bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relationship between Carbon Isotope Discrimination, Ash Content and Grain Yield in Wheat in the Peninsular Zone of India
Authors: Misra S. C. , Randive R. , Rao V. S. , Sheshshayee M. S. , Serraj R. , Monneveux P. 
Published: September 2006

AbstractCarbon isotope discrimination (Δ) and ash content (ma) have been proposed as indirect selection criteria for grain yield in wheat. The associations between Δ, ma and grain yield were found, however, to depend highly on the environmental conditions, the organ sampled and the time of sampling. In this study, carried out in the warm conditions of the Peninsular Zone of India, the relationship between Δ, ma and yield was studied in 30 bread and durum wheat cultivars under residual soil moisture stress (RSMS), post‐anthesis water stress (PAWS) and well‐watered (WW) conditions. Both Δ and ma were analysed in young seedlings (four‐leaf stage), leaves at anthesis and grain at maturity. Ash content was also evaluated in leaves at booting stage and maturity. Grain Δ was lower under PAWS and RSMS than under WW, while seedling and leaf Δ did not significantly differ among water regimes. Grain yield was positively correlated to grain Δ under PAWS and negatively correlated to grain ma under RSMS. A significant positive correlation was noted under RSMS and WW treatments between maLm and grain yield. Ash content in leaf at maturity consequently appears to be a useful indirect selection criterion in environments where Δ does not show any correlation with yield. The results highlight the potential of Δ and ma as indirect selection criteria for wheat yield in the conditions of the Peninsular Zone of India.
Bilateral Testicular Leydig Cells Tumour in a Donkey
Authors: Galofaro V , Rapisarda G , Ferrara G , Marino F 
Published: September 2006

ContentsA rare case of a bilateral Leydig cells tumour located in the testis of a 15‐year‐old donkey slaughtered normally is presented. Histologically, the testicular tumour showed neoplastic Leydig cells arranged in solid growth as a pseudoadenomatous packet type. To our knowledge, this is the first bilateral Leydig cells tumour, a neoplasm never reported in the donkey.
Long‐lasting synaptic loss after repeated induction of LTD: independence to the means of LTD induction
Authors: Kamikubo Yuji , Egashira Yoshihiro , Tanaka Tsunehiro , Shinoda Yo , Tominaga‐Yoshino Keiko , Ogura Akihiko 
Published: September 2006

AbstractShort‐ and long‐lasting synaptic plasticity is assumed to be the cellular basis of short‐ and long‐lasting memory, respectively. However, the cellular consequences leading to the long‐lasting synaptic plasticity, assumed to include the processes of synapse formation and elimination, remain unknown. Using hippocampal slices maintained stably in culture, we found previously that the repeated induction of long‐term potentiation (LTP) triggered a slowly developing long‐lasting enhancement in synaptic transmission strength accompanied by synapse formation, which was separate from LTP itself. We recently reported a phenomenon apparently of a mirror‐image effect. The repeated activations of metabotropic glutamate receptor (mGluR), which induces long‐term depression (LTD), triggered a long‐lasting reduction in synaptic strength accompanied by synapse elimination. To clarify whether the reported long‐lasting effect was specific to the drugs used previously and whether the effect was specific to mGluR‐mediated LTD, we exposed the cultured slices repeatedly to another Group I metabotropic glutamate receptor (mGluR) agonist, an N‐methyl‐d‐aspartate receptor agonist, and a Na+/K+‐pump inhibitor. All these treatments resulted in an equivalent long‐lasting synaptic reduction/elimination when repeated three times, indicating that the repeated LTD induction leads to synapse elimination. The independence of synapse elimination to the means of LTD induction suggests that the signals leading to short‐term plasticity and long‐term plasticity are independent. Detailed inspections in the representative case of mGluR activation revealed that the reduction in synaptic strength developed with a ∼1‐week delay from the decrease in the number of synaptic structures. This synapse elimination should be unique as it is activity‐dependent rather than inactivity‐dependent.
Altered PPARγ expression and activation after transient focal ischemia in rats
Authors: Victor N. A. , Wanderi E. W. , Gamboa J. , Zhao X. , Aronowski J. , Deininger K. , Lust W.D. , Landreth G. E. , Sundararajan S. 
Published: September 2006

