bluuebunny/crossref_metadata_2025_split huggingface dataset:
Urodynamic effects of α1‐blocker tamsulosin on voiding dysfunction in patients with neurogenic bladder
Authors: KAKIZAKI HIDEHIRO , AMEDA KANAME , KOBAYASHI SHINYA , TANAKA HIROSHI , SHIBATA TAKASHI , KOYANAGI TOMOHIKO 
Published: October 2003

AbstractBackgroud:  The therapeutic role of α‐blockers in the treatment of voiding disorders due to benign prostatic hyperplasia has been extensively examined. To investigate a possible effect of α1‐blocker on urodynamic voiding parameters in patients with neurogenic bladder, we conducted a clinical trial using tamsulosin.Methods:  Twenty‐four patients (14 men and 10 women) ranging from 24 to 82 years of age (mean age 61 years) with neurogenic bladder were analyzed. Urodynamic studies were performed before and after treatment with 0.4 mg tamsulosin daily for 4 weeks.Results:  On uroflowmetry, the average flow rate (from 4.6 ± 3.3 to 6.7 ± 3.0 mL/s, P = 0.04), maximum flow rate (from 9.4 ± 6.8 to 14.1 ± 7.0 mL/s, P = 0.016) and residual urine rate (from 46 ± 29 to 32 ± 21%, P = 0.02) improved significantly. In patients with detrusor contraction during voiding, detrusor opening pressure and detrusor pressure at maximum flow decreased significantly from 69.0 ± 36.2 to 49.2 ± 26.4 cmH2O (P = 0.046) and from 66.7 ± 34.6 to 53.6 ± 26.5 cmH2O (P = 0.007), respectively. On the other hand, in patients with detrusor areflexia, vesical opening pressure (from 78.2 ± 23.4 to 61.6 ± 25.2 cmH2O), or vesical pressure at maximum flow (from 68.6 ± 23.2 to 62.9 ± 25.2 cmH2O) did not change significantly after treatment.Conclusion:  Tamsulosin reduces functional urethral resistance during voiding and improves flow rate in patients with neurogenic bladder. It has more beneficial urodynamic effects in patients with detrusor contraction during voiding than in patients with detrusor areflexia.
Usefulness of tamsulosin hydrochloride and naftopidil in patients with urinary disturbances caused by benign prostatic hyperplasia: A comparative, randomized, two‐drug crossover study
Authors: IKEMOTO ISAO , KIYOTA HIROSHI , OHISHI YUKIHIKO , ABE KAZUHIRO , GOTO HIROKAZU , KISHIMOTO KOUICHI , MIKI KENTA 
Published: October 2003

AbstractBackground:  The aim of the study presented here was to stratify drug therapy for patients with benign prostatic hyperplasia (BPH) displaying various voiding symptoms.Methods:  Two different α1‐adrenoceptor antagonists; tamsulosin hydrochloride (Tam) and naftopidil (Naf ), were administered to 96 patients with BPH for 8 weeks in a crossover study.Results:  With the administration of both drugs, the International Prostate Symptom Score (I‐PSS) significantly decreased and the maximum urinary flow significantly increased. Whereas Naf monotherapy decreased the I‐PSS for storage symptoms, Tam monotherapy decreased the I‐PSS for voiding symptoms. In both the Naf‐to‐Tam and Tam‐to‐Naf groups, crossover was effective when the initial drug was judged subjectively and objectively to have been ineffective. Compliance was acceptable with both drugs.Conclusion:  Our results show that either Naf or Tam can be used to treat patients on the basis of objective and subjective assessment of voiding symptoms. Our findings should be helpful for patient guidance and treatment of BPH.
c‐Src kinase activation regulates preprotachykinin gene expression and substance P secretion in rat sensory ganglia
Authors: Igwe Orisa J. 
Published: October 2003

