bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ischemic preconditioning attenuates the lipid peroxidation and remote lung injury in the rat model of unilateral lower limb ischemia reperfusion
Authors: Olguner Ç. , Koca U. , Kar A. , Karci A. , İşlekel H. , Canyilmaz M. , Mavioĝlu Ö. , Kizildaĝ S. , Ünlü G. , Elar Z. 
Published: January 2006

Background:  Ischemia and reperfusion of the skeletal muscle tissue may cause remote lung injury. We aimed to evaluate the protective effect of ischemic preconditioning (IP) on the lung during unilateral lower limb ischemia reperfusion (IR).Methods:  Four groups of rats were used in this study: (i) the sham group (sham, n = 6) served as time controls, they remained anesthetized for the whole duration of the study; (ii) the ischemia and reperfusion group (IR, n = 10) underwent 4 h of left lower limb ischemia followed by 2 h of reperfusion; (iii) the ischemic preconditioning group (IP, n = 10), the left lower limbs of rats were exposed to three cycles of IP (10 min of ischemia followed by 10 min of reperfusion); and (iv) the ischemic preconditioning plus ischemia reperfusion group (IP/IR, n = 10) underwent IP followed by IR as in the IP and IR groups. Plasma and tissue samples were taken at the end of the study period for determination of lung tissue myeloperoxidase activity (MPO) and polymorphonuclear leukocyte count (PMNL), histological lung injury score and plasma thiobarbituric acid reactive substances (TBARS) level.Results:  PMNL count and MPO activity in the lung tissue, and plasma TBARS level were higher in the IR group compared with other groups while there were no differences between the sham and the IP and between the sham and the IP/IR groups. Histological lung injury score was higher in the IR group than in the IP/IR and sham groups. The plasma TBARS level in the IP group was significantly lower than in the IP/IR group.Conclusion:  IP pretreatment reduces lipid peroxidation and lung injury caused by lower limb IR.
Diversity of laminar connections linking periarcuate and lateral intraparietal areas depends on cortical structure
Authors: Medalla M. , Barbas H. 
Published: January 2006

AbstractLateral prefrontal and intraparietal cortices have strong connectional and functional associations but it is unclear how their common visuomotor, perceptual and working memory functions arise. The hierarchical scheme of cortical processing assumes that prefrontal cortex issues ‘feedback’ projections to parietal cortex. However, the architectonic heterogeneity of these cortices raises the question of whether distinct areas have laminar‐specific interconnections underlying their complex functional relationship. Using quantitative procedures, we showed that laminar‐specific connections between distinct prefrontal (areas 46 and 8) and lateral intraparietal (LIPv, LIPd and 7a) areas in Macaca mulatta, studied with neural tracers, varied systematically according to rules determined by the laminar architecture of the linked areas. We found that axons from areas 46 and rostral 8 terminated heavily in layers I–III of all intraparietal areas, as did caudal area 8 to area LIPv, suggesting ‘feedback’ communication. However, contrary to previous assumptions, axons from caudal area 8 terminated mostly in layers IV–V of LIPd and 7a, suggesting ‘feedforward’ communication. These laminar patterns of connections were highly correlated with consistent differences in neuronal density between linked areas. When neuronal density in a prefrontal origin was lower than in the intraparietal destination, most terminations were found in layer I with a concomitant decrease in layer IV. The opposite occurred when the prefrontal origin had a higher neuronal density than the target. These findings indicate that the neuronal density of linked areas can reliably predict their laminar connections and may form the basis of understanding the functional complexity of prefrontal–intraparietal interactions in cognition.
Macrophages and neurons are targets of retinoic acid signaling after spinal cord contusion injury
Authors: Schrage Kirsten , Koopmans Guido , Joosten Elbert A. J. , Mey Jörg 
Published: January 2006