AbstractStroke is a devastating disease with limited treatment options. Recently, we found that the peroxisome proliferator‐activated receptor‐γ (PPARγ) agonists troglitazone and pioglitazone reduce injury and inflammation in a rat model of transient cerebral ischemia. The mechanism of this protection is unclear, as these agents can act through PPAR‐γ activation or through PPAR‐γ‐independent mechanisms. Therefore, we examined PPAR‐γ expression, DNA binding and transcriptional activity following stroke. In addition, we used a PPAR‐γ antagonist, T0070907, to determine the role of PPAR‐γ during ischemia. Using immunohistochemical techniques and real‐time PCR, we found low levels of PPAR‐γ mRNA and PPAR‐γ immunoreactivity in nonischemic brain; however, PPAR‐γ expression dramatically increased in ischemic neurons, peaking 24 h following middle cerebral artery occlusion. Interestingly, we found that in both vehicle‐ and agonist‐treated brains, DNA binding was reduced in the ischemic hemisphere relative to the contralateral hemisphere. Expression of a PPAR‐γ target gene, lipoprotein lipase, was also reduced in ischemic relative to nonischemic brain. Both DNA binding and lipoprotein lipase expression were increased by the addition of the PPAR‐γ agonist rosiglitazone. Finally, we found that rosiglitazone‐mediated protection after stroke was reversed by the PPAR‐γ antagonist T0070907. Interestingly, infarction size was also increased by T0070907 in the absence of PPAR‐γ agonist, suggesting that endogenous PPAR‐γ ligands may mitigate the effects of cerebral ischemia.
The vasopressin‐induced excitation of hypoglossal and facial motoneurons in young rats is mediated by V1a but not V1b receptors, and is independent of intracellular calcium signalling
Authors: Reymond‐Marron I. , Tribollet E. , Raggenbass M. 
Published: September 2006

AbstractAs a hormone, vasopressin binds to three distinct receptors: V1a and V1b receptors, which induce phospholipase‐Cβ (PLCβ) activation and Ca2+ mobilization; and V2 receptors, which are coupled to adenylyl cyclase. V1a and V1b receptors are also present in neurons. In particular, hypoglossal (XII) and facial (VII) motoneurons are excited following vasopressin‐V1a receptor binding. The aim of the present study was double: (i) to determine whether V1b receptors contribute to the excitatory effect of vasopressin in XII and VII motoneurons; and (ii) to establish whether the action of vasopressin on motoneurons is mediated by Ca2+ signalling. Patch‐clamp recordings were performed in brainstem slices of young rats. Vasopressin depolarized the membrane or generated an inward current. By contrast, [1‐deamino‐4‐cyclohexylalanine] arginine vasopressin (d[Cha4]AVP), a V1b agonist, had no effect. The action of vasopressin was suppressed by Phaa‐d‐Tyr(Et)‐Phe‐Gln‐Asn‐Lys‐Pro‐Arg‐NH2, a V1a antagonist, but not by SSR149415, a V1b antagonist. Thus, the vasopressin‐induced excitation of brainstem motoneurons was exclusively mediated by V1a receptors. Light microscopic autoradiography failed to detect V1b binding sites in the facial nucleus. In motoneurons loaded with GTP‐γ‐S, a non‐hydrolysable analogue of GTP, the effect of vasopressin was suppressed, indicating that neuronal V1a receptors are G‐protein‐coupled. Intracellular Ca2+ chelation suppressed a Ca2+‐activated potassium current, but did not affect the vasopressin‐evoked current. H7 and GF109203, inhibitors of protein kinase C, were without effect on the vasopressin‐induced excitation. U73122 and D609, PLCβ inhibitors, were also without effect. Thus, excitation of brainstem motoneurons by V1a receptor activation is probably mediated by a second messenger distinct from that associated with peripheral V1a receptors.
CA3 NMDA receptors are crucial for rapid and automatic representation of context memory
Authors: Cravens Catherine J. , Vargas‐Pinto Noelia , Christian Kimberly M. , Nakazawa Kazu 
Published: September 2006

