriched‐environment or standard living cages throughout adolescence [postnatal days (pnd) 22–43]. Juvenile rats from stressed pregnancies had a prominent depression of affiliative/playful behaviour and of basal circulating CD4 T lymphocytes, CD8 T lymphocytes and T4/T8 ratio. They also showed increased emotionality and spleen and brain frontal cortex levels of pro‐inflammatory interleoukin‐1β (IL‐1β) cytokine. A more marked response to cyclophosphamide (CPA: two 2 mg/kg IP injections) induced immunosuppression was also found in prenatal stressed rats. Enriched housing increased the amount of time adolescent PS rats spent in positive species‐typical behaviours (i.e. play behaviour), reduced emotionality and reverted most of immunological alterations. In addition to its effects in PS rats, enriched housing increased anti‐inflammatory IL‐2 and reduced pro‐inflammatory IL‐1β production by activated splenocytes, also producing a marked alleviation of CPA‐induced immune depression. In the brain, enriched housing increased IL‐1β values in hypothalamus, while slightly normalizing these values in the frontal cortex from PS rats. This is a first indication that an environmental intervention, such as enriched housing, during adolescence can beneficially affect basal immune parameters and rats response to both early stress and drug‐induced immunosuppression.
Unique accumulation of neuropeptides in an insect: FMRFamide‐related peptides in the cockroach, Periplaneta americana
Authors: Predel R. , Neupert S. , Wicher D. , Gundel M. , Roth S. , Derst C. 
Published: September 2004

AbstractFMRFamides belong to the most extensively studied neuropeptides in invertebrates and exhibit diverse physiological effects on different target organs, such as muscles, intestine and the nervous system. This study on the American cockroach confirms for the first time that extended FMRFamides occur in non‐dipteran insects. By means of tandem mass spectrometry, these neuropeptides were structurally elucidated, and sequence information was used for subsequent cloning of the cockroach FMRFamide gene. This precursor gene encodes for 24 putative peptides and shows sufficient similarity with the Drosophila FMRFamide gene. Of the 24 peptides, 23 were detected by mass spectrometric methods; it is the highest number of neuropeptide forms shown to be expressed from a single precursor in any insect. The expression was traced back to single neurons in the thoracic ganglia. The unique accumulation of these FMRFamide‐related peptides in thoracic perisympathetic organs provides the definite evidence for a tagma‐specific distribution of peptidergic neurohormones in neurohaemal release sites of the insect CNS. Excitatory effects of the cockroach FMRFamides were observed on antenna–heart preparations. In addition, the newly described FMRFamides reduce the spike frequency of dorsal‐unpaired median neurons and reduce the intracellular calcium concentration, which may affect the peripheral release of the biogenic amine octopamine.
SNAP‐25 in hippocampal CA1 region is involved in memory consolidation
Authors: Hou Qiuling , Gao Xiang , Zhang Xuehan , Kong Lingwei , Wang Xinming , Bian Wei , Tu Yanyang , Jin Meilei , Zhao Guoping , Li Baoming , Jing Naihe , Yu Lei 
Published: September 2004

AbstractAs a synaptosomal protein, SNAP‐25 plays a role in a number of neuronal functions including axonal growth, dendrite formation, fusion of synaptic vesicles with membrane and the expression of long‐term potentiation (LTP) in the hippocampus. Using a learning/memory behavior screening, we identified SNAP‐25 as one of the differentially expressed genes in the hippocampus upon behavioral training. The inhibition of SNAP‐25 with intracerebroventricular antisense oligonucleotide caused a deficit in long‐ but not short‐term memory for step‐down inhibitory avoidance. Intra‐CA1 infusion of the SNAP‐25 antisense oligonucleotide impaired long‐term contextual fear memory and spatial memory and interfered with the LTP of synaptic transmission in the CA1 region. The inhibitory effect on LTP was not mediated by a pre‐synaptic mechanism because paired pulse facilitation of synaptic transmission was not affected after administration of the antisense oligonucleotide. Together, the results suggest that SNAP‐25 in the CA1 region is involved in memory consolidation.
Monocarboxylate transport inhibition alters retinal function and cellular amino acid levels
Authors: Bui Bang V. , Vingrys Algis J. , Wellard John W. , Kalloniatis Michael 
Published: September 2004

AbstractWe assessed the effect of the in vivo application of monocarboxylate transport inhibitors on retinal function and amino acid immunocytochemistry. We wanted to determine the impact that altered aerobic metabolite availability has on retinal function and the characteristics of amino acid shunting into metabolic pools. Electroretinograms were collected from anaesthetized rats at various times after intravitreal injection of the monocarboxylate transport inhibitors α‐cyano‐4‐hydroxycinnamate (4‐CIN; 2 µL, 0.1–10 mm) or p‐(dipropylsulphamoyl)benzoic acid (probenecid; 1–10 mm). Changes in retinal function were compared with quantitative amino acid immunocytochemical changes in retinas harvested 20 and 40 min after either 4‐CIN or vehicle treatment. The injection of 4‐CIN resulted in a dose‐dependent reduction of the ON‐bipolar cell P2 wave amplitude (20–80%) and delay in its implicit time. The phototransduction sensitivity was mildly reduced whereas the ON‐bipolar cell P2 sensitivity was unaffected. Probenecid induced functional changes similar to those observed with 4‐CIN. We also mapped the amino acid alterations within specific cell classes induced by 4‐CIN application. All neurones displayed a reduced glutamate content averaging 48%; reduced GABA (31%) and glycine (28%) were found within amacrine cells and glutamine was reduced in all cell classes except photoreceptor and Müller cells. All cell classes in the retina demonstrated increases in aspartate (57%), whereas leucine (24%) and ornithine (21%) were only significantly increased in photoreceptor and bipolar cells. The reduction in glutamate immunolabelling in specific retinal cell classes was mirrored by an increase in aspartate levels at these locations. In addition, attenuated glutamine immunolabelling also closely matched the spatial pattern observed for glutamate. Our immunocytochemical analysis provides evidence that monocarboxylate transport inhibition induces a shift in the equilibrium of glutamate transamination reactions involving aspartate throughout the retina whereas photoreceptor and bipolar cells also use glutamate transamination reactions involving ornithine and leucine. The distribution pattern of glutamine secondary to monocarboxylate inhibition suggests that this amino acid is a major precursor for glutamate throughout the retina.
Adrenoceptor subtype‐specific acceleration of the hypoxic depression of excitatory synaptic transmission in area CA1 of the rat hippocampus
Authors: Pearson Tim , Frenguelli Bruno G. 
Published: September 2004