AbstractThe physiological reactions after spinal cord injury are accompanied by local synthesis of the transcriptional activator retinoic acid (RA). RA exerts its effects by binding to retinoic acid receptors (RAR) which heterodimerize with retinoid X receptors (RXR) and then act as ligand‐activated transcription factors. To identify possible cellular targets of RA we investigated protein levels and cellular distribution of retinoid receptors in the rat spinal cord at 4, 7, 14 and 21 days after a contusion injury. In the nonlesioned spinal cord, immunoreactivity for RARα, RXRα, RXRβ and RXRγ was localized in the cytosol of neurons, that of RXRα and RXRβ in astrocytes and that of RARα, RXRα and RXRγ in some oligodendrocytes. After contusion injury RARα and all RXRs appeared in the cell nuclei of reactive microglia and macrophages. This nuclear staining began at 4 days, was most prominent at 7 and 14 days and had decreased at 21 days after injury. A similar nuclear translocation was also observed for the RARα, RXRα and RXRβ staining in neurons situated around the border of the contusion. These observations suggest that RA participates as a signal for the physiological responses of microglia and neurons after CNS injury.
1‐HydroxyPGE1 reduces infarction volume in mouse transient cerebral ischemia
Authors: Ahmad Muzamil , Saleem Sofiyan , Zhuang Hean , Ahmad Abdullah Shafique , Echeverria Valentina , Sapirstein Adam , Doré Sylvain 
Published: January 2006

AbstractDifferential neurological outcomes due to prostaglandin E2 activating G‐protein‐coupled prostaglandin E (EP) receptors have been observed. Here, we investigated the action of the EP4/EP3 agonist 1‐hydroxyPGE1 (1‐OHPGE1) in modulating transient ischemic brain damage. C57BL/6 mice were pretreated 50 min before transient occlusion of the middle cerebral artery with an intraventricular injection of 1‐OHPGE1 (0.1, 0.2, 2.0 nmol/0.2 µL). Brain damage 4 days after reperfusion, as estimated by infarct volume, was significantly reduced by more than 19% with 1‐OHPGE1 in the two higher‐dose groups (P < 0.05). To further address whether protection also was extended to neurons, primary mouse cultured neuronal cells were exposed to N‐methyl‐d‐aspartate. Co‐treatment with 1‐OHPGE1 resulted in significant neuroprotection (P < 0.05). To better understand potential mechanisms of action and to test whether changes in cyclic adenosine monophosphate (cAMP) levels and downstream signaling would be neuroprotective, we measured cAMP levels in primary neuronal cells. Brief exposure to 1‐OHPGE1 increased cAMP levels more than twofold and increased the phosphorylation of extracellular‐regulated kinases at positions Thr‐202/Tyr‐204. In a separate cohort of animals, 1‐OHPGE1 at all doses tested produced no significant effect on the physiological parameters of core body temperature, mean arterial pressure and relative cerebral blood flow observed following drug treatment. Together, these results suggest that modulation of PGE2 receptors that increase cAMP levels and activate extracellular‐regulated kinases 1/2 caused by treatment with 1‐OHPGE1 can be protective against neuronal injury induced by focal ischemia.
Identification of ventricular‐side‐enriched molecules regulated in a stage‐dependent manner during cerebral cortical development
Authors: Ajioka Itsuki , Maeda Takuya , Nakajima Kazunori 
Published: January 2006

AbstractRadial glial cells are the main component of the embryonic cortical ventricular zone (VZ), producing deep‐layer excitatory neurons in the early stage and upper‐layer excitatory neurons in the late stage of development. Previous studies have suggested that the laminar fate of deep‐layer neurons might be determined by early‐stage‐specific secretory or transmembrane molecules (S/TMs) in the VZ. However, the different properties required to produce the different types of neurons in early‐stage and late‐stage VZ cells are largely unknown. Herein, we investigated the stage‐dependent transcriptional profiles of the ventricular side of the mouse cortex, which was manually dissected at embryonic day (E)12, E14 and E16, and identified 3985 ‘VZ‐enriched’ genes, regulated stage‐dependently, by GeneChip analysis. These molecules were classified into nine types based on stage‐dependent regulation patterns. Prediction programs for the S/TMs revealed 659 ‘VZ‐enriched’ S/TMs. In situ hybridization and real‐time PCR analysis for several of these molecules showed results consistent with the statistical analysis of the GeneChip experiments. Moreover, we identified 17 cell cycle‐related early‐stage and ‘VZ‐enriched’ molecules. These molecules included not only those involved in cell cycle progression, but also essential molecules for DNA double‐strand break repair, such as Rad51 and Rpa1. These results suggest that the early stage‐VZ cells, which produce both deep‐ and upper‐layer neurons, and the late‐stage VZ cells, which produce only upper‐layer neurons, are intrinsically different. The gene lists presented here will be useful for the investigation of stage‐dependent changes in VZ cells and their regulatory mechanisms in the developing cortex.
Motor learning changes GABAergic terminals on spinal motoneurons in normal rats
Authors: Wang Yu , Pillai Shreejith , Wolpaw Jonathan R. , Chen Xiang Yang 
Published: January 2006