AbstractIncreased synthesis of substance P (SP) in the dorsal root ganglia (DRG) and enhanced axonal transport to and secretion from the primary afferent sensory neurons might enhance pain signalling in the spinal dorsal horn by modifying pronociceptive pathways. IL‐1β increases SP synthesis by enhancing the expression of preprotachykinin (PPT) mRNA encoding for SP and other tachykinins in the DRG. Stimulation of IL‐1 receptor by IL‐1β may induce the phosphorylation of tyrosine residues in many effector proteins through the activation of p60c‐src kinase. The hypothesis that the synthesis of SP in and secretion from the primary sensory ganglia are regulated by the activation of p60c‐src kinase induced by IL‐1β was tested. Pretreatment of DRG neurons in culture with herbimycin A, genistein or PP2, three structurally different nonreceptor tyrosine kinase inhibitors that act by different mechanisms, decreased the kinase activity of p60c‐src induced by the activation of IL‐1 receptor. PP3, a negative control for the Src family of tyrosine kinase inhibitor PP2 had no effect. Herbimycin A and genistein also decreased IL‐1β‐induced expression of PPT mRNA‐encoding transcripts and the levels of SP‐li synthesized in the cells and secreted into the culture medium in a concentration‐dependent manner. SB 203580 [a p38 mitogen‐activated protein kinase (p38 MAPK) inhibitor] and PD 98059 (a p44/42 MAPK kinase inhibitor) were ineffective in modulating IL‐1β‐induced SP synthesis and secretion, and p60c‐src kinase activity in DRG neurons. Whereas, IL‐1 receptor antagonist and cycloheximide inhibited IL‐1β‐evoked secretion of SP‐like immunoreactivity (SP‐li), actinomycin D decreased it significantly but did not entirely abolish it. These findings show that phosphorylation of specific protein tyrosine residue(s) following IL‐1 receptor activation might play a key role in IL‐1β signalling to modulate PPT gene expression and SP secretion in sensory neurons. In view of the role of SP as an immunomodulator, these studies provide a new insight into neural‐immune intercommunication in pain regulation in the sensory ganglia through the IL‐1β‐induced p60c‐src activation.
Involvement of Nurr1 in specifying the neurotransmitter identity of ventral midbrain dopaminergic neurons
Authors: Smits Simone M. , Ponnio Tiia , Conneely Orla M. , Burbach J. Peter H. , Smidt Marten P. 
Published: October 2003

AbstractThe mesencephalic dopaminergic (mesDA) system is involved in many brain functions including motor control and motivated behaviour, and is of clinical importance because of its implication in psychiatric disorders and Parkinson's disease. Nurr1, a member of the nuclear hormone receptor superfamily of transcription factors, is essential for establishing the dopaminergic phenotype, because expression of tyrosine hydroxylase (TH), the rate‐limiting enzyme in dopamine synthesis, requires Nurr1. In addition, Nurr1 plays an important role in the maintenance of mesDA neurons. Neonatal Nurr1 knockout mice lack expression of the dopamine transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) andl‐aromatic amino acid decarboxylase (AADC) in addition to TH specifically in mesDA neurons. It is unclear whether the lack of expression of these dopaminergic markers is caused by a maintenance defect or whether the induction of these markers depends on Nurr1 expression. To address this problem, the expression of DAT, VMAT2 and AADC was analysed at embryonic day 12.5 and 14.5. Here we demonstrate that induction of VMAT2 and DAT specifically in mesDA neurons requires Nurr1 expression, whereas AADC expression in mesDA neurons is induced independently of Nurr1 function.
Interleukin 1 beta enhances conditioned fear memory in rats: possible involvement of glucocorticoids
Authors: Song Cai , Phillips Anthony G. , Leonard Brian 
Published: October 2003

AbstractCentral administration of 15 ng interleukin (IL)‐1β in the rat significantly enhanced conditioned fear memory assessed by a passive avoidance task, when retested at 24 and 48 h post‐training. Pain threshold was unaffected by 15 ng IL‐1β administration. IL‐1β treatment also increased serum corticosterone. This increase in serum corticosterone was further enhanced in rats given both IL‐1β and footshock. Furthermore, the glucocorticoid receptor antagonist mifepristone blocked IL‐1β‐induced elevation in corticosterone and also attenuated the enhanced conditioned fear memory. Central administration of IL‐1β significantly increased prostaglandin E2 and decreased the anti‐inflammatory cytokine IL‐10 release from whole blood cultures; therefore this treatment appears to be effective in inducing an inflammatory response in both the periphery and the brain. The present study confirms that IL‐1β can enhance conditioned fear memory, an effect which is correlated with changes in glucocorticoid function. This facilitation of defensive behaviour could reflect adaptive responses which may enhance survival during sickness.
Modulation of olfactory learning in young rats through intrabulbar GABAB receptors
Authors: Okutani Fumino , Zhang Jing‐Ji , Otsuka Tomoko , Yagi Fumio , Kaba Hideto 
Published: October 2003

