bluuebunny/crossref_metadata_2025_split huggingface dataset:
UMODL1/Olfactorin is an extracellular membrane‐bound molecule with a restricted spatial expression in olfactory and vomeronasal neurons
Authors: Di Schiavi Elia , Riano Elena , Heye Babett , Bazzicalupo Paolo , Rugarli Elena I. 
Published: July 2005

AbstractThe olfactory system provides a unique model for developmental neurobiology. Precise targeting of axonal projections from sensory neurons located in the olfactory epithelium to specific neurons in the olfactory bulb establishes a highly refined spatial sensory map. Distinctively, this process is not restricted to embryonic stages, but continues during the entire life of mammals. A number of secreted and membrane molecules have been implicated in guidance and targeting of olfactory sensory neurons. Here we describe olfactorin, the protein product of the mouse Umodl1 gene, as a potential new element in this process. Olfactorin is a secreted modular protein containing several domains typically present in extracellular matrix proteins (EMI, WAP, FNIII, Ca2+‐binding EGF‐like, SEA and ZP domains). By in situ hybridization we find that during embryonic development expression of the Umodl1 gene is detectable only in the olfactory epithelium and vomeronasal organ starting at embryonic day 16.5. At this stage, Umodl1 expression within the olfactory epithelium is punctate, and is restricted to only some of the sensory neurons. At birth and postnatally, expression in these organs continues and involves more neurons. Kallmann syndrome is a genetic disease in which olfactory axons fail to connect to target neurons in the bulb. We tested whether olfactorin might be responsible for an autosomal form of this disease and show that this is not the case. However, based on its domain composition and on the expression in olfactory neurons we suggest that olfactorin may play a role in correct olfactory axon navigation to the brain.
Essential roles of Homer‐1a in homeostatic regulation of pyramidal cell excitability: a possible link to clinical benefits of electroconvulsive shock
Authors: Sakagami Yu , Yamamoto Kenji , Sugiura Shigeki , Inokuchi Kaoru , Hayashi Takuji , Kato Nobuo 
Published: July 2005

AbstractHomer‐1a/Vesl1S, a member of the scaffold protein family Homer/Vesl, is expressed during seizure and serves to reduce seizure susceptibility. Cellular mechanisms for this feedback regulation were studied in neocortex pyramidal cells by injecting Homer‐1a protein intracellularly. The injection reduced membrane excitability as demonstrated in two ways. First, the resting potential was hyperpolarized by 5–10 mV. Second, the mean frequency of spikes evoked by depolarizing current injection was decreased. This reduction of excitability was prevented by applying each of the followings: the calcium chelator BAPTA, the calcium store depletor cyclopiazonic acid (CPA), the insitol‐1,4,5‐trisphosphate receptor (IP3R) blocker heparin, the phospholipase C (PLC) inhibitor U‐73122, the metabotropic glutamate receptor (mGluR) antagonist 2‐methyl‐6‐(phenylethynyl)‐pyridine (MPEP), and the large‐conductance calcium activated potassium channel (BK channel) antagonist charybdotoxin. The small‐conductance calcium activated potassium channel (SK channel) blocker dequalinium was ineffective. These findings suggest that activation of mGluR by Homer‐1a produced IP3, which caused inositol‐induced calcium release and a consequent BK channel opening, thus hyperpolarizing the injected neurons. In slices from rats subjected to electroconvulsive shock (ECS), a comparable reduction of excitability was observed without Homer‐1a injection. The ECS‐induced reduction of excitability was abolished by MPEP, charybdotoxin, heparin or BAPTA. Intracellular injection of anti‐Homer‐1a antibody was suppressive as well, but anti‐Homer‐1b/c antibody was not. We propose that ECS‐induced Homer‐1a stimulated the same pathway as did the injected Homer‐1a, thereby driving a feedback regulation of excitability.
Two‐way active avoidance training‐specific increases in phosphorylated cAMP response element‐binding protein in the dorsal hippocampus, amygdala, and hypothalamus
Authors: Saha Subhash , Datta Subimal 
Published: July 2005