AbstractIt is argued that the hippocampus contributes to acquisition of context‐specific memory although neural mechanisms have not been clarified. To evaluate the role of CA3 in context‐specific memory, we developed one‐trial context discrimination tasks to test acquisition and retrieval of contextual memory in CA3 pyramidal cell‐restricted N‐methyl‐d‐aspartate (NMDA) receptor knockout mice. Mutants were unable to discriminate conditioned and no‐shock contexts 3 h after one‐trial avoidance training. These phenotypes were not evident 24 h after one‐trial training or 3 h after multi‐trial training. Following one‐trial contextual fear conditioning, mutants showed a selective deficit in context discrimination during a retention test 3 h after acquisition, although overall freezing levels were similar to those of the control mice. As in the avoidance task, this context discrimination impairment was not observed 24 h after initial conditioning. Interestingly, extending the post‐shock period to 3 min during the one‐trial fear conditioning task eliminated the discrimination deficit observed at the 3 h retention interval. These results suggest that: (i) impaired rapid context discrimination during the recall test is dependent on the duration of post‐shock period during conditioning; (ii) CA3 NMDA receptors are critically involved in rapid and automatic formation of a unified context memory representation from the sensory information; (iii) CA3 NMDA receptors support contextual pattern separation; (iv) fear memory to foot‐shock is acquired without CA3 NMDA receptors. It appears that rapid and automatic context memory representations from one‐time experience are mediated, at least in part, by CA3 NMDA receptors.
Effects of early life stress on adult male aggression and hypothalamic vasopressin and serotonin
Authors: Veenema Alexa H. , Blume Annegret , Niederle Daniela , Buwalda Bauke , Neumann Inga D. 
Published: September 2006

AbstractEarly life stress in humans enhances the risk for psychopathologies, including excessive aggression and violence. In rodents, maternal separation is a potent early life stressor inducing long‐lasting changes in emotional and neuroendocrine responsiveness to stress, associated with depression‐ and anxiety‐like symptoms. However, effects of maternal separation on adult male aggression and underlying neurobiological mechanisms remain unknown. Therefore, we investigated the effects of maternal separation on adult intermale aggression in Wistar rats and on hypothalamic arginine vasopressin (AVP) mRNA expression, and AVP and serotonin (5‐HT) immunoreactivity, as both AVP and 5‐HT have been implicated in stress‐coping and aggression. We showed that maternal separation induced depression‐like behaviour (increased immobility) and higher adrenocorticotropin hormone responses to an acute stressor (forced swimming). Intermale aggression (lateral threat, offensive upright and keep down) was significantly higher in maternally separated rats compared with control rats. AVP mRNA expression and AVP immunoreactivity were higher in the hypothalamic paraventricular and supraoptic nuclei upon resident‐intruder test exposure, whereas 5‐HT immunoreactivity was decreased in the anterior hypothalamus of maternally separated rats. Moreover, 5‐HT immunoreactivity in the anterior hypothalamus and supraoptic nucleus correlated negatively with aggression. These findings show that exposure to early life stress increases adult male aggression in an animal model of maternal separation. Furthermore, the maternal separation‐induced changes in hypothalamic AVP and 5‐HT systems may underlie these behavioural alterations.
Smoking and structural brain deficits: a volumetric MR investigation
Authors: Gallinat Jürgen , Meisenzahl Eva , Jacobsen Leslie K. , Kalus Peter , Bierbrauer Jeffrey , Kienast Thorsten , Witthaus Henning , Leopold Karolina , Seifert Frank , Schubert Florian , Staedtgen Mario 
Published: September 2006

AbstractGrowing evidence from animal studies indicates brain‐damaging properties of nicotine exposure. Investigations in humans found a wide range of functional cerebral effects of nicotine and cigarette smoking, but studies focusing on brain damage are sparse. In 22 smokers and 23 never‐smokers possible differences of the cerebral structures were investigated using magnetic resonance imaging and voxel‐based morphometry. Significantly smaller grey matter volume and lower grey matter density (P = 0.05, corrected) were observed in the frontal regions (anterior cingulate, prefrontal and orbitofrontal cortex), the occipital lobe and the temporal lobe including parahippocampal gyrus, in smokers than in never‐smokers. Group differences of either grey matter volume or grey matter density were also found in the thalamus, cerebellum and substantia nigra, among other regions. Smokers did not show greater volumes than never‐smokers in any cerebral region. Magnitude of lifetime exposure to tobacco smoke (pack‐years) was inversely correlated with volume of frontal and temporal lobes and cerebellum (P = 0.001, uncorrected). The data indicate structural deficits of several cortical and subcortical regions in smokers relative to never‐smokers. The topographic profile of the group differences show some similarities to brain networks known to mediate drug reinforcement, attention and working memory processing. The present findings may explain in part the frequently reported cognitive dysfunctions in chronic cigarette consumers.
Localization of heterotypic gap junctions composed of connexin45 and connexin36 in the rod pathway of the mouse retina
Authors: Dedek Karin , Schultz Konrad , Pieper Mario , Dirks Petra , Maxeiner Stephan , Willecke Klaus , Weiler Reto , Janssen‐Bienhold Ulrike 
Published: September 2006

