bluuebunny/crossref_metadata_2025_split huggingface dataset:
Brain targeting and glomerulus formation of two olfactory neuron populations expressing related receptor types
Authors: Conzelmann Sidonie , Malun Dagmar , Breer Heinz , Strotmann Jörg 
Published: March 2003

AbstractOlfactory sensory neurons expressing different members of the mOR37 odourant receptor subfamily send their axons to distinct glomeruli located in the immediate vicinity in the olfactory bulb [Strotmann, J., Conzelmann, S., Beck, A., Feinstein, P., Breer, H. & Mombaerts, P. (2000) J. Neurosci., 20, 6927–6938]. In this study, the potential of transgenic mouse lines was used to explore the onset of receptor expression, the outgrowth of axons as well as the glomerulus formation for two neuron populations expressing different mOR37 subtypes. The data indicate a synchronous time course of these features for both neuron populations. From E15 until the day of birth, the axons of the two mOR37 populations terminate in a common, small area of the presumptive olfactory bulb. During a short postnatal phase, the two axon populations segregate into distinct, protoglomerular structures; some aberrant fibers can still be observed during this period.
Organization of inputs from cingulate motor areas to basal ganglia in macaque monkey
Authors: Takada M. , Tokuno H. , Hamada I. , Inase M. , Ito Y. , Imanishi M. , Hasegawa N. , Akazawa T. , Hatanaka N. , Nambu A. 
Published: March 2003

AbstractThe cingulate motor areas reside within regions lining the cingulate sulcus and are divided into rostral and caudal parts. Recent studies suggest that the rostral and caudal cingulate motor areas participate in distinct aspects of motor function: the former plays a role in higher‐order cognitive control of movements, whereas the latter is more directly involved in their execution. Here, we investigated the organization of cingulate motor areas inputs to the basal ganglia in the macaque monkey. Identified forelimb representations of the rostral and caudal cingulate motor areas were injected with different anterograde tracers and the distribution patterns of labelled terminals were analysed in the striatum and the subthalamic nucleus. Corticostriatal inputs from the rostral and caudal cingulate motor areas were located within the rostral striatum, with the highest density in the striatal cell bridges and the ventrolateral portions of the putamen, respectively. There was no substantial overlap between these input zones. Similarly, a certain segregation of input zones from the rostral and caudal cingulate motor areas occurred along the mediolateral axis of the subthalamic nucleus. It has also been revealed that corticostriatal and corticosubthalamic input zones from the rostral cingulate motor area considerably overlapped those from the presupplementary motor area, while the input zones from the caudal cingulate motor area displayed a large overlap with those from the primary motor cortex. The present results indicate that a parallel design underlies motor information processing in the cortico‐basal ganglia loop derived from the rostral and caudal cingulate motor areas.
Characterization of the single‐channel properties of NMDA receptors in laminae I and II of the dorsal horn of neonatal rat spinal cord
Authors: Green G. Mark , Gibb Alasdair J. 
Published: March 2003

AbstractThe single‐channel properties of native NMDA receptors in laminae I and II of the dorsal horn of the neonatal rat spinal cord were studied using outside‐out patch‐clamp techniques. These receptors were found to have several features that distinguish them from native NMDA receptors elsewhere in the CNS. Single‐channel currents activated by NMDA (100 nm) and glycine (10 µm) exhibited five distinct amplitude components with slope‐conductance values of 19.9 ± 0.8, 32.9 ± 0.6, 42.2 ± 1.1, 53.0 ± 1.0 and 68.7 ± 1.5 pS. Direct transitions were observed between all conductance levels but transitions between 69‐pS openings and 20‐, 33‐ and 42‐pS openings were rare. There was no significant difference in the frequency of direct transitions from 42‐ to 20‐pS compared to 20‐ to 42‐pS transitions. The Kb (0 mV) for Mg2+ was 89 µm. The Mg2+ unblocking rate constant was similar to other reported values. However, the Mg2+ blocking rate constant was larger than other reported values, suggesting an unusually high sensitivity to Mg2+. The NR2B subunit‐selective antagonist, ifenprodil, had no significant effect on overall channel activity but significantly decreased the mean open time of 53‐pS openings. These results suggest neonatal laminae I and II NMDA receptors are not simply composed of NR1 and NR2B subunits or NR1 and NR2D subunits. It is possible that these properties are due to an as yet uninvestigated combination of two NR2 subunits with the NR1 subunit or a combination of NR3A, NR2 and NR1 subunits.
C‐type natriuretic peptide (CNP) regulates cocaine‐induced dopamine increase and immediate early gene expression in rat brain
Authors: Thiriet Nathalie , Jouvert Peggy , Gobaille Serge , Solov'Eva Olga , Gough Bobby , Aunis Dominique , Ali Syed , Zwiller Jean 
Published: March 2003