AbstractAfter training with an odour paired with foot shock on postnatal day 11, rat pups show an aversion to the odour in testing on postnatal day 12. The mechanisms underlying this aversive olfactory learning involve disinhibition of mitral/tufted cells in the olfactory bulb by the somatosensory stimulation‐induced activation of centrifugal noradrenergic fibres originating in the locus coeruleus. The activity of mitral/tufted cells is regulated through γ‐aminobutyric acidA (GABAA) receptors in the external plexiform layer and GABAB receptors in the glomerular layer. We have previously presented that aversive olfactory learning in young rats is modulated through GABAA receptors in the olfactory bulb. In the present study we examined the consequence of manipulating GABAB receptors in the olfactory bulb during training. Baclofen, a GABAB receptor agonist when infused into the olfactory bulb during the pairing of an odour with foot shock, prevented aversive olfactory learning in a dose‐dependent manner. Infusion of saclofen, a GABAB receptor antagonist, during training with a citral odour in the absence of foot shock produced aversive responses not only to the odour, but also to strange odours (benzaldehyde and vanillin) not previously presented. Such olfactory aversions were observed even if saclofen was infused without odour exposure. These results suggest that olfactory learning in young rats is modulated through GABAB receptors in the olfactory bulb.
VIP‐containing deep short‐axon cells of the olfactory bulb innervate interneurons different from granule cells
Authors: Gracia‐Llanes Francisco Javier , Crespo Carlos , Blasco‐Ibáñez José Miguel , Marqués‐Marí Ana Isabel , Martínez‐Guijarro Francisco José 
Published: October 2003

AbstractThis study investigates the targets of the population of vasoactive intestinal polypeptide (VIP)‐containing deep short‐axon cells of the rat olfactory bulb (OB), combining single‐ and double‐immunocytochemical approaches under light and electron microscopy. It has been assumed that deep short‐axon cells innervate granule cells in the mammalian OB, but their synaptic connectivity has not been demonstrated to date. Our results indicate that, instead of the accepted scheme of the bulbar circuitry, VIP‐containing deep short‐axon cells are γ‐aminobutyric acid (GABA)ergic interneurons specialized in the selective innervation of other GABAergic deep short‐axon cells. Their axons contact with the perisomatic region and the dendritic portions of subsets of deep short‐axon cells that contain VIP, calbindin D‐28k and neuropeptide Y. Electron microscopy reveals axo‐somatic and axo‐dendritic symmetrical synapses from VIP‐containing boutons. Taken altogether, our data show that the VIP‐containing deep short‐axon cells of the rat OB form an interneuronal network that modulates the function of other interneurons different from granule cells. They might be involved indirectly in the inhibition or disinhibition of principal cells or might participate in the generation of oscillatory activity and in the synchronization of populations of interneurons and, then, of principal cells. Present data demonstrate that modulation of the OB by local circuits is more complex than the simple inhibition from periglomerular cells and granule cells, and remark the importance of considering the contribution of other classes of GABAergic interneurons different from periglomerular cells and granule cells to the bulbar circuitry.
Cannabinoids inhibit the release of [3H]glutamate from rodent hippocampal synaptosomes via a novel CB1 receptor‐independent action
Authors: Köfalvi Attila , Vizi E. Sylvester , Ledent Catherine , Sperlágh Beáta 
Published: October 2003

AbstractIn this study we investigated the effect of cannabinoids on [3H]glutamate release from hippocampal synaptosomes of rat and CB1‐null mutant mouse. In the rat, cannabinoid receptor agonists, i.e. CP55,940 (EC50, 0.84 μm), WIN55,212‐2 (EC50, 3.47 μm), ACEA (EC50, 17.8 μm), and R‐(+)‐methanandamide (EC50, 19.8 μm) concentration‐dependently inhibited the 25‐mm‐K+ depolarization‐evoked release of [3H]glutamate and, among them, WIN55,212‐2 displayed the greatest efficacy. The CB1 receptor antagonists SR141716A (1–5 μm) and AM251 (1 μm) and the VR1 vanilloid receptor antagonist capsazepine (10 μm) did not antagonize the effect of the agonists. SR141716A by itself attenuated the evoked [3H]glutamate release. WIN55,212‐2 inhibited the release of [3H]glutamate in \mathrm{CB}^{\,‐/‐\,}_{1} mice as well. These data demonstrate that the action of cannabinoids on glutamate release in the hippocampus is pharmacologically distinct and independent from the cloned CB1 receptor.
Developmental study of dendritic bundles in layer 1 of the rat granular retrosplenial cortex with special reference to a cell adhesion molecule, OCAM
Authors: Ichinohe Noritaka , Yoshihara Yoshihiro , Hashikawa Tsutomu , Rockland Kathleen S. 
Published: October 2003

