bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sodium hyaluronate in trabeculectomy: effect on early complications
Authors: Gulkılık Gokhan , Kocabora Selim , Engın Gunay , Taskapılı Muhittin , Yılmazlı Cemil , Kucuksahın Hasan 
Published: May 2006

AbstractPurpose:  To evaluate the effect of sodium hyaluronate on the early complications of trabeculectomy.Methods:  In this prospective study, trabeculectomy was performed in 51 eyes of 51 patients with different types of glaucoma. Patients were divided into two groups randomly. In 24 eyes (study group) sodium hyaluronate was injected into the anterior chamber after suturing the scleral flap. In the remaining 27 eyes (control group) only balanced salt solution was injected. Visual acuities, intraocular pressures and early complications were evaluated.Results:  Preoperative mean intraocular pressures were similar in the two groups (34.5 ± 18.7 mmHg in the study group and 37.2 ± 18.1 mmHg in the control group). In the first postoperative day mean intraocular pressure difference was significant (16.8 ± 7.1 mmHg in the study group and 9.0 ± 6.6 mmHg in the control group, P < 0.01). There was significant difference in occurrence of hypotony (8.3% study vs. 40.7% control), anterior chamber shallowing (8.3% study vs. 37% control) and choroidal detachment (none in study vs. 33.3% control) between the two groups (P < 0.01). Early intraocular pressure peak, occurred more common in the study group (20.8%) than in the control group (11.1%), but the difference was not significant (P > 0.01). Hyphema occurred in two (8.3%) eyes in the study group, and three (11.1%) in the control group. This was not significant (P > 0.01). The clearance time of blood from the anterior chamber (less than 1 week) was also similar in the two groups.Conclusion:  Sodium hyaluronate‐assisted trabeculectomy decreased the incidence of early postoperative complications like anterior chamber shallowing, choroidal detachment and hypotony, but it did not have any effect on hyphema or its clearance.
Selective tuning of cortical sound‐feature processing by language experience
Authors: Tervaniemi M. , Jacobsen T. , Röttger S. , Kujala T. , Widmann A. , Vainio M. , Näätänen R. , Schröger E. 
Published: May 2006

AbstractIn ‘quantity‐languages’, such as Japanese or Finnish, sound duration is linguistically relevant. We showed that quantity‐language speakers were superior to speakers of a non‐quantity language in discriminating the duration of even non‐speech sounds. In contrast, there was no group difference in the discrimination of sound frequency. This result, obtained both by behavioural and neural indices at attentive and automatic levels of processing, indicates precise feature‐specific tuning of the auditory‐cortex functions by the mother tongue.
Short periods of concordant binocular vision prevent the development of deprivation amblyopia
Authors: Mitchell Donald E. , Kind Peter C. , Sengpiel Frank , Murphy Kathryn 
Published: May 2006

AbstractBased in part on deprivation studies, it is generally agreed that the development of vision and of the central visual pathways of higher mammals such as cats and primates is experience‐dependent. Past deprivation experiments employed periods of exclusively abnormal early visual input. Because of the absence of any normal visual input, such studies indicate only the extremes to which the visual system can change in response to visually driven activity (i.e. its capabilities) rather than provide insight into the role of early visual input in normal development (i.e. what it actually does). We examined the possibility that certain visual input, i.e. normal concordant binocular vision, may be more efficacious than others with respect to its effects on the developing visual system and on vision. On a daily basis, one type of visual input, i.e. normal binocular experience (BE), was pitted against abnormal (monocular exposure, ME) input in order to see if one was more effective. We show that 2 h of daily normal concordant, but not discordant, BE outweighs or protects against as much as 5 h of daily abnormal input to permit the development of normal grating acuity and alignment accuracy in the two eyes. Further, we show that splitting the period of BE into two 1‐h periods straddling the period of ME was ineffective, thereby indicating the 2 h of BE each day must be continuous to protect against the development of amblyopia.
ERP and fMRI correlates of endogenous and exogenous focusing of visual‐spatial attention
Authors: Natale E. , Marzi C. A. , Girelli M. , Pavone E. F. , Pollmann S. 
Published: May 2006