AbstractThe neuropeptide C‐type natriuretic peptide (CNP) is the primary biologically active natriuretic peptide in brain. Using in situ hybridization, the present report demonstrates that CNP regulates egr‐1, c‐fos and junB immediate early gene expression in rat brain. In the frontal cortex, CNP induced immediate early gene expression whereas it inhibited dose‐dependently the cocaine‐induced early gene expression in the dopaminergic projection fields nucleus accumbens and caudate–putamen. CNP may produce its effect directly on dopaminergic neurons because we found that its receptor, guanylyl cyclase GC‐B, was expressed in the mesencephalon where dopaminergic neurons originate, as well as in their projection fields. The inhibition by CNP of the early gene expression elicited by cocaine in the caudate–putamen is correlated with a CNP‐evoked decrease in cocaine‐induced rise in extracellular dopamine, measured by in vivo microdialysis experiments. The significance of the inhibition of cocaine‐induced dopamine release and early gene induction by the endogenous peptide CNP is demonstrated by data indicating that CNP reduced the cocaine‐induced spontaneous locomotor activation. By inhibiting dopaminergic neuronal activity, CNP represents a potential negative regulator of related behavioural effects of cocaine.
Putative glycine receptors in Hydra: a biochemical and behavioural study
Authors: Pierobon Paola , Minei Rosario , Porcu Patrizia , Sogliano Cristiana , Tino Angela , Marino Giuseppe , Biggio Giovanni , Concas Alessandra 
Published: March 2003

AbstractGlycine acts as an inhibitory transmitter in the lower brain stem and spinal cord of vertebrate species, while very few data are yet available to support a similar role in invertebrate nervous systems. Here we report the identification and characterization of glycine receptors in the freshwater polyp Hydra vulgaris (Cnidaria, Hydrozoa) by biochemical and behavioural studies. Saturation experiments revealed the occurrence of one population of binding sites of nanomolar affinity (KD = 33 nm) and low capacity (Bmax= 79 fmol/mg protein) for [3H]strychnine. The addition of glycine or taurine (0.1 µm–1 mm) produced a dose‐dependent inhibition of [3H]strychnine binding. β‐alanine (0.1–1 mm) did not significantly affect [3H]strychnine binding. The pharmacological properties of these receptors compare with those of vertebrate glycine receptors. Stimulation of Hydra polyps by reduced glutathione resulted in a significant increase in the duration of mouth opening in the presence of glycine, taurine or β‐alanine. The enhancement of the response was related both to amino acid (10–100 µm) and to glutathione concentration (1–10 µm). The effects of glycine or its agonists were suppressed by strychnine (1–10 µm). d‐serine, a glycine agonist at the vertebrate NMDA receptor, produced opposite effects to those of glycine. The effects of d‐serine were suppressed by 5,7‐dichlorokynurenic acid but not by strychnine. In vitro, [3H]strychnine binding was not displaced by d‐serine. These results indicate a dual action of glycine in Hydra tissues. The hypothesis that NMDA receptors may also be present in this elementary nervous system is proposed.
Immune surveillance of mouse brain perivascular spaces by blood‐borne macrophages
Authors: Bechmann Ingo , Priller Josef , Kovac Adam , Böntert Matthias , Wehner Tim , Klett Francisco Fernandez , Bohsung Joerg , Stuschke Martin , Dirnagl Ulrich , Nitsch Robert 
Published: March 2003