AbstractThe role of spinal cord plasticity in motor learning is largely unknown. This study explored the effects of H‐reflex operant conditioning, a simple model of motor learning, on GABAergic input to spinal motoneurons in rats. Soleus motoneurons were labeled by retrograde transport of a fluorescent tracer and GABAergic terminals on them were identified by glutamic acid decarboxylase (GAD)67 immunoreactivity. Three groups were studied: (i) rats in which down‐conditioning had reduced the H‐reflex (successful HRdown rats); (ii) rats in which down‐conditioning had not reduced the H‐reflex (unsuccessful HRdown rats) and (iii) unconditioned (naive) rats. The number, size and GAD density of GABAergic terminals, and their coverage of the motoneuron, were significantly greater in successful HRdown rats than in unsuccessful HRdown or naive rats. It is likely that these differences are due to modifications in terminals from spinal interneurons in lamina VI–VII and that the increased terminal number, size, GAD density and coverage in successful HRdown rats reflect and convey a corticospinal tract influence that changes motoneuron firing threshold and thereby decreases the H‐reflex. GABAergic terminals in spinal cord change after spinal cord transection. The present results demonstrate that such spinal cord plasticity also occurs in intact rats in the course of motor learning and suggest that this plasticity contributes to skill acquisition.
Cytosolic labile zinc: a marker for apoptosis in the developing rat brain
Authors: Lee Joo‐Yong , Hwang Jung Jin , Park Mi‐Ha , Koh Jae‐Young 
Published: January 2006

AbstractCytosolic zinc accumulation was thought to occur specifically in neuronal death (necrosis) following acute injury. However, a recent study demonstrated that zinc accumulation also occurs in adult rat neurons undergoing apoptosis following target ablation, and in vitro experiments have shown that zinc accumulation may play a causal role in various forms of apoptosis. Here, we examined whether intraneuronal zinc accumulation occurs in central neurons undergoing apoptosis during development. Embryonic and newborn Sprague–Dawley rat brains were double‐stained for terminal deoxynucleotidyl transferase‐mediated dUTP‐biotin nick end labelling (TUNEL) detection of apoptosis and immunohistochemical detection of stage‐specific neuronal markers, such as nestin, proliferating cell nuclear antigen (PCNA), TuJ1 and neuronal nuclear specific protein (NeuN). The results revealed that apoptotic cell death occurred in neurons of diverse stages (neural stem cells, and dividing, young and adult neurons) throughout the brain during the embryonic and early postnatal periods. Further staining of brain sections with acid fuchsin or zinc‐specific fluorescent dyes showed that all of the apoptotic neurons were acidophilic and contained labile zinc in their cell bodies. Cytosolic zinc accumulation was also observed in cultured cortical neurons undergoing staurosporine‐ or sodium nitroprusside (SNP)‐induced apoptosis. In contrast, zinc chelation with CaEDTA or N,N,N′,N′‐tetrakis(2‐pyridylmethyl)ethylenediamine (TPEN) reduced SNP‐induced apoptosis but not staurosporine‐induced apoptosis, indicating that cytosolic zinc accumulation does not play a causal role in all forms of apoptosis. Finally, the specific cytosolic zinc accumulation may have a practical application as a relatively simple marker for neurons undergoing developmental apoptosis.
Functional contribution of specific brain areas to absence seizures: role of thalamic gap‐junctional coupling
Authors: Proulx Éliane , Leshchenko Yevgen , Kokarovtseva Larisa , Khokhotva Vladislav , El‐Beheiry Mostafa , Snead O. Carter , Perez Velazquez Jose L. 
Published: January 2006