AbstractThe depression of excitatory synaptic transmission by hypoxia in area CA1 of the hippocampus is largely dependent upon the activation of adenosine A1 receptors on presynaptic glutamatergic terminals. As well as adenosine, norepinephrine levels increase in the hypoxic/ischemic hippocampus. We sought to determine the influence of α‐ and β‐adrenoceptor (AR) activation on the hypoxic depression of synaptic transmission utilizing electrophysiological, pharmacological and adenosine sensor techniques. Norepinephrine depressed synaptic transmission and significantly accelerated the hypoxic depression of synaptic transmission. The α‐AR agonist 6‐fluoronorepinephrine mimicked both of these effects whilst the α2‐AR antagonist yohimbine, but not the α1‐AR antagonist urapidil, prevented the actions of 6‐fluoronorepinephrine. In contrast, the β‐AR agonist isoproterenol enhanced synaptic transmission and only accelerated the hypoxic depression of transmission in hypoxia‐conditioned slices in which the hypoxic release of adenosine is reduced. The effects of isoproterenol were blocked by the non‐selective β‐AR antagonist propranolol and the selective β1‐AR antagonist betaxolol. Using an enzyme‐based adenosine sensor we observed that the application of the β‐AR agonist resulted in increased extracellular adenosine during repeated hypoxia. Our results suggest that α2‐AR activation facilitates the hypoxic depression of synaptic transmission probably via the known α2‐AR‐mediated inhibition of presynaptic calcium channels whereas β1‐AR activation does so via increased extracellular adenosine and greater activation of inhibitory adenosine A1 receptors.
Developmental expression of the Ca2+‐binding proteins calretinin and parvalbumin at the calyx of Held of rats and mice
Authors: Felmy Felix , Schneggenburger Ralf 
Published: September 2004

AbstractCa2+‐binding proteins of the EF‐hand family are widely expressed in the CNS, and contribute to intracellular Ca2+ buffering in neurons. In nerve terminals, Ca2+‐binding proteins are likely to regulate transmitter release probability and synaptic short‐term‐plasticity. Here, we investigated the developmental expression pattern of calretinin and parvalbumin at a large excitatory synapse, the calyx of Held in the medial nucleus of the trapezoid body (MNTB) of rats and mice. We used two‐colour immunofluorescence imaging with primary antibodies detecting one of the Ca2+‐binding proteins, and a presynaptic marker protein, Rab‐3A. Calretinin was found in nerve terminals of the calyx of Held, but not in postsynaptic principal cells. The presynaptic density of Calretinin staining, and the degree of colocalization with Rab‐3A increased during postnatal development (P6–P31). Surprisingly, not all calyces of Held expressed calretinin. In rats, calretinin‐containing calyces were irregularly interspersed with calretinin‐negative calyces, whereas in mice, calretinin‐positive calyces were preferentially located in the lateral portion of the MNTB. The percentage of calretinin‐positive calyces increased during development, to about 75% and 20% at P30 in rats and in mice, respectively. Parvalbumin was present in the presynaptic calyces of Held and in the nerve fibres entering the MNTB, as well as in the somata of the MNTB principal neurons. An up‐regulation of calretinin and parvalbumin in calyces of Held probably increases the presynaptic Ca2+ buffering strength during postnatal development, but the unexpected heterogeneity of calretinin expression might cause differences in Ca2+ signalling and transmitter release probability between calyces of Held.
Reduced plasticity of cortical whisker representation in adult tenascin‐C‐deficient mice after vibrissectomy
Authors: Cybulska‐Klosowicz Anita , Zakrzewska Renata , Pyza Elzbieta , Kossut Malgorzata , Schachner Melitta 
Published: September 2004

AbstractThe effect of the extracellular matrix recognition molecule tenascin‐C on cerebral plasticity induced by vibrissectomy was investigated with 2‐deoxyglucose (2DG) brain mapping in tenascin‐C‐deficient mice. Unilateral vibrissectomy sparing row C of vibrissae was performed in young adult mice. Two months later, cortical representations of spared row C vibrissae and control row C on the other side of the snout were visualized by [14C]2DG autoradiography. In both wild‐type and tenascin‐C‐deficient mice, cortical representation of the spared row was expanded in all layers of the barrel cortex. However, the effect was significantly more extensive in wild‐type animals than in the mutant. Elimination of tenascin‐C by genetic manipulation thus reduces the effect of vibrissectomy observed in the somatosensory cortex. No increase in number of fibres in the vibrissal nerve of spared vibrissae was seen, and occurrence of additional nerve to the spared follicle was very rare. Thus, in tenascin‐C‐deficient mice functional plasticity seems to be impaired within the CNS.