AbstractVirchow–Robin's perivascular spaces lie between the basement membrane around pericytes and the basement membrane at the surface of the glia limitans of the brain vessels. They are directly connected to the subpial space and harbour a population of cells distinct from pericytes, perivascular microglia and other cells within perivascular spaces (e.g. T cells and mast cells) in their ability to quickly phagocytose particles from the cerebrospinal fluid (CSF). Morphology, function, and cell surface proteins of these perivascular cells suggest an origin from the monocyte/macrophage lineage. It is currently unclear to what extent these brain perivascular cells represent a resident population of histiocytes or undergo continuous supplementation from blood monocytes. Using transplants of green‐fluorescent‐protein (GFP)‐transfected bone marrow cells, we therefore investigated the replacement of perivascular cells by blood‐borne macrophages in adult mice. GFP‐positive cells in the perivascular spaces were found as early as 2 weeks post transplantation. The substitution of host perivascular cells by donor‐derived macrophages was then evaluated using immunocytochemistry and intraventricular injection of hydrophilic rhodamine‐fluorescent tracers. Such tracers diffuse along perivascular spaces and are subsequently phagocytosed by perivascular cells leading to stable phagocytosis‐dependent labelling. Thus, the population of newly immigrated macrophages could be related to the total number of perivascular macrophages. This approach revealed a continuous increase of donor‐derived perivascular cells. At 14 weeks post transplantation, all perivascular cells were donor‐derived. These data show that brain perivascular cells are a population of migratory macrophages and not resident histiocytes.
Forelimb locomotor generators and quadrupedal locomotion in the neonatal rat
Authors: Ballion Bérangère , Morin Didier , Viala Denise 
Published: March 2003

AbstractThe spinal localization of the forelimb locomotor generators and their interactions with other spinal segments were investigated on in vitro brainstem–spinal cord preparations of new‐born rats. Superfusion of the cervicothoracic cord (C1–T4) with high K+/low Mg2+ artificial cerebrospinal fluid (aCSF) evoked rhythmic motor root activity that was limited to low cervical (C7, C8) and high thoracic (T1) spinal levels. This activity consisted of synchronous, homolateral bursts and a typical alternating bilateral pattern. Rhythmic activity with similar locomotor‐like characteristics could be induced with either serotonin (5‐HT, 5 µm), N‐methyl‐d‐aspartate (NMDA, 5 µm), kainate (10 µm) or a ‘cocktail’ of 5‐HT (5 µm) and NMDA (5 µm). During 5‐HT/NMDA perfusion of the cervicothoracic cord, induced bursting was no longer restricted to C7–T1 levels, but also occurred at cervical C3–C5 levels and with C5–C8 homolateral alternation. Spinal transections between C6 and C7 cervical segments did not abolish rhythmic activity in C7–T1, but suppressed locomotor‐like rhythmicity at C3–C5 levels. Reduced regions comprising the C7–C8 or C8–T1 segments maintained rhythmicity. Superfusion of the whole cord with 5‐HT/NMDA induced ventral root bursting with similar frequencies at all recorded segments (cervical, thoracic and lumbar). After isolation, the T3–T10 cord was unable to sustain any rhythmic activity while cervical and lumbar segmental levels continued to burst, albeit at different frequencies. We also found that the faster caudal and the slower rostral locomotor generators interact to produce coordinated locomotor‐like activity in all segments of the intact spinal cord. In conclusion, C7–T1 spinal levels display a strong motor rhythmogenic ability; with the lumbar generators, they contribute to coordinated rhythmic activity along the entire spinal cord of a quadrupedal locomoting mammal.
Reduction in CNS scar formation without concomitant increase in axon regeneration following treatment of adult rat brain with a combination of antibodies to TGFβ1 and β2
Authors: Moon L. D. F. , Fawcett J. W. 
Published: March 2003