AbstractPrevious studies have demonstrated that the activation of pontine‐wave (P‐wave) generating cells in the brainstem during post‐training rapid eye movement (REM) sleep is critical for the consolidation of memory for two‐way active avoidance (TWAA) learning in the rat. Here, using immunocytochemistry, we investigated the spatio‐temporal distribution of CREB phosphorylation within different parts of the dorsal hippocampus, amygdala, and hypothalamus following a session of TWAA training in the rat. We show that the TWAA training trials increased phosphorylation of CREB (p‐CREB) in the dorsal hippocampus, amygdala, amygdalo‐hippocampal junction (AHi), and hypothalamus. However, the time intervals leading to training‐induced p‐CREB activity were different for different regions of the brain. In the dorsal hippocampus, p‐CREB activity was maximal at 90 min and this activity disappeared by 180 min. In the AHi, activity of the p‐CREB peaked by 180 min and disappeared by 360 min. In the amygdala, the p‐CREB activity peaked at 180 min and still remained higher than the control at the 360 min interval. In the hypothalamus, at 90 min p‐CREB activity was present only in the ventromedial hypothalamus; however, by 180 min this p‐CREB activity was also present in the dorsal hypothalamus, perifornical area, and lateral hypothalamus. By 360 min, p‐CREB activity disappeared from the hypothalamus. This TWAA training trials‐induced spatiotemporal characteristic of CREB phosphorylation, for the first time, suggests that REM sleep P‐wave generator activation‐dependent memory processing involves different parts of the dorsal hippocampus, amygdala, and hypothalamus.
Anterior cingulate error‐related activity is modulated by predicted reward
Authors: Amiez Céline , Joseph Jean‐Paul , Procyk Emmanuel 
Published: July 2005

AbstractLearning abilities depend on detection and exploitation of errors. In primates, this function involves the anterior cingulate cortex. However, whether anterior cingulate error‐related activity indicates occurrence of inappropriate responses or results from other computations is debated. Here we have tested whether reward‐related parameters modulate error‐related activity of anterior cingulate neurons. Recordings in monkeys performing stimulus–reward associations and preliminary data obtained with a problem‐solving task revealed major properties of error‐related unit activity: (i) their amplitude varies with the amount of predicted reward or the proximity to reward delivery; (ii) they appear both after execution and performance errors; (iii) they do not indicate which error occurred or which correction to make; and (iv), importantly, the activity of these neurons also increases following an external signal indicating the necessity to shift response. Hence, we conclude that anterior cingulate ‘error’ activity might represent a negative deviation from a predicted goal, and does not only reflect error detection but signals events interrupting potentially rewarded actions.
Developmental downregulation of low‐voltage‐activated Ca2+ channels in Cajal‐Retzius cells of the mouse visual cortex
Authors: Kirmse Knut , Grantyn Rosemarie , Kirischuk Sergei 
Published: July 2005

AbstractCajal‐Retzius (CR) cells have been demonstrated to fulfil an important secretory function in the developing neocortex. On the other hand, the contribution of CR cell electrical activity during cortex development is still unclear. Using the whole‐cell patch‐clamp technique, we studied low‐voltage‐activated (LVA) Ca2+ channels in CR cells in the layer I of the mouse visual cortex. CR cells were found to display a transient Ca2+ current (IT) in response to a depolarization step from −100 mV to −40 mV. IT showed: (i) typical for LVA Ca2+ channels voltage dependence of activation (half‐activation at −55 mV) and inactivation (half‐inactivation at −76 mV); (ii) fast activation and inactivation kinetics, with time constants of 1.4 and 28 ms, respectively, at −40 mV; (iii) fast recovery from steady‐state inactivation (time constant: 290 ms); (iv) a complete block by 1 µm mibefradil; and (v) a partial block (to 55%) by 100 µm Ni2+. The density of IT dramatically decreased between postnatal day (P) 1 and P9. Immunostaining demonstrated the presence and postnatal downregulation of the α1G‐subunit of LVA Ca2+ channels in CR cells. Experiments performed in the current‐clamp mode revealed that mibefradil delayed an action potential generation in response to a suprathreshold depolarizing current at P1, but not at P8–9. We suggest that LVA Ca2+ channels might influence CR cell excitability during the first postnatal week and thereby contribute to the shaping of synaptic connectivity in the neocortical layer I.
Primary afferent nociceptor mechanisms mediating NGF‐induced mechanical hyperalgesia
Authors: Malik‐Hall Misbah , Dina Olayinka A. , Levine Jon D. 
Published: July 2005