AbstractThe aim of this study was to investigate the neural correlates of the functional distinction underlying attentional mechanisms of endogenous‐sustained and exogenous‐transient spatial selection. We recorded event related potentials (ERPs) and used functional magnetic resonance imaging (fMRI) in separate experiments while subjects performed a simple reaction time (RT) to the same visual stimulus displayed to one of several field locations. Endogenous‐sustained or exogenous‐transient focusing of attention onto target location were obtained by presenting the stimulus in blocks of same‐point vs. randomised‐point trials, respectively. Same‐point stimuli yielded overall faster RT than randomised stimuli, indicating a facilitating effect of endogenous‐sustained spatial attention on the perceptual processing of the impending stimulus. Moreover, same‐point vs. randomised presentations revealed significant increases in the fMRI signal in the bilateral lingual and fusiform gyri as well as in the right calcarine sulcus, in conjunction with a larger amplitude of the posterior P1 component of ERPs, but no modulation of the amplitude of the N1 component. Rather, a larger amplitude of N1 was found in the reverse contrast, randomised minus same‐point trials, which revealed increases in the fMRI signal along the posterior left superior frontal sulcus and bilaterally in the superior precuneus. These findings indicate that N1 indexes exogenous orienting of attention and is likely to represent the activity of frontal and parietal components of the attention network involved in eliciting attention changes. In contrast, the effects of those changes, resulting in a modulation of activation in visual occipital areas, are indexed by P1.
Intrinsic bursting of immature CA3 pyramidal neurons and consequent giant depolarizing potentials are driven by a persistent Na+ current and terminated by a slow Ca2+‐activated K+ current
Authors: Sipilä Sampsa T. , Huttu Kristiina , Voipio Juha , Kaila Kai 
Published: May 2006

AbstractThe CA3 area of the mature hippocampus is known for its ability to generate intermittent network activity both in physiological and in pathological conditions. We have recently shown that in the early postnatal period, the intrinsic bursting of interconnected CA3 pyramidal neurons generates network events, which were originally called giant depolarizing potentials (GDPs). The voltage‐dependent burst activity of individual pyramidal neurons is promoted by the well‐known depolarizing action of endogenous GABA on immature neurons. In the present work, we show that a persistent Na+ current, I‐Nap, accounts for the slow regenerative depolarization that triggers the intrinsic bursts in the neonatal rat CA3 pyramidal neurons (postnatal day 3–6), while a slow Ca2+‐activated K+ current, sI‐K(Ca), is primarily responsible for the postburst slow afterhyperpolarization and consequent burst termination. In addition, we exploited pharmacological data obtained from intracellular recordings to study the mechanisms involved in network events recorded with field potential recordings. The data as a whole indicate that I‐Nap and sI‐K(Ca) are involved in the initiation and termination, respectively, of the pyramidal bursts and consequent network events underlying GDPs.
L‐DOPA‐induced dyskinesia in adult rats with a unilateral 6‐OHDA lesion of dopamine neurons is paralleled by increased c‐fos gene expression in the subthalamic nucleus
Authors: Soghomonian Jean‐Jacques 
Published: May 2006

AbstractLevodopa (L‐DOPA), the metabolic precursor of dopamine, is widely used as a pharmacological agent for the symptomatic treatment of Parkinson's disease. However, long‐term L‐DOPA use results in abnormal involuntary movements such as dyskinesias. There is evidence that abnormal cell signaling in the basal ganglia is involved in L‐DOPA‐induced dyskinesia. The subthalamic nucleus (STN) plays a key role in the circuitry of the basal ganglia and in the pathophysiology of Parkinson's disease. However, the contribution of the STN to L‐DOPA‐induced dyskinesias remains unclear. The objective of this work was to study the effects of acute or chronic systemic administration of L‐DOPA to adult rats with a unilateral 6‐hydroxydopamine (6‐OHDA) lesion of dopamine neurons on c‐fos expression in the STN and test the hypothesis that these effects correlate with L‐DOPA‐induced dyskinesias. c‐fos mRNA expression was measured in the STN by in situ hybridization histochemistry at the single cell level. Our results confirm earlier evidence that the chronic administration of L‐DOPA to rats with a unilateral 6‐OHDA lesion increases c‐fos expression in the STN. We also report that c‐fos expression can be increased following an acute injection of L‐DOPA to 6‐OHDA‐lesioned rats but not following a chronic injection of L‐DOPA to sham‐operated, unlesioned rats. Finally, we provide evidence that the occurrence and severity of dyskinesia is correlated with c‐fos mRNA levels in the ipsilateral STN. These results suggest that altered cell signaling in the STN is involved in some of the behavioral effects induced by systemic L‐DOPA administration.
Cannabinoids modulate spontaneous neuronal activity and evoked inhibition of locus coeruleus noradrenergic neurons
Authors: Muntoni Anna Lisa , Pillolla Giuliano , Melis Miriam , Perra Simona , Gessa Gian Luigi , Pistis Marco 
Published: May 2006