AbstractIn this study we investigated whether CNS axons regenerate following attenuation of scar formation using a combination of antibodies against two isoforms of transforming growth factor beta (TGFβ). Anaesthetized adult rats were given unilateral mechanical lesions of the nigrostriatal tract. Implantation of transcranial cannulae allowed wounds to be treated with a combination of antibodies against TGFβ1 and TGFβ2 once daily for 10 days postaxotomy. Eleven days post‐transection brains from animals under terminal anaesthesia were recovered for histological evaluation. Gliosis, inflammation and the response of dopaminergic nigral axons were assessed by immunolabelling. Treatment with antibodies against TGFβ1 and TGFβ2 attenuated (but did not abolish) the response of glial fibrillary acidic protein (GFAP)‐immunoreactive astrocytes and of NG2‐immunoreactive glia but did not attenuate the response of CR3‐immunoreactive microglia and macrophages. However, this reduction in scar formation was not accompanied by growth of cut dopaminergic nigral axons. We conclude that treatment of injured adult rat brain with a combination of antibodies against TGFβ1 and TGFβ2 results in a reduction of scar formation but that this is not sufficient to enhance spontaneous long distance CNS axon regeneration.
The α1I T‐type calcium channel exhibits faster gating properties when overexpressed in neuroblastoma/glioma NG 108‐15 cells
Authors: Chemin Jean , Monteil Arnaud , Dubel Steve , Nargeot Joël , Lory Philippe 
Published: March 2003

AbstractThe recently cloned T‐type calcium channel α1I (Cav3.3) displays atypically slow kinetics when compared to native T‐channels. Possible explanations might involve alternative splicing of the α1I subunit, or the use of expression systems that do not provide a suitable environment (auxiliary subunit, phosphorylation, glycosylation…). In this study, two human α1I splice variants, the α1I‐a and α1I‐b isoforms that harbour distinct carboxy‐terminal regions were studied using various expression systems. As the localization of the α1I subunit is primarily restricted to neuronal tissues, its functional expression was conducted in the neuroblastoma/glioma cell line NG 108‐15, and the results compared to those obtained in HEK‐293 cells and Xenopus oocytes. In Xenopus oocytes, both isoforms exhibited very slow current kinetics compared to those obtained in HEK‐293 cells, but the α1I‐b isoform generated faster currents than the α1I‐a isoform. Both activation and inactivation kinetics of α1I currents were significantly faster in NG 108‐15 cells, while deactivating tail currents were two times slower, compared to those obtained in HEK‐293 cells. Moreover, the α1I‐b isoform showed significantly slower deactivation kinetics both in NG 1080‐15 and in HEK‐293 cells. Altogether, these data emphasize the advantage of combining several expression systems to reveal subtle differences in channel properties and further indicate that the major functional differences between both human α1I isoforms are related to current kinetics. More importantly, these data suggest that the expression of the α1I subunit in neuronal cells contributes to the ‘normalization’ of current kinetics to the more classical, fast‐gated T‐type Ca2+ current.
Motion processing in the auditory cortex of the rufous horseshoe bat: role of GABAergic inhibition
Authors: Firzlaff U. , Schuller G. 
Published: March 2003

AbstractThis study examined the influence of inhibition on motion‐direction‐sensitive responses of neurons in the dorsal fields of auditory cortex of the rufous horseshoe bat. Responses to auditory apparent motion stimuli were recorded extracellularly from neurons while microiontophoretically applying γ‐aminobutyric acid (GABA) and the GABAA receptor antagonist bicuculline methiodide (BMI). Neurons could respond with a directional preference exhibiting stronger responses to one direction of motion or a shift of receptive field (RF) borders depending on direction of motion. BMI influenced the motion direction sensitivity of 53% of neurons. In 21% of neurons the motion‐direction sensitivity was decreased by BMI by decreasing either directional preference or RF shift. In neurons with a directional preference, BMI increased the spike number for the preferred direction by a similar amount as for the nonpreferred direction. Thus, inhibition was not direction specific. BMI increased motion‐direction sensitivity by either increasing directional preference or magnitude of RF shifts in 22% of neurons. Ten percent of neurons changed their response from a RF shift to a directional preference under BMI. In these neurons, the observed effects could often be better explained by adaptation of excitation rather than inhibition. The results suggest, that adaptation of excitation, as well as cortex specific GABAergic inhibition, contribute to motion‐direction sensitivity in the auditory cortex of the rufous horseshoe bat.
Role of the corpus callosum in bimanual coordination: a comparison of patients with congenital and acquired callosal damage
Authors: Serrien Deborah J. , Nirkko Arto C. , Wiesendanger Mario 
Published: March 2003

