bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stage‐specific activity patterns affect motoneuron axonal retraction and outgrowth during the metamorphosis of Manduca sexta
Authors: Duch C. , Mentel T. 
Published: December 2004

AbstractDuring the metamorphosis of holometabolous insects, most larval muscles and sensory neurons are replaced by new adult elements, whereas most motoneurons persist and are remodelled to serve new adult functions. In Manduca sexta, the formation of the anlagen of the adult dorsal longitudinal flight muscle (DLM) is characterized by retraction of axonal terminals and dendrites of persisting larval motoneurons, partial target muscle degeneration and myoblast accumulation during late larval life. Most of these structural changes have been attributed to hormonal control, not only because ecdysteroids govern metamorphosis, but also because motoneurons express ecdysteroid receptors and experimental manipulations of ecdysteroid titres perturb normal development. To test whether activity‐dependent mechanisms also came into play, chronic extracellular recordings were conducted in vivo from the five future DLM motoneurons throughout the last 3 days of larval life. Motoneuron activity is regulated developmentally. The types of motoneurons recruited, the number of motor spikes and the duration of bursts change in a stereotypical fashion during different stages, indicating an internal control of motor activity. A characteristic cessation in the activity of the five future DLM motoneurons coincides in time with the retraction of their dendrites and their terminal arborizations, whereas their activation during ecdysis coincides with the onset of new outgrowth. Inducing advanced activity by stimulating the motoneurons selectively with ecdysis‐like patterns results in significant outgrowth of their terminal arborizations. Therefore, steroids might act in concert with activity‐dependent mechanisms during the postembryonic modifications of neuromuscular systems.
Direct and indirect interactions between cannabinoid CB1 receptor and group II metabotropic glutamate receptor signalling in layer V pyramidal neurons from the rat prefrontal cortex
Authors: Barbara Jean‐Gaël , Auclair Nathalie , Roisin Marie‐Paule , Otani Satoru , Valjent Emmanuel , Caboche Jocelyne , Soubrie Philippe , Crepel Francis 
Published: December 2004

AbstractAt proximal synapses from layer V pyramidal neurons from the rat prefrontal cortex, activation of group II metabotropic glutamate receptors (group II mGlu) by (2S,2′R,3′R)‐2‐(2′,3′‐dicarboxycyclopropyl) glycine (DCG IV) induced a long‐lasting depression of excitatory postsynaptic currents. Paired‐pulse experiments suggested that the depression was expressed presynaptically. Activation of type 1 cannabinoid receptors (CB1) by WIN 55,212‐2 occluded the DCG IV‐induced depression in a mutually occlusive manner. At the postsynaptic level, WIN 55,212‐2 and DCG IV were also occlusive for the activation of extracellular signal‐regulated kinase. The postsynaptic localization of active extracellular signal‐regulated kinase was confirmed by immunocytochemistry after activation of CB1 receptors. However, phosphorylation of extracellular signal‐regulated kinase in layer V pyramidal neurons was dependent on the activation of N‐methyl‐d‐aspartate receptors, consequently to a release of glutamate in the local network. Group II mGlu were also shown to be involved in long‐term changes in synaptic plasticity induced by high frequency stimulations. The group II mGlu antagonist (RS)‐alpha‐methylserine‐O‐phosphate monophenyl ester (MSOPPE) favoured long‐term depression. However, no interaction was found between MSOPPE, WIN 55,212‐2 and the CB1 receptor antagonist SR 141716A on the modulation of long‐term depression or long‐term potentiation and the effects of these drugs were rather additive. We suggest that CB1 receptor and group II mGlu signalling may interact through a presynaptic mechanism in the induction of a DCG IV‐induced depression. Postsynaptically, an indirect interaction occurs for activation of extracellular signal‐regulated kinase. However, none of these interactions seem to play a role in synaptic plasticities induced with high frequency stimulations.
Basolateral amygdala modulation of the nucleus accumbens dopamine response to stress: role of the medial prefrontal cortex
Authors: Stevenson C. W. , Gratton A. 
Published: December 2004