AbstractThe noradrenergic pathway arising from the locus coeruleus (LC) is involved in the regulation of attention, arousal, cognitive processes and sleep. These physiological activities are affected byCannabisexposure − both in humans and laboratory animals. In addition, exogenous cannabinoids, as well as pharmacological and genetic manipulation of the endocannabinoid system, are known to influence emotional states (e.g. anxiety) for which a contributory role of the LC‐noradrenergic system has long been postulated. However, whether cannabinoid administration would affect the LC neuronal activityin vivois still unknown. To this end, single‐unit extracellular recordings were performed from LC noradrenergic cells in anaesthetized rats. Intravenous injection of both the synthetic cannabinoid agonist, WIN55212‐2, and the main psychoactive principle ofCannabis, Δ9‐tetrahydrocannabinol, dose‐dependently increased the firing rate of LC noradrenergic neurons, with WIN55212‐2 being the most efficacious. Similar results were obtained by the administration of these drugs into a lateral ventricle. Cannabinoid‐induced stimulation of LC noradrenergic neuronal activity was counteracted by SR141716A, a cannabinoid receptor antagonist/reverse agonist, which by itself slightly reduced LC discharge rate. Moreover, WIN55212‐2 suppressed the inhibition of noradrenergic cells produced by stimulation of the major γ‐aminobutyric acid (GABA)ergic afferent to the LC, the nucleus prepositus hypoglossi. Altogether, these findings suggest the involvement of noradrenergic pathways in some consequences ofCannabisintake (e.g. cognitive and attention deficits, anxiety reactions), as well as a role for cannabinoid receptors in basic brain activities sustaining arousal and emotional states.
T‐type Cav3.3 calcium channels produce spontaneous low‐threshold action potentials and intracellular calcium oscillations
Authors: Chevalier Marc , Lory Philippe , Mironneau Chantal , Macrez Nathalie , Quignard Jean‐François 
Published: May 2006

AbstractThe precise contribution of T‐type Ca2+ channels in generating action potentials (APs), burst firing and intracellular Ca2+ signals needs further elucidation. Here, we show that Cav3.3 channels can trigger repetitive APs, generating spontaneous membrane potential oscillations (MPOs), and a concomitant increase in the intracellular Ca2+ concentration ([Ca2+]i) when overexpressed in NG108‐15 cells. MPOs were dependent on Cav3.3 channel activity given that they were recorded from a potential range of −55 to −70 mV, blocked by nickel and mibefradil, as well as by low external Ca2+ concentration. APs of distinct duration were recorded: short APs (sAP) or prolonged APs (pAP) with a plateau potential near −40 mV. The voltage‐dependent properties of the Cav3.3 channels constrained the AP duration and the plateau potential was supported by sustained calcium current through Cav3.3 channels. The sustained current amplitude decreased when the resting holding potential was depolarized, thereby inducing a switch of AP shape from pAP to sAP. Duration of the [Ca2+]i oscillations was also closely related to the shape of APs. The Cav3.3 window current was the oscillation trigger as shown by shifting the Cav3.3 window current potential range as a result of increasing the external Ca2+ concentration, which resulted in a corresponding shift of the AP threshold. Overall, the data demonstrate that the Cav3.3 window current is critical in triggering intrinsic electrical and [Ca2+]i oscillations. The functional expression of Cav3.3 channels can generate spontaneous low‐threshold calcium APs through its window current, indicating that Cav3.3 channels can play a primary role in pacemaker activity.
Maturation of otolith‐related brainstem neurons in the detection of vertical linear acceleration in rats
Authors: Lai Suk‐King , Lai Chun‐Hong , Yung Ken K. L. , Shum Daisy K. Y. , Chan Ying‐Shing 
Published: May 2006