AbstractThe synchronized discharges typical of seizures have a multifactorial origin at molecular, cellular and network levels. During recent years, the functional role of gap‐junctional coupling has received increased attention as a mechanism that may participate in seizure generation. We have investigated the possible functional roles of thalamic and hippocampal gap‐junctional communication (GJC) in the generation of spike‐and‐wave discharges in a rodent model of atypical absence seizures. Seizures in this model spread throughout limbic, thalamic and neocortical areas. Rats were chronically implanted with cannulae to deliver drugs or saline, and local field potentials recordings were performed using intracerebral electrodes positioned in distinct brain areas. Initially, the effects on synaptic transmission of the gap‐junctional blockers used in this study were determined. Neither carbenoxolone (CBX) nor 18‐α‐glycyrrhetinic acid altered chemical synaptic transmission at the concentrations tested. These two compounds, when injected via cannulae into the reticular nucleus of the thalamus (NRT), decreased significantly the duration of seizures as compared with saline injections or injections of the CBX inactive derivative glycyrrhizic acid. CBX injections into the hippocampus resulted in diminished seizure activity as well. NRT injections of trimethylamine, which presumably causes intracellular alkalinization (thereby promoting gap‐junctional opening), enhanced seizures and spindle activity. These observations suggest that, in this rodent model, thalamic and limbic areas are involved in the synchronous paroxysmal activity and that GJC contributes to the spike‐and‐wave discharges.
Effects of Emx2 inactivation on the gene expression profile of neural precursors
Authors: Gangemi Rosaria M. R. , Daga Antonio , Muzio Luca , Marubbi Daniela , Cocozza Serena , Perera Marzia , Verardo Sara , Bordo Domenico , Griffero Fabrizio , Capra Maria C. , Mallamaci Antonello , Corte Giorgio 
Published: January 2006

AbstractEmx2 plays a crucial role in the development of the diencephalon and dorsal telencephalon. Thus, Emx2‐null mutants have abnormal cortical lamination and a reduction in size of the caudal and medial areas of the prosencephalon. Emx2 is expressed in neural precursors of the subventricular zone in vivo and in cultured neurospheres in vitro where it controls the size of the transit‐amplifying population, affecting proliferation and clonal efficiency of neural stem cells. To identify the cellular processes mastered by Emx2, and possibly the molecular mechanisms by which the gene exerts its action, we compared the expression profile of cultured neurospheres derived from wild‐type and Emx2‐null mouse embryos. The differential expression of several genes was also confirmed by semiquantitative RT‐PCR, real‐time PCR and cytofluorimetric analysis in different preparations of neurospheres, and by in situ hybridization. The gene expression profile suggested a role for Emx2 in regulating the differentiation and migration properties of neural precursor cells. This involvement was confirmed in vitro, where the altered clonogenicity and impaired migration of Emx2‐null cells were partially corrected by transduction of the Emx2 gene. Taken together, our results indicate that Emx2 is indeed involved in the transition between resident early progenitors (perhaps stem cells) and more mature precursors capable of migrating out of the ventricular zone, becoming postmitotic and differentiating into the appropriate cell type, and help explain the alterations observed in the brains of knock‐out mice.
Difference in sleep regulation between morning and evening circadian types as indexed by antero‐posterior analyses of the sleep EEG
Authors: Mongrain Valérie , Carrier Julie , Dumont Marie 
Published: January 2006

AbstractCircadian types classify individuals according to their preferred timing for activity and sleep, morning and evening types showing, respectively, early or late preferences. This characteristic has been associated with corresponding differences in circadian sleep propensity. In this study, quantitative analysis of the sleep EEG in antero‐posterior derivations was used to test the hypothesis that morning and evening types differ not only in the circadian aspect of sleep regulation but also in the homeostatic aspect. Morning types and evening types (six men and six women per group, aged 19–34 years) were selected using the Morningness–Eveningness Questionnaire. They were studied by polysomnography according to their preferred sleep schedule. Spectral activity in four midline derivations (Fz, Cz, Pz, Oz) was calculated separately in nonrapid eye movement (NREM) sleep and in rapid eye movement (REM) sleep. In NREM sleep, morning types showed a steeper decrease of slow‐wave activity (SWA; 1–5 Hz) per sleep cycle in the fronto‐central derivations and a steeper increase in 13–14 Hz activity in the parieto‐occipital derivations than did evening types. Nonlinear regression analysis revealed that the exponential decay rate of relative values of SWA in NREM sleep was faster in morning than evening types, in the frontal derivation. In REM sleep, morning types showed a steeper decrease of high sigma (14–16 Hz) and beta (16–24 Hz) activities across the night in centro‐parietal derivations than did evening types. These results show for the first time a clear difference between morning types and evening types in homeostatic sleep regulation.
Prenatal stress: opposite effects on anxiety and hypothalamic expression of vasopressin and corticotropin‐releasing hormone in rats selectively bred for high and low anxiety
Authors: Bosch Oliver J. , Krömer Simone A. , Neumann Inga D. 
Published: January 2006