AbstractThe objective of the study was to investigate temporal control in patients with congenital as compared to acquired pathology of the corpus callosum during two different bimanual paradigms: (i) a drawer‐opening task during which one hand opened a drawer while the other hand reached and grasped a small object, and (ii) rhythmical circling movements that were executed according to the in‐phase or antiphase mode. Synchronization values revealed that patients with acquired callosal dysfunction generally showed optimal behaviour during the goal‐directed and familiar drawer‐opening task but demonstrated strong tendencies towards desynchronization during circling movements, which became most apparent for antiphase coordination. Whereas one patient with callosal agenesis showed a similar performance, the other acallosal patients performed both activities successfully. These observations indicate that patients with congenital absence of the corpus callosum can make use of compensatory mechanisms for allowing temporal synchronization during bimanual movements whereas patients with acquired callosal dysfunction are severely hampered when the task places significant demands on the control processes. The data also underline that the ability of callosal patients to precisely time events in coordinated actions depend on the task constraints.
Glial‐derived arginine, the nitric oxide precursor, protects neurons from NMDA‐induced excitotoxicity
Authors: Grima Gilbert , Benz Beatrix , Do Kim Q. 
Published: March 2003

AbstractExcitotoxic neuronal cell death is characterized by an overactivation of glutamate receptors, in particular of the NMDA subtype, and the stimulation of the neuronal nitric oxide synthase (nNOS), which catalyses the formation of nitric oxide (NO) from l‐arginine (L‐Arg). At low L‐Arg concentrations, nNOS generates NO and superoxide (O2•–), favouring the production of the toxin peroxynitrite (ONOO–). Here we report that NMDA application for five minutes in the absence of added L‐Arg induces neuronal cell death, and that the presence of L‐Arg during NMDA application prevents cell loss by blocking O2•– and ONOO– formation and by inhibiting mitochondrial depolarization. Because L‐Arg is transferred from glial cells to neurons upon activation of glial glutamate receptors, we hypothesized that glial cells play an important modulator role in excitotoxicity by releasing L‐Arg. Indeed, as we further show, glial‐derived L‐Arg inhibits NMDA‐induced toxic radical formation, mitochondrial dysfunction and cell death. Glial cells thus may protect neurons from excitotoxicity by supplying L‐Arg. This potential neuroprotective mechanism may lead to an alternative approach for the treatment of neurodegenerative diseases involving excitotoxic processes, such as ischemia.
Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nucleus in the rat
Authors: Breit Sorin , Bouali‐Benazzouz Rabia , Benabid Alim‐Louis , Benazzouz Abdelhamid 
Published: March 2003

AbstractThe role of the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease is still unclear. Using microrecordings, we investigated the changes occurring in PPN neurons after lesions of the substantia nigra compacta (SNc) and the role of the subthalamic nucleus (STN) in these changes. In normal rats the firing rate of PPN neurons was 10.6 ± 1.4 spikes/s, the majority of neurons (91%) having a regular firing pattern, 6% irregular and 3% in bursts. In rats with 6‐hydroxydopamine lesions of the SNc, the firing rate increased significantly to 18.3 ± 3.0 spikes/s compared with normal rats. In addition, the firing pattern changed significantly: 70% of the neurons discharged regularly, 27% irregularly and 3% in bursts. In rats with ibotenic acid lesions of the STN, the firing rate decreased significantly to 7.2 ± 0.9 spikes/s and the firing pattern changed significantly: 50% of the neurons discharged regularly, 43% irregularly and 7% in bursts. The rats with combined SNc and STN lesions showed no change in the firing rate (8.5 ± 1.0 spikes/s) compared to normal rats. The firing pattern changed significantly: 69% of the cells discharged regularly, 26% irregularly and 5% in bursts. These findings demonstrate that PPN neurons are overactive and more irregular in the 6‐hydroxydopamine‐lesioned rats, suggesting the implication of this nucleus in the pathophysiology of parkinsonism. Moreover, the fact that STN lesions induced a reduction in the firing rate of the PPN in normal rats and a normalization of the firing rate in rats with 6‐hydroxydopamine lesions suggests that this nucleus is under major control of the STN.