AbstractIn the granular retrosplenial cortex (GRS) of adult rats, callosally projecting pyramidal neurons in layer 2 form dendritic bundles, 30–100 µm wide, in layer 1. The distinctness of these bundles makes the GRS an attractive model system for investigating the developmental, microcircuitry, and basic organizational features related to dendritic modularity. In this report, we investigate the developmental time course of the dendritic bundles, visualized by immunohistochemistry for microtubule‐associated protein 2 (MAP2) and glutamate receptor subunits 2/3 (GluR2/3). Bundles in layer 1 are apparent as early as postnatal day 5, first with GluR2/3 and then, from postnatal day 14, with MAP2. As a step toward understanding the mechanisms of dendritic aggregation, we further investigated the ontogeny of expression of the cell adhesion molecule OCAM. OCAM exhibits a patchy distribution in layer 1 from postnatal day 3 to adult, and the regions of weak OCAM immunoreactivity selectively correspond to the dendritic bundles (in both GluR2/3 and MAP2). The periodic geometry of OCAM‐immunoreactive regions, the time course of their appearance and the distinct localization complementary to the bundles support the possibility that this molecule is one contributor to the establishment and maintenance of dendritic modules. The interdigitating relationship between regions of high OCAM immunoreactivity and the dendritic bundles in layer 1 suggests that OCAM may have a repellent influence on the formation of these bundles.
Perirhinal cortex neuronal activity related to long‐term familiarity memory in the macaque
Authors: Hölscher Christian , Rolls Edmund T. , Xiang Jianzhong 
Published: October 2003

AbstractLesion studies suggest that the perirhinal cortex plays a role in object recognition memory. To analyse its role, the activity of single neurons in the perirhinal cortex was recorded in three rhesus monkeys (Macaca mulatta) performing a delayed matching‐to‐sample task with up to three intervening stimuli. A set of familiar visual stimuli was used. Some neurons had activity related to working memory, in that they responded more to the sample than to the match image within a trial, as shown previously. However, when a novel set of stimuli was introduced, the neuronal responses were on average only 47% of the magnitude of the responses to the familiar set of stimuli. Moreover, it was shown in eight different replications in three monkeys that the responses of the perirhinal cortex neurons gradually increased over hundreds of presentations of the new set of (initially novel) stimuli to become as large as with the already familiar stimuli. The mean number of 1.3‐s presentations to induce this effect was 400 occurring over 7–13 days. These results show that perirhinal cortex neurons represent the very long‐term familiarity of visual stimuli. A representation of the long‐term familiarity of visual stimuli may be important for many aspects of social behaviour, and part of the impairment in temporal lobe amnesia may be related to the difficulty of building representations of the degree of familiarity of stimuli.
Hypocretin‐1 causes G protein activation and increases ACh release in rat pons
Authors: Bernard René , Lydic Ralph , Baghdoyan Helen A. 
Published: October 2003

AbstractThe effects of the arousal‐promoting peptide hypocretin on brain stem G protein activation and ACh release were examined using 16 adult Sprague‐Dawley rats. In vitro[35S]GTPγS autoradiography was used to test the hypothesis that hypocretin‐1‐stimulated G protein activation is concentration‐dependent and blocked by the hypocretin receptor antagonist SB‐334867. Activated G proteins were quantified in dorsal raphe nucleus (DR), locus coeruleus (LC) and pontine reticular nucleus oral part (PnO) and caudal part (PnC). Concentration–response data revealed a significant (P < 0.001) effect of hypocretin‐1 (2–2000 nm) in all brain regions examined. Maximal increases over control levels of [35S]GTPγS binding were 37% (DR), 58% (LC), 52% (PnO) and 44% (PnC). SB‐334867 (2 µm) significantly (P < 0.002) blocked hypocretin‐1 (200 nm)‐stimulated [35S]GTPγS binding in all four nuclei. This is the first autoradiographic demonstration that hypocretin‐1 activates G proteins in arousal‐related brain stem nuclei as a result of specific receptor interactions. This finding suggests that some hypocretin receptors in brain stem couple to inhibitory G proteins. In vivo microdialysis was used to test the hypothesis that PnO administration of hypocretin‐1 increases ACh release in PnO. Dialysis delivery of hypocretin‐1 (100 µm) significantly (P < 0.002) increased (87%) ACh release. This finding is consistent with the interpretation that one mechanism by which hypocretin promotes arousal is by enhancing cholinergic neurotransmission in the pontine reticular formation.
Preshaping and continuous evolution of motor cortical representations during movement preparation
Authors: Bastian Annette , Schöner Gregor , Riehle Alexa 
Published: October 2003