AbstractThe primary rod pathway in mammals contains gap junctions between AII amacrine cells and ON cone bipolar cells which relay the rod signal into the cone pathway under scotopic conditions. Two gap junctional proteins, connexin36 (Cx36) and connexin45 (Cx45), appear to play a pivotal role in this pathway because lack of either protein leads to an impairment of visual transmission under scotopic conditions. To investigate whether these connexins form heterotypic gap junctions between ON cone bipolar and AII amacrine cells, we used newly developed Cx45 antibodies and studied the cellular and subcellular distribution of this protein in the mouse retina. Specificity of the Cx45 antibodies was determined, among others, by Western blot and immunostaining of mouse heart, where Cx45 is abundantly expressed. In mouse retina, Cx45 immunosignals were detected in both plexiform layers and the ganglion cell layer. Double staining for Cx45 and Cx36 revealed a partial overlap in the punctate patterns in the ON sublamina of the inner plexiform layer of the retina. We quantified the distributions of these two connexins in the ON sublamina, and detected 30% of the Cx45 signals to be co‐localized with or in close apposition to Cx36 signals. Combining immunostaining and intracellular dye injection revealed an overlap or tight association of Cx36 and Cx45 signals on the terminals of injected AII amacrine and two types of ON cone bipolar cells. Our results provide direct evidence for heterotypic gap junctions composed of Cx36 and Cx45 between AII amacrine and certain types of ON cone bipolar cells.
ERK1/2 but not p38 MAP kinase is essential for the long‐term depression in mouse cerebellar slices
Authors: Ito‐Ishida Aya , Kakegawa Wataru , Yuzaki Michisuke 
Published: September 2006

AbstractMitogen‐activated protein kinase (MAPK) cascade is essential for synaptic plasticity and learning. In the hippocampus, three different MAPK subfamilies, extracellular signal‐regulated kinase 1/2 (ERK1/2), p38 MAPK and c‐Jun NH2‐terminal protein kinase (JNK), selectively regulate activity‐dependent glutamate receptor trafficking during long‐term potentiation (LTP), long‐term depression (LTD), and depotentiation after LTP, respectively. Although LTP and LTD at cerebellar parallel fibre (PF)–Purkinje cell synapses are thought to be controlled by glutamate receptor trafficking, the involvement of MAPK subfamilies has not been systemically studied in cerebellar slice preparations. To clarify the role of the MAPK cascade in cerebellar LTD, we performed biochemical and electrophysiological analyses using ICR mouse cerebellar slices. Immunoblot analyses using phosphorylation‐specific antibodies for MAPKs revealed that among the three MAPKs, ERK1/2 was specifically activated by phorbol ester, which could induce LTD in cerebellar slices. In addition, U0126, a specific inhibitor of the MAPK kinase‐ERK1/2 pathway, abrogated the induction of LTD in cerebellar slices, whereas SB203580 and SP600125, specific inhibitors of p38 MAPK and JNK, respectively, had no effect. Although metabotropic glutamate receptor 1 (mGluR1) has been suggested as a possible downstream target of ERK1/2 in cell‐culture preparations, mGluR1‐activated slow excitatory postsynaptic currents (EPSCs) were not affected by U0126 treatment in slices. These findings indicate that unlike hippocampal LTD mediated by p38 MAPK, glutamate receptor trafficking during cerebellar LTD was regulated by a distinct mechanism involving ERK1/2 in slice preparations.
A double dissociation of dorsal and ventral hippocampal function on a learning and memory task mediated by the dorso‐lateral striatum
Authors: McDonald Robert J. , Jones Jana , Richards Blake , Hong Nancy S. 
Published: September 2006