AbstractWe studied the mechanisms of genetic–early environmental interactions to modulate adult stress‐coping and tested the hypothesis that prenatal stress (PS) can differentially alter the consequences of a genetic predisposition to either hyper‐ or hypo‐anxiety. Exposure of male Wistar rats, bred for high (HAB) or low (LAB) anxiety‐related behaviour, to PS between pregnancy days 4 and 18 resulted in opposite effects on anxiety in adulthood, i.e. HAB rats became less and LAB rats became more anxious compared with their unstressed controls (plus‐maze and holeboard). The high anxiety of HAB controls was accompanied by elevated expression of vasopressin and corticotropin‐releasing hormone (CRH) mRNA within the hypothalamic paraventricular nucleus compared with LAB rats. PS reduced CRH mRNA expression in HAB rats but increased vasopressin mRNA expression in LAB rats, which may explain the opposite effects of PS on adult emotionality. Differential effects of PS were also found with respect to hypothalamo‐pituitary‐adrenal axis reactivity; the hypothalamo‐pituitary‐adrenal hyper‐response in virgin female HAB controls became attenuated after PS, without affecting plasma corticosterone concentrations in LAB rats. Differences in maternal plasma corticosterone measured between pregnancy days 6 and 14 of HAB and LAB dams or differential effects of PS on maternal behaviour can be excluded. In conclusion, exposure of rats with genetically determined high or low emotionality to PS mitigates the extremes in behavioural and neuroendocrine stress‐coping, thus allowing adequate and similar behavioural responses to potentially dangerous stimuli in adulthood. Differential effects of PS on the activity of the brain vasopressin and CRH systems might represent possible underlying molecular mechanisms.
Sensorineural hearing loss in insulin‐like growth factor I‐null mice: a new model of human deafness
Authors: Cediel R. , Riquelme R. , Contreras J. , Díaz A. , Varela‐Nieto I. 
Published: January 2006

AbstractIt has been reported that mutations in the gene encoding human insulin‐like growth factor‐I (IGF‐I) cause syndromic hearing loss. To study the precise role of IGF‐I in auditory function and to hypothesize the possible morphological and electrophysiological changes that may occur in the human inner ear, we have analysed the auditory brainstem response in a mouse model of IGF‐I deficiency. We show here that homozygous Igf‐1–/– mice present an all‐frequency involved bilateral sensorineural hearing loss. Igf‐1–/– mice also present a delayed response to acoustic stimuli; this increases along the auditory pathway, indicating a contribution of the central nervous system to the hearing loss in Igf‐1–/– mice. These results support the use of the Igf‐1–/– mouse as a new model for the study of human syndromic deafness.
The vomeronasal organ is required for the expression of lordosis behaviour, but not sex discrimination in female mice
Authors: Keller Matthieu , Pierman Sylvie , Douhard Quentin , Baum Michael J. , Bakker Julie 
Published: January 2006

AbstractThe role of the vomeronasal organ (VNO) in mediating neuroendocrine responses in female mice is well known; however, whether the VNO is equally important for sex discrimination is more controversial as evidence exists for a role of the main olfactory system in mate recognition. Therefore, we studied the effect of VNO removal (VNOx) on the ability of female mice to discriminate between volatile and non‐volatile odours of conspecifics of the two sexes and in different endocrine states using Y‐maze tests. VNOx female mice were able to reliably distinguish between male and female or male and gonadectomized (gdx) male volatile odours. However, when subjects had to discriminate between male and female or gdx male non‐volatile odours, VNOx females were no longer able to discriminate between sex or different endocrine status. These results thus show that the VNO is primarily involved in the detection and processing of non‐volatile odours, and that female mice can use volatile odours detected and processed by the main olfactory system for mate recognition. However, VNO inputs are needed to promote contact with the male, including facilitation of lordosis responses to his mounts. A single subcutaneous injection with gonadotropin‐releasing hormone (GnRH) partially reversed the deficit in lordosis behaviour observed in VNOx females suggesting that VNO inputs may reach hypothalamic GnRH neurons to influence the display of sexual behaviour.