AbstractWhile a goal‐directed movement is prepared, motor cortical neurons selectively change their activity in relation to prior information about movement direction. Only little is known, however, about the neuronal representation of partial information about this parameter. We investigated this question by training monkeys in a multidirectional centre‐out pointing task. A preparatory signal provided prior information about one, two or three possible adjacent targets, thus manipulating the level of certainty about movement direction. After a 1‐s delay, the response signal specified one of the precued targets to indicate the actual movement to be performed. Based on the directional tuning curves of individual motor cortical neurons determined during the reaction time interval, we constructed distributions of the population activation (DPAs), which we were then able to estimate as well during the preparatory period. We found that these distributions were preshaped by prior information, with peaks of activation centred over the range of precued movement directions. These peaks sharpened as the response signal approached, and shifted to the specified movement direction subsequent to that signal. Wider ranges of precued movement directions were represented by broader DPAs. Trials in which monkeys produced short reaction times were characterized by narrower distributions than trials with long reaction times. Our study thus provides evidence for (i) a graded preshaping of the neuronal population representation of movement direction by partial information about this parameter, and (ii) the continuous evolution of the preshaped population representation during the preparatory period towards movement initiation.
Characterization of the rat A2A adenosine receptor gene: a 4.8‐kb promoter‐proximal DNA fragment confers selective expression in the central nervous system
Authors: Lee Yi‐Chao , Chien Chen‐Li , Sun Chung‐Nan , Huang Chuen‐Lin , Huang Nai‐Kuei , Chiang Ming‐Chang , Lai Hsing‐Lin , Lin Yow‐Sien , Chou Szu‐Yi , Wang Chi‐Kuang Leo , Tai Ming‐Hong , Liao Wen‐Lin , Lin Teng‐Nan , Liu Fu‐Chin , Chern Yijuang 
Published: October 2003

AbstractWe isolated and characterized a 4.8‐kb 5′ flanking region of the rat A2A adenosine receptor (A2A‐R) gene in the present study. Promoter activity was observed with this DNA fragment in PC12 cells and C6 cells which contain endogenous A2A‐Rs. A fusion fragment consisting of the 4.8‐kb promoter‐proximal DNA fragment of the A2A‐R gene, and the coding region of lacZ was utilized to produce mice harbouring the fusion gene. In three independent founder lines, proteins and transcripts of the transgene were found in many areas of the central nervous system (CNS), but not in three peripheral tissues examined. Double immunohistochemical analyses revealed that the transgene was coexpressed with endogenous A2A‐R and proper neuronal markers in the brain. Specifically, the transgene in the striatum was found in the enkephalin‐containing GABAergic neurons and in the cholinergic neurons as was found for the endogenous A2A‐R. However, a selectively enriched striatal expression of the transgene was not found as was observed for the endogenous A2A‐R. Collectively, the 4.8‐kb promoter‐proximal DNA fragment of the rat A2A‐R gene contains important element(s) to direct its expression in the CNS where functional A2A‐R are found, but were not sufficient to confer the highly concentrated expression of the striatal A2A‐R. Furthermore, expressions of A2A‐R and the transgene were found in both neurons and astrocytes, suggesting that adenosine might mediate its function through A2A‐R in both cell types.
Retrospective and prospective persistent activity induced by Hebbian learning in a recurrent cortical network
Authors: Mongillo Gianluigi , Amit Daniel J. , Brunel Nicolas 
Published: October 2003

AbstractRecordings from cells in the associative cortex of monkeys performing visual working memory tasks link persistent neuronal activity, long‐term memory and associative memory. In particular, delayed pair‐associate tasks have revealed neuronal correlates of long‐term memory of associations between stimuli. Here, a recurrent cortical network model with Hebbian plastic synapses is subjected to the pair‐associate protocol. In a first stage, learning leads to the appearance of delay activity, representing individual images ('retrospective' activity). As learning proceeds, the same learning mechanism uses retrospective delay activity together with choice stimulus activity to potentiate synapses connecting neural populations representing associated images. As a result, the neural population corresponding to the pair‐associate of the image presented is activated prior to its visual stimulation ('prospective' activity). The probability of appearance of prospective activity is governed by the strength of the inter‐population connections, which in turn depends on the frequency of pairings during training. The time course of the transitions from retrospective to prospective activity during the delay period is found to depend on the fraction of slow, N‐methyl‐d‐aspartate‐like receptors at excitatory synapses. For fast recurrent excitation, transitions are abrupt; slow recurrent excitation renders transitions gradual. Both scenarios lead to a gradual rise of delay activity when averaged over many trials, because of the stochastic nature of the transitions. The model reproduces most of the neuro‐physiological data obtained during such tasks, makes experimentally testable predictions and demonstrates how persistent activity (working memory) brings about the learning of long‐term associations.