AbstractThe objectives of this research were to further delineate the neural circuits subserving proposed memory‐based behavioural subsystems in the hippocampal formation. These studies were guided by anatomical evidence showing a topographical organization of the hippocampal formation. Briefly, perpendicular to the medial/lateral entorhinal cortex division there is a second system of parallel circuits that separates the dorsal and ventral hippocampus. Recent work from this laboratory has provided evidence that the hippocampus incidentally encodes a context‐specific inhibitory association during acquisition of a visual discrimination task. One question that emerges from this dataset is whether the dorsal or ventral hippocampus makes a unique contribution to this newly described function. Rats with neurotoxic lesions of the dorsal or ventral hippocampus were assessed on the acquisition of the visual discrimination task. Following asymptotic performance they were given reversal training in either the same or a different context from the original training. The results showed that the context‐specific inhibition effect is mediated by a circuit that includes the ventral but not the dorsal hippocampus. Results from a control procedure showed that rats with either dorso‐lateral striatum damage or dorsal hippocampal lesions were impaired on a tactile/spatial discrimination. Taken together, the results represent a double dissociation of learning and memory function between the ventral and dorsal hippocampus. The formation of an incidental inhibitory association was dependent on ventral but not dorsal hippocampal circuitry, and the opposite dependence was found for the spatial component of a tactile/spatial discrimination.
Retinotopic distribution of chromatic responses in human primary visual cortex
Authors: Vanni S. , Henriksson L. , Viikari M. , James A. C. 
Published: September 2006

AbstractIn non‐human primates at least three anatomically and functionally distinct channels convey signals from the retina to the primary visual cortex (V1). Two of these channels, the parvocellular and the koniocellular, are sensitive to chromatic contrasts and form the basis of color vision. In humans, common phylogenetic history with other primates and psychophysical experiments suggest identical retinocortical mechanisms but separate evaluation of the distinct anatomical channels has been difficult because signals are already combined in V1. We studied the spatial distribution of activation to chromatic stimuli along the two opponent chromatic axes in human V1 with multifocal functional magnetic resonance imaging. The signal strength was quantified from three experiments with stimuli up to 20° eccentricity. The hypothesis was that, although the parvo‐ and koniocellular signals are mixed in V1, distinct distributions of signal strength would be evident. We found that whereas different conditions activated the same areas of cortex, indicating that they have identical magnification factors, the responses to red/green stimulation were stronger close to the fovea whereas the blue/yellow responses were much less diminished with increasing eccentricity. Both chromatic axes showed saturating contrast response functions. Our measure directly from human V1 is in line with earlier psychophysical studies suggesting relatively stronger parvocellular channel representation close to the fovea, and more uniform distribution of the koniocellular and achromatic channels. In addition, our study presents a way to rapidly quantify retinotopic signal transmission in distinct retinocortical pathways of individual subjects.
Dendritic excitability and calcium signalling in the mitral cell distal glomerular tuft
Authors: Zhou Zhishang , Xiong Wenhui , Zeng Shaoqun , Xia Andong , Shepherd Gordon M. , Greer Charles A. , Chen Wei R. 
Published: September 2006

AbstractThe processing of odour information starts at the level of the olfactory glomerulus, where the mitral cell distal dendritic tuft not only receives olfactory nerve sensory input but also generates dendrodendritic output to form complicated glomerular synaptic circuits. Analysing the membrane properties and calcium signalling mechanisms in these tiny dendritic branches is crucial for understanding how the glomerular tuft transmits and processes olfactory signals. With the use of two‐photon Ca2+ imaging in rat olfactory bulb slices, we found that these distal dendritic branches displayed a significantly larger Ca2+ signal than the soma and primary dendrite trunk. A back‐propagating action potential was able to trigger a Ca2+ increase throughout the entire glomerular tuft, indicative of the presence of voltage‐gated Ca2+ conductances in all branches at different levels of ramification. In response to a train of action potentials evoked at 60 Hz from the soma, the tuft Ca2+ signal increased linearly with the number of action potentials, suggesting that these glomerular branches were able to support repetitive penetration of Na+ action potentials. When a strong olfactory nerve excitatory input was paired with an inhibition from mitral cell basal dendrites, a small spike‐like fast prepotential was revealed at both the soma and distal primary dendrite trunk. Corresponding to this fast prepotential was a Ca2+ increase confined locally within the glomerular tuft. In summary, the mitral cell distal dendritic tuft possesses both Na+ and Ca2+ voltage‐dependent conductances which can mediate glomerular Ca2+ responsiveness critical for dendrodendritic output and synaptic plasticity.