AbstractTo investigate the critical maturation time of otolith‐related neurons in processing vertical orientations, rats (postnatal day 4 to adults) were studied for functional activation of c‐fos expression in brainstem neurons by immuno‐/hybridization histochemistry. Conscious rats were subjected to sinusoidal linear acceleration along the vertical plane. Labyrinthectomized and/or stationary controls showed only sporadically scattered Fos‐labeled neurons in the vestibular nuclei, confirming an otolithic origin of c‐fos expression. Functionally activated Fos expression in neurons of the medial and spinal vestibular nuclei and group x were identifiable by P7 and those in group y by P9. A small number of Fos‐labeled neurons characterized by small soma size were found in the ventral part of lateral vestibular nucleus by P9. Other vestibular‐related areas such as prepostitus hypoglossal nucleus, gigantocellular reticular nucleus and locus coeruleus of normal experimental rats showed functionally activated c‐fos expression at P7. Neurons in dorsal medial cell column and beta subnucleus of the inferior olive only showed functionally activated c‐fos expression by the second postnatal week. These findings revealed a unique critical maturation time for each of the vestibular‐related brainstem areas in the recognition of gravity‐related vertical head orientations. By mapping the three‐dimensional distribution of Fos‐immunoreactive neurons, we found an even distribution of otolith‐related neurons within the spinal vestibular nucleus in groups x and y but a clustered distribution in the middle–lateral–ventral part of the medial vestibular nucleus. Taken together, our findings reveal the developmental profile of neuronal subpopulations within the vertical otolith system, thereby providing an anatomical basis for postnatal coding of gravity‐related vertical head movements.
Requirement for Id1 in opioid‐induced oligodendrogenesis in cultured adult rat hippocampal progenitors
Authors: Persson Anders I. , Bull Cecilia , Eriksson Peter S. 
Published: May 2006

AbstractGrowth factors and peptides playing important roles during early development of the central nervous system have also been shown to maintain their regulation of cell genesis in the adult brain. We have previously described that endogenous opioids, expressed in the developing hippocampus, regulate proliferation and differentiation in the adult rat hippocampus. The aim of this study was to investigate the effects of the opioid β‐endorphin on gene expression and glial differentiation in cultures of adult rat hippocampal progenitors (AHPs). Changes in gene expression after stimulation of AHPs with β‐endorphin for 48 h were investigated using cDNA arrays. Confirmation experiments verified that stimulation with β‐endorphin increased the mRNA levels of myelin basic protein, glutathione S‐transferase pi, c‐junD and rab16 (P < 0.05), genes that are associated with oligodendrogenesis. Furthermore, β‐endorphin increased the levels of Id1, but not Id3, mRNA on the arrays. Incubation of AHPs with β‐endorphin resulted in a threefold increase in oligodendrogenesis (P < 0.01) but no significant change in astrogliogenesis. No effect on oligodendrogenesis was observed in the presence of the opioid antagonist naloxone. Coincubation of β‐endorphin with Id1 antisense oligonucleotides for 10 days also entirely blocked the induced oligodendrogenesis in our AHP cultures. Moreover, a subpopulation of AHPs (25%) showed nuclear expression of the proneural transcriptional activator Mash1 that was reduced to approximately 5% of the cells when exposed to β‐endorphin. We suggest a requirement for Id1 in opioid‐induced oligodendrogenesis in cultured AHPs possibly acting on opioid‐responsive AHPs expressing the proneural transcriptional activator Mash1.
Rapid phosphorylation of histone H2A.X following ionotropic glutamate receptor activation
Authors: Crowe Samantha L. , Movsesyan Vilen A. , Jorgensen Timothy J. , Kondratyev Alexei 
Published: May 2006