AbstractThe basolateral amygdala (BLA) is involved in modulating affective responses to stress and, along with the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), receives a stress‐responsive dopamine (DA) projection from the ventral tegmental area. The present study was undertaken to characterize the role of BLA DA D1 and D2/D3 receptor subtypes in modulating the NAc and mPFC DA responses to stress. Voltammetry was used to monitor, in freely behaving rats, stress‐induced DA release in NAc or mPFC after injection of D1 (SCH 23390) or D2/D3 (raclopride) receptor antagonist into BLA. Intra‐BLA SCH 23390 injection potentiated stress‐induced NAc DA release but attenuated the mPFC DA stress response; raclopride had no effect on either the NAc or mPFC DA responses to stress. Based on these results, we also examined the possibility that BLA can indirectly modulate the NAc DA stress response via its projection to mPFC. To do so we studied the effects of intra‐mPFC co‐administration of D1 (SKF 38393) and D2/D3 (quinpirole) receptor agonists on the potentiated NAc DA stress response resulting from intra‐BLA SCH 23390 injection. Alone, mPFC D1 and D2/D3 receptor co‐activation had no effect on stress‐induced NAc DA release, but did prevent the potentiated NAc DA stress response produced by BLA D1 receptor blockade. These findings indicate that BLA DA modulates the NAc and mPFC DA stress responses via activation of the D1 receptor subtype. They also suggest that BLA DA modulates stress‐induced NAc DA release indirectly by modulating the mPFC DA response to stress.
Neuronal lineage‐specific induction of phospholipase Cε expression in the developing mouse brain
Authors: Wu Dongmei , Tadano Makoto , Edamatsu Hironori , Masago‐Toda Misa , Yamawaki‐Kataoka Yuriko , Terashima Toshio , Mizoguchi Akira , Minami Yasuhiro , Satoh Takaya , Kataoka Tohru 
Published: December 2004

AbstractPhospholipase C is a key enzyme of intracellular signal transduction in the central nervous system. We and others recently discovered a novel class of phospholipase C, phospholipase Cε, which is regulated by Ras and Rap small GTPases. As a first step toward analysis of its function, we have examined the spatial and temporal expression patterns of phospholipase Cε during mouse development byin situhybridization and immunohistochemistry. Around embryonic day 10.5, abundant expression of phospholipase Cε is observed specifically in the outermost layer of the neural tube. On embryonic day 12 and later, it is observed mainly in the marginal zone of developing brain and spinal cord as well as in other regions undergoing neuronal differentiation, such as the retina and olfactory epithelium. The phospholipase Cε‐expressing cells almost invariably express microtubule‐associated protein 2, but hardly express nestin or glial fibrillary acidic protein, indicating that the expression of phospholipase Cε is induced specifically in cells committed to the neuronal lineage. The expression of phospholipase Cε persists in the terminally differentiated neurons and exhibits no regional specificity. Further, anin vitroculture system of neuroepithelial stem cells is employed to show that abundant expression of phospholipase Cε occurs in parallel with the loss of nestin expression as well as with the induction of microtubule‐associated protein 2 expression and neuronal morphology. Also, glial fibrillary acidic protein‐positive glial lineage cells do not exhibit the high phospholipase Cε expression. These results suggest that the induction of phospholipase Cε expression may be a specific event associated with the commitment of the neural precursor cells to the neuronal lineage.
Separate processing mechanisms for encoding of geometric and landmark information in the avian hippocampus
Authors: Tommasi Luca , Gagliardo Anna , Andrew Richard J. , Vallortigara Giorgio 
Published: December 2004

AbstractDomestic chicks bilaterally or unilaterally lesioned to the hippocampus were trained to search for food hidden beneath sawdust by ground‐scratching in the centre of a large enclosure, the correct position of food being indicated by a local landmark in the absence of any extra‐enclosure visual cues. At test, the landmark was removed or displaced at a distance from its original position. Results showed that sham‐operated chicks and chicks with a lesion of the left hippocampus searched in the centre, relying on large‐scale geometric information provided by the enclosure, whereas chicks with a lesion of either the right hippocampus or both hippocampi were completely disoriented (landmark removed) or searched close to the landmark shifted from the centre (landmark displaced). These results indicate that encoding of geometric features of an enclosure occurs in the right hippocampus even when local information provided by a landmark would suffice to localize the goal; encoding based on local information, in contrast, seems to occur outside the hippocampus. These findings provide evidence that the left and right avian hippocampi play different roles in spatial cognition, a phenomenon which had been documented previously only for the human hippocampus.
A hot spot for hotfoot mutations in the gene encoding the δ2 glutamate receptor
Authors: Wang Ying , Matsuda Shinji , Drews Valerie , Torashima Takashi , Meisler Miriam H. , Yuzaki Michisuke 
Published: December 2004