AbstractThe underlying mechanism for nerve growth factor (NGF) evoked pain and long‐lasting mechanical hyperalgesia remains poorly understood. Using intrathecal antisense against the NGF receptor, receptor tyrosine kinase (TrkA), we found NGF to act at the primary afferent nociceptor directly in the Sprague–Dawley rat. Inhibitors of the three major pathways for TrkA receptor signalling, extracellular signal‐related kinase (ERK)/mitogen‐activated protein kinase kinase (MEK) (ERK/MEK), phosphatidylinositol 3‐kinase (PI3K), and phospholipase Cγ (PLCγ) all attenuate NGF‐induced hyperalgesia. Although inhibitors of kinases downstream of PI3K and PLCγ[glycogen synthetase kinase 3 (GSK3), calmodulin‐dependent protein kinase II (CAMII‐K) or protein kinase C (PKC)] do not reduce mechanical hyperalgesia, hyperalgesia induced by activation of PI3K was blocked by ERK/MEK inhibitors, suggesting cross‐talk from the PI3K to the ERK/MEK signalling pathway. As integrins have been shown to modulate epinephrine and prostaglandin E2‐induced hyperalgesia, we also evaluated a role for integrins in NGF‐induced mechanical hyperalgesia using β1‐integrin‐specific antisense or antibodies.
Prolongation and enhancement of γ‐aminobutyric acidA receptor mediated excitation by chronic treatment with estradiol in developing rat hippocampal neurons
Authors: Nuñez Joseph L. , Bambrick Linda L. , Krueger Bruce K. , McCarthy Margaret M. 
Published: July 2005

AbstractGABAA receptor activation during brain development is a critical source of excitation. This is due to the positive equilibrium potential for chloride relative to resting membrane potential, resulting in membrane depolarization sufficient to open voltage sensitive calcium channels. The gonadal steroid estradiol has pronounced trophic effects on the developing hippocampus, promoting cell survival and synaptogenesis. In the current study, we investigated the effect of estradiol on GABAA receptor‐mediated calcium transients in cultured neonatal hippocampal neurons, from Sprague–Dawley rats, using the calcium sensitive dye, Fura‐2‐AM. Treatment of hippocampal neurons with physiological levels of estradiol significantly increased the peak amplitude of calcium transients, increased the number of cells responding to the GABAA agonist muscimol with membrane depolarization, and delayed the rate of clearance of free intracellular calcium. These effects were significantly attenuated by pretreatment with the oestrogen receptor antagonist ICI‐182,780. This suggests that estradiol, via its action on the oestrogen receptor, prolongs the developmental duration of depolarizing GABA. Estradiol likely maintains GABA‐mediated excitation by promoting increased protein levels of the active/phosphorylated form of the chloride cotransporter Na+K+2CL– and L‐type voltage sensitive calcium channels containing the α1C subunit. We propose that a component of the trophic effects of estradiol on hippocampal development results from enhanced calcium influx subsequent to GABAA receptor activation.
Distribution and regulation of L‐type calcium channels in deep dorsal horn neurons after sciatic nerve injury in rats
Authors: Dobremez E. , Bouali‐Benazzouz R. , Fossat P. , Monteils L. , Dulluc J. , Nagy F. , Landry M. 
Published: July 2005

AbstractDeep dorsal horn neurons are involved in the processing of nociceptive information in the spinal cord. Previous studies revealed a role of the intrinsic bioelectrical properties (plateau potentials) of deep dorsal horn neuron in neuronal hyperexcitability, indicating their function in pain sensitization. These properties were considered to rely on L‐type calcium currents. Two different isotypes of L‐type calcium channel alpha 1 subunit have been cloned (CaV1.2 and CaV1.3). Both are known to be expressed in the spinal cord. However, no data were available on their subcellular localization. Moreover, possible changes in CaV1.2 and CaV1.3 expression had never been investigated in nerve injury models. Our study provides evidence for a differential expression of CaV1.2 and CaV1.3 subunits in the somato‐dendritic compartment of deep dorsal horn neurons. CaV1.2 immunoreactivity is restricted to the soma and proximal dendrites whereas CaV1.3 immunoreactivity is found in the whole somato‐dendritic compartment, up to distal dendritic segments. Moreover, these specific immunoreactive patterns are also found in electrophysiologically identified deep dorsal horn neurons expressing plateau potentials. After nerve injury, namely total axotomy or partial nerve ligation, CaV1.2 and CaV1.3 expression undergo differential changes, showing up‐ and down‐regulation, respectively, both at the protein and at the mRNA levels. Taken together, our data support the role of L‐type calcium channels in the control of intrinsic biolectrical regenerative properties. Furthermore, CaV1.2 and CaV1.3 subunits may have distinct and specific roles in sensory processing in the dorsal horn of the spinal cord, the former being most likely involved in long‐term changes after nerve injury.
Tetrodotoxin resets the clock
Authors: Noguchi Takako , Watanabe Kazuto 
Published: July 2005