AbstractExcessive activation of ionotropic glutamate receptors increases oxidative stress, contributing to the neuronal death observed following neurological insults such as ischemia and seizures. Post‐translational histone modifications may be key mediators in the detection and repair of damage resulting from oxidative stress, including DNA damage, and may thus affect neuronal survival in the aftermath of insults characterized by excessive glutamate release. In non‐neuronal cells, phosphorylation of histone variant H2A.X (termed γ‐H2AX) occurs rapidly following DNA double‐strand breaks. We investigated γ‐H2AX formation in rat cortical neurons (daysin vitro14) following activation ofN‐methyl‐d‐aspartate (NMDA) or α‐amino‐3‐hydroxyl‐5‐methyl‐4‐isoxazolepropionic acid (AMPA)/kainate glutamate receptors using fluorescent immunohistochemical techniques. Moreover, we evaluated the co‐localization of γ‐H2AX ‘foci’ with Mre11, a double‐strand break repair protein, to provide further evidence for the activation of this DNA damage response pathway. Here we show that minimally cytotoxic stimulation of ionotropic glutamate receptors was sufficient to evoke γ‐H2AX in neurons, and that NMDA‐induced γ‐H2AX foci formation was attenuated by pretreatment with the antioxidant, Vitamin E, and the intracellular calcium chelator, BAPTA‐AM. Moreover, a subset of γ‐H2AX foci co‐localized with Mre11, indicating that at least a portion of γ‐H2AX foci is damage dependent. The extent of γ‐H2AX induction following glutamate receptor activation corresponded to the increases we observed following conventional DNA damaging agents [i.e. non‐lethal doses of gamma‐radiation (1 Gy) and hydrogen peroxide (10 µm)]. These data suggest that insults not necessarily resulting in neuronal death induce the DNA damage‐evoked chromatin modification, γ‐H2AX, and implicate a role for histone alterations in determining neuronal vulnerability following neurological insults.
EEG evidence for the presence of an action observation–execution matching system in children
Authors: Lepage Jean‐François , Théoret Hugo 
Published: May 2006

AbstractIn the adult human brain, passive observation of actions performed by others activates some of the same cortical areas that are involved in the execution of actions, thereby contributing to action recognition. This mechanism appears to occur through activation of a population of action‐coding cells known as mirror neurons (MN). In the adult motor cortex, performing actions and observing human movement reduces the magnitude of the mu (8–13 Hz) rhythm, possibly reflecting MN system activity. Despite the wealth of information available regarding the adult MN system, little is known about its existence in children. Here, we used EEG to probe mu rhythm modulation in 15 children during observation and execution of hand actions. Our data show that mu rhythm attenuation occurs in children under 11 years old during observation of hand movements. Similarly to what has been reported in adults, observation of goal/object‐orientated movement produces greater modulation of the mu rhythm than intransitive movement. These data confirm the existence of an observation–execution matching system in the immature human brain and may be of clinical value in the understanding of neurodevelopmental disorders associated with a faulty MN system, such as autism spectrum disorder.
In vivo synaptic plasticity in the dentate gyrus of mice deficient in the neural cell adhesion molecule NCAM or its polysialic acid
Authors: Stoenica Luminita , Senkov Oleg , Gerardy‐Schahn Rita , Weinhold Birgit , Schachner Melitta , Dityatev Alexander 
Published: May 2006

AbstractThe neural cell adhesion molecule NCAM and its associated polysialic acid (PSA) play important roles in synaptic plasticity in the CA1 and/or CA3 regions of the hippocampus in vitro. Here, we address the question of whether NCAM and PSA are involved in regulation of synaptic transmission and plasticity also in vivo at synapses formed by entorhinal cortex axons in the dentate gyrus of mice anaesthetized with urethane. We show that basal synaptic transmission, measured as the slope of field excitatory postsynaptic potentials, was reduced strongly in mice lacking ST8SiaII/STX, the enzyme involved in polysialylation of NCAM in stem cell‐derived immature granule cells, but not in mice deficient either in the NCAM glycoprotein or the enzyme ST8SiaIV/PST involved in polysialylation of NCAM in mature neurons. Strikingly, only mice deficient in NCAM, but not in PST or STX, were impaired in long‐term potentiation (LTP) induced by theta‐burst stimulation, suggesting that LTP in the dentate gyrus depends on the NCAM glycoprotein alone rather than on its associated PSA. As also patterns of synaptic activity during and immediately after induction of LTP were impaired in NCAM‐deficient mice, it is likely that induction of LTP requires NCAM. These data are the first to describe that NCAM is necessary for induction of synaptic plasticity in identified synapses in vivo and suggest that polysialylation of NCAM expressed by immature granule cells in the dentate gyrus supports development of basal excitatory synaptic transmission in this region.