AbstractThe orphan glutamate receptor δ2 is selectively expressed in Purkinje cells and plays a crucial role in cerebellar functions. Recently, ataxia in the hotfoot mouse ho4J was demonstrated to be caused by a deletion in the δ2 receptor gene (Grid2) removing the N‐terminal 170 amino acids of the δ2 receptor. To understand how δ2 receptors function, we characterized mutations in eight additional spontaneously occurring hotfoot alleles of Grid2. The mouse Grid2 gene consists of 16 exons, spanning approximately 1.4 Mb. Genomic DNA analysis showed that seven hotfoot mutants had a deletion of one or more exons encoding the N‐terminal domain of δ2 receptors. The exception is ho5J, which has a point mutation in exon 12. Deletions in ho7J, ho9J, ho11J and ho12J mice result in the in‐frame deletion of between 40 and 95 amino acids. Expression of constructs containing these deletions in HEK293 cells resulted in protein retention in the endoplasmic reticulum or cis‐Golgi without transport to the cell surface. Coimmunoprecipitation assays indicated that these deletions also reduce the intermolecular interaction between individual δ2 receptors. These results indicate that the deleted N‐terminal regions are crucial for oligomerization of δ2 receptors and their subsequent transport to the cell surface of Purkinje cells. The relatively large size of the Grid2 gene may be one of the reasons why many spontaneous mutations occur in this gene. In addition, the frequent occurrence of in‐frame deletions within the N‐terminal domain in hotfoot mutants suggests the importance of this domain in the function of δ2 receptors.
Aversive conditioning following repeated withdrawal from ethanol and epileptic kindling
Authors: Ripley Tamzin L. , Brown Geraldine , Dunworth Sarah J. , Stephens David N. 
Published: December 2004

AbstractRepeated withdrawal from ethanol, a procedure which resembles amygdala kindling in increasing seizure sensitivity, impairs the acquisition of fear conditioning (Stephens et al., 2001, Eur. J. Neurosci.,14, 2023–31). In contrast, rats previously kindled by repeated electrical stimulation of basolateral amygdala, or repeated administration of pentylenetetrazol, showed increased suppression of operant responding during the presentation of a stimulus conditioned to footshock when conditioning took place several weeks following the kindling experience. Neither form of kindling nor repeated ethanol withdrawal altered taste aversion conditioning, though rats treated chronically with ethanol and given a single withdrawal experience showed enhanced taste aversion conditioning. These results suggest that, despite evidence suggesting a common neuronal mechanism underlying seizure sensitivity following these types of kindling, they differ in their effects on fear conditioning.
Bidirectional synaptic plasticity as a consequence of interdependent Ca2+‐controlled phosphorylation and dephosphorylation pathways
Authors: D'Alcantara Pablo , Schiffmann Serge N. , Swillens Stéphane 
Published: December 2004

AbstractPostsynaptic Ca2+ signals of different amplitudes and durations are able to induce either long‐lasting potentiation (LPT) or depression (LTD). The bidirectional character of synaptic plasticity may result at least in part from an increased or decreased responsiveness of the glutamatergic α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid receptor (AMPA‐R) due to the modification of conductance and/or channel number, and controlled by the balance between the activities of phosphorylation and dephosphorylation pathways. AMPA‐R depression can be induced by a long‐lived Ca2+ signal of moderate amplitude favouring the activation of the dephosphorylation pathway, whereas a shorter but higher Ca2+ signal would induce AMPA‐R potentiation resulting from the preferential activation of the phosphorylation pathway. Within the framework of a model involving calcium/calmodulin‐dependent protein kinase II (CaMKII), calcineurin (PP2B) and type 1 protein phosphatase (PP1), we aimed at delineating the conditions allowing a biphasic U‐shaped relationship between AMPA‐R and Ca2+ signal amplitude, and thus bidirectional plasticity. Our theoretical analysis shows that such a property may be observed if the phosphorylation pathway: (i) displays higher cooperativity in its Ca2+‐dependence than the dephosphorylation pathway; (ii) displays a basal Ca2+‐independent activity; or (iii) is directly inhibited by the dephosphorylation pathway. Because the experimentally observed inactivation of CaMKII by PP1 accounts for this latter characteristic, we aimed at verifying whether a realistic model using reported parameters values can simulate the induction of either LTP or LTD, depending on the time and amplitude characteristics of the Ca2+ signal. Our simulations demonstrate that the experimentally observed bidirectional nature of Ca2+‐dependent synaptic plasticity could be the consequence of the PP1‐mediated inactivation of CaMKII.
Objects automatically potentiate action: an fMRI study of implicit processing
Authors: Grèzes J. , Tucker M. , Armony J. , Ellis R. , Passingham R. E. 
Published: December 2004