AbstractIn mammals, circadian rhythms are driven by a pacemaker located in the suprachiasmatic nucleus (SCN) of the hypothalamus. We measured the rhythm of arginine vasopressin release in rat organotypic SCN slices following application of tetrodotoxin (TTX) or N‐methyl‐d‐aspartate (NMDA) at various times throughout the circadian cycle. TTX resets the clock in a manner similar to dark pulses. A 4‐h application of TTX starting in mid subjective day, at around circadian time (CT) 7.0, induced phase advances, while TTX treatment started in early subjective morning, at about CT 2.0, induced phase delays. On the other hand, NMDA resets the clock in a manner similar to a light pulse; that is, NMDA treatment in the early evening induced phase delays while treatment in the late night induced phase advances. The data indicate that deprivation of neuronal firing changes the circadian rhythm.
Food Stamp Benefits and Child Poverty
Authors: Jolliffe Dean , Gundersen Craig , Tiehen Laura , Winicki Joshua 
Published: July 2005

AbstractIn 2000, 8.8 million children lived in households participating in the Food Stamp Program, making this assistance program a crucial component of the social safety net. Despite its importance, little research has examined food stamps' effect on children's overall well‐being. Using the Current Population Survey from 1989 to 2001, we consider the impact of food stamps on three measures of poverty—the headcount, the poverty gap, and the squared poverty gap. We find that in comparison to the headcount measure, food stamp benefits lead to large reductions in the poverty gap and squared poverty gap measures.
Forecast Encompassing as the Necessary Condition to Reject Futures Market Efficiency: Fluid Milk Futures
Authors: Sanders Dwight R. , Manfredo Mark R. 
Published: July 2005

AbstractThe traditional necessary condition for futures market inefficiency is the existence of alternative forecasting methods that produce mean squared forecast errors smaller than the futures market. Here, a more exacting requirement for futures market efficiency is proposed—forecast encompassing. Using the procedure of Harvey and Newbold, multiple forecast encompassing is tested using Chicago Mercantile Exchange fluid milk futures. Time series models and USDA experts provide competing forecasts. Results suggest milk futures do not encompass the information contained in the USDA forecasts at a two‐quarter horizon. While the competing forecasts generate positive revenues, it is unlikely that returns exceed transaction costs in this relatively new market.
Genetically Modified Crops and Product Differentiation: Trade and Welfare Effects in the Soybean Complex
Authors: Sobolevsky Andrei , Moschini GianCarlo , Lapan Harvey 
Published: July 2005

AbstractA partial equilibrium four‐region world trade model for the soybean complex is developed in which Roundup Ready (RR) products are weakly inferior substitutes to conventional ones, RR seeds are priced at a premium, and costly segregation is necessary to separate conventional and biotech products. Solution of the calibrated model illustrates how incomplete adoption of RR technology arises in equilibrium. The United States, Argentina, Brazil, and the Rest of the World (ROW) all gain from the introduction of RR soybeans, although some groups may lose. The impacts of RR production or import bans by the ROW or Brazil are analyzed. U.S. price support helps U.S. farmers, despite hurting the United States and has the potential to improve world efficiency.
The Significance and Insignificance of Demand Analysis in Evaluating Promotion Programs
Authors: Davis George C. 
Published: July 2005