AbstractBehavioural data have shown that the perception of an object automatically potentiates motor components (affordances) of possible actions toward that object, irrespective of the subject's intention. We carried out an event‐related fMRI study to investigate the influence of the intrinsic properties of an object on motor responses which were either compatible or incompatible with the action that the object affords. The subjects performed power or precision grip responses based on the categorization of objects into natural or man‐made. The objects were either ‘small’ (usually grasped with a precision grip) or ‘large’ (usually grasped with a power grip). As expected, the motor responses were fastest to objects that afforded the same grip (congruent) and slowest to objects that afforded the other grip (incongruent). Imaging revealed activations which covaried with compatibility in the parietal, dorsal premotor and inferior frontal cortex. We suggest that the greater the difference in reaction times between congruent and incongruent trials, the greater the competition between the action afforded by the object and the action specified by the task, and thus the greater the activation within this network.
Formation of dendritic spines in cultured striatal neurons depends on excitatory afferent activity
Authors: Segal Menahem , Greenberger Varda , Korkotian Eduard 
Published: December 2004

AbstractThe role of afferent innervation in the formation of dendritic spines was studied in cultured rat striatum. The striatum is a unique structure in that it contains highly spiny GABAergic projection neurons, with no known local excitation. Grown alone in culture, striatal neurons did not express spontaneous network activity and were virtually devoid of dendritic spines. Adding GFP‐expressing mouse cortical neurons to the striatal culture caused the appearance of spontaneous and evoked excitatory synaptic currents in the striatal neurons and a 10‐fold increase in the density of spines on their dendrites. This effect was blocked by a continuous presence of TTX in the growth medium, while removal of the drug caused a rapid appearance of spines. Exposure to glutamate, or the presence of cortex‐conditioned medium did not mimic the effect of cortical neurons on formation of spines in the striatal neurons. Also, the cortical innervation did not cause a selective enhancement of survival of specific subtypes of spiny striatal neurons. These experiments demonstrate that excitatory afferents are necessary for the formation of dendritic spines in striatal neurons.
Increased vulnerability to kainic acid‐induced epileptic seizures in mice underexpressing the scaffold protein Islet‐Brain 1/JIP‐1
Authors: Magara Fulvio , Haefliger Jacques‐Antoine , Thompson Nancy , Riederer Beat , Welker Egbert , Nicod Pascal , Waeber Gérard 
Published: December 2004

AbstractIslet‐Brain 1, also known as JNK‐interacting protein‐1 (IB1/JIP‐1) is a scaffold protein mainly involved in the regulation of the pro‐apoptotic signalling cascade mediated by c‐Jun–N‐terminal kinase (JNK). IB1/JIP‐1 organizes JNK and upstream kinases in a complex that facilitates JNK activation. However, overexpression of IB1/JIP‐1 in neurons in vitro has been reported to result in inhibition of JNK activation and protection against cellular stress and apoptosis. The occurrence and the functional significance of stress‐induced modulations of IB1/JIP‐1 levels in vivo are not known. We investigated the regulation of IB1/JIP‐1 in mouse hippocampus after systemic administration of kainic acid (KA), in wild‐type mice as well as in mice hemizygous for the gene MAPK8IP1, encoding for IB1/JIP‐1. We show here that IB1/JIP‐1 is upregulated transiently in the hippocampus of normal mice, reaching a peak 8 h after seizure induction. Heterozygous mutant mice underexpressing IB1/JIP‐1 showed a higher vulnerability to the epileptogenic properties of KA, whereas hippocampal IB1/JIP‐1 levels remained unchanged after seizure induction. Subsequently, an increasing activation of JNK in the 8 h following seizure induction was observed in IB1/JIP‐1 haploinsufficient mice, which also underwent more severe excitotoxic lesions in hippocampal CA3, as assessed histologically 3 days after KA administration. Taken together, these data indicate that IB1/JIP‐1 in hippocampus participates in the regulation of the neuronal response to excitotoxic stress in a level‐dependent fashion.
Calcium‐activated cationic channel in rat sensory neurons
Authors: Cho Hawon , Kim Man Su , Shim Won Sik , Yang Young Duk , Koo Jaeyeon , Oh Uhtaek 
Published: December 2004

AbstractIon channels in sensory neurons are molecular sensors that detect external stimuli and transduce them to neuronal signals. Although Ca2+‐activated nonselective cation (CAN) channels were found in many cell types, CAN channels in mammalian sensory neurons are not yet identified. In the present study, we describe an ion channel that is activated by intracellular Ca2+ in cultured rat sensory neurons. Half‐maximal concentration of Ca2+ in activating the CAN channel was approximately 780 µm. The current–voltage relationship of this channel was linear with a unit conductance of 28.8 ± 0.4 pS at −60 mV in symmetrical 140 mm Na+ solution. The CAN channel was permeable to monovalent cations such as Na+, K+, Cs+, and Li+, but poorly permeable to Ca2+. The CAN channel in mammalian sensory neurons was reversibly blocked by intracellular adenine nucleotides, such as ATP, ADP, and AMP. Interestingly, single‐channel currents activated by Ca2+ were blocked by fenamates, such as flufenamic acid, a class of nonsteroidal anti‐inflammatory drugs. Thus, these results suggest that CAN channels in mammalian sensory neurons would participate in modulating nociceptive neural transmission in response to ever‐changing intracellular Ca2+ in the local microenvironment.
Greater orbitofrontal activity predicts better memory for faces
Authors: Frey Stephen , Petrides Michael 
Published: December 2004

AbstractHaving demonstrated recently that the orbitofrontal cortex is selectively involved when novel abstract visual information is encoded, we investigated whether the same orbitofrontal area would be activated during the encoding of novel human faces. The present positron emission tomography study demonstrated that area 11 in the right orbitofrontal region, which is directly linked to the medial temporal lobe, is a critical frontal area selectively activated when normal human subjects are engaged in encoding visually presented faces. Furthermore, better face recognition performance correlated with greater cerebral blood flow specifically in this orbitofrontal area.
Degeneration of sensory outer hair cells following pharmacological blockade of cochlear KCNQ channels in the adult guinea pig
Authors: Nouvian Régis , Ruel Jérôme , Wang Jing , Guitton Matthieu J. , Pujol Rémy , Puel Jean‐Luc 
Published: December 2004

AbstractIn the inner ear, hair cell function is inextricably linked with intracellular potassium homeostasis. KCNQ potassium channels may play an important role by preventing accumulation of potassium in the hair cells. Linopirdine, a tool useful in targeting native or heterologous KCNQ channels, was used to study the role of KCNQ channels in the guinea pig cochlea. When perfused into intact cochlea, linopirdine transiently increases the summating potential and endocochlear potential, suggesting that it alters K+ homeostasis. The concomitant decrease in cochlear microphonic potential and distortion product otoacoustic emission amplitude indicates that linopirdine has an effect on the outer hair cells (OHCs). To determine the pathological consequences of the inhibition of cochlear KCNQ channels, we developed a hearing loss model based on a chronic intracochlear perfusion of linopirdine via an osmotic minipump. Ultrastructural analysis reveals that KCNQ channel blockade leads to OHC degeneration. Together, these results demonstrate that KCNQ channels, most probably of the KCNQ4 subtype, are crucial for the function and survival of sensory OHCs. Clinically, KCNQ4 channel dysfunction is known to be associated with the DFNA2 form of nonsyndromic dominant deafness. Our study shows that OHC KCNQ4 dysfunction could contribute to the early (40dB) hearing loss, but not for the profound deafness observed at the final stage of this disease.