AbstractThe estimated effects of promotion on demand are often small and insignificant. Yet, the estimated effects of promotion on industry profit are often positive and large. This puzzle is explained by demonstrating that (in)significance of promotion in a demand equation does not imply, and is not implied by, (in)significance of promotion in an industry profit equation. A Monte Carlo example is provided. The econometric modeling implications are discussed. The short‐run marginal effect of a dollar of generic beef promotion on slaughter cattle industry profit is estimated to be about $9.84 with a standard error of 3.77 for 1997.
Coupon Redemption and Its Effect on Household Cheese Purchases
Authors: Dong Diansheng , Kaiser Harry M. 
Published: July 2005

AbstractBy endogenizing unit value and coupon redemption, we estimate U.S. household cheese purchase, quality choice, and coupon redemption equations simultaneously. Zero purchases and missing values on coupons and unit values are taken into account in the model to correct for selectivity bias. Correlations among the three equations are found to be significant. Empirical findings show that high‐quality choice significantly decreases cheese purchases, while cheese coupon usage significantly increases purchases. We find that higher income households select higher quality cheese, while larger households choose lower quality cheese. For coupon redemption, we find that African‐American and Hispanic households redeem less, while Asian households have no significant difference compared to Caucasian households.
Somatostatin down‐regulates the expression and release of endozepines from cultured rat astrocytes via distinct receptor subtypes
Authors: Masmoudi Olfa , Gandolfo Pierrick , Tokay Tursonjan , Leprince Jérôme , Ravni Aurélia , Vaudry Hubert , Tonon Marie‐Christine 
Published: July 2005

AbstractEndozepines, a family of regulatory peptides related to diazepam‐binding inhibitor (DBI), are synthesized and released by astroglial cells. Because rat astrocytes express various subtypes of somatostatin receptors (sst), we have investigated the effect of somatostatin on DBI mRNA level and endozepine secretion in rat astrocytes in secondary culture. Somatostatin reduced in a concentration‐dependent manner the level of DBI mRNA in cultured astrocytes. This inhibitory effect was mimicked by the selective sst4 receptor agonist L803‐087 but not by the selective sst1, sst2 and sst3 receptor agonists L779‐591, L779‐976 and L797‐778, respectively. Somatostatin was unable to further reduce DBI mRNA level in the presence of the MEK inhibitor U0126. Somatostatin and the sst1, sst2 and sst4 receptor agonists induced a concentration‐dependent inhibition of endozepine release. Somatostatin and the sst1, sst2 and sst4 receptor agonists also inhibited cAMP formation dose‐dependently. In addition, somatostatin reduced forskolin‐induced endozepine release. H89 mimicked the inhibitory effect of somatostatin on endozepine secretion. In contrast the PLC inhibitor U73122, the PKC activator PMA and the PKC inhibitor calphostin C had no effect on somatostatin‐induced inhibition of endozepine release. The present data demonstrate that somatostatin reduces DBI mRNA level mainly through activation of sst4 receptors negatively coupled to the MAPK pathway, and inhibits endozepine release through activation of sst1, sst2 and sst4 receptors negatively coupled to the adenylyl cyclase/PKA pathway.
Changes in calcineurin expression induced in the rat brain by the administration of antipsychotics
Authors: Rushlow W. J. , Seah Y. H. , Belliveau D. J. , Rajakumar N. 
Published: July 2005

AbstractCalcineurin (CN) was recently identified as a susceptibility gene for schizophrenia as well as showing altered RNA expression levels in the post‐mortem brains of individuals with schizophrenia. CN knockout mice show a number of behaviours associated with schizophrenia, including deficits in sensorimotor gating, suggesting a link between CN and psychosis. Concurrently, we found, using genome screening techniques, that antipsychotics alter CN expression levels. Therefore, western blotting, in situ hybridization, immunocytochemistry and phosphatase assays were employed to determine what effect antipsychotics have on CN. The results indicate that clozapine, risperidone and haloperidol cause substantial reductions in the A subunit of CN but not CN B at both the RNA and protein levels in the striatum and prefrontal cortex. The changes could only be observed after repeated treatment with antipsychotics but not after acute administration. The alterations in CN protein levels were specific to antipsychotics and mediated by D2 dopamine receptor antagonism. However, despite reductions in CN protein levels, the phosphatase activity of CN was significantly elevated after treatment with antipsychotics. Collectively the results suggest that CN may be a common target for antipsychotics and that antipsychotic‐induced alterations in CN may represent one of the mechanisms by which antipsychotics alleviate psychosis.