bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Influence of Premotor lnterneuron Populations on the Frequency of the Spinal Pattern Generator for Swimming in Xenopus Embryos: A Simulation Study
Authors: Wolf E. , Roberts A. 
Published: April 2006

AbstractOur aim was to test the hypothesis that the frequency of neuronal rhythm‐generating networks is partly controlled by the size of the active premotor interneuron population. We have tested possible mechanisms for frequency changes in a population model of the Xenopus laevis embryo spinal rhythm‐generating networks for swimming. After initiation by a brief sensory excitation, the frequency of swimming activity decreases to a steady level determined by the properties of the 24 interneurons and their connections. The initial frequency decrease was dependent on the time‐course of initiating sensory synaptic excitation. When some premotor excitatory interneurons were given weaker synaptic connections to reflect the variability in the spinal cord, they could drop out and stop firing during the initial frequency decrease while swimming activity continued. If the synaptic input of such weak excitatory interneurons was graded finely, they could drop out consecutively. This led to further decreases in the level of tonic excitation and in network frequency which depended on the number, type and distribution of excitatory interneurons that stopped firing. Silent weak excitatory interneurons could be recruited by a second sensory excitation and cause an increase in tonic depolarization and frequency which outlasted the sensory input. Such recruitment could occur on both sides after local sensory stimulation to only one region or one side of the model. We conclude that these computer simulations support the hypothesis that premotor interneuron drop‐out and recruitment is one mechanism which can control frequency in a locomotor central pattern generator.
Ontogeny of the D1 Dopamine Receptor in the Rat Striatonigral System: an lmmunohistochemical Study
Authors: Caille I. , Dumartin B. , Le Moine C. , Begueret J. , Bloch B. 
Published: April 2006

AbstractAntibodies were raised against a recombinant protein to analyse the pre‐ and postnatal ontogeny of the neurons expressing the D1 dopamine receptor in the striatum by immunohistochemistry. We report that D1 immunoreactivity is detectable from gestational day (G) 15 and is distributed homogeneously throughout the striatum from G15 to G18. From G19–20 to postnatal day (P) 3, D1 immunoreactivity becomes heterogeneous and predominates in cell bodies of the patch Compartment while very limited immunoreactivity is detectable in the matricial compartment. The differential intensity between patches and matrix reaches its peak around PO. From P2, the pattern of D1 immunoreactivity progressively assumes the homogeneous distribution characteristic of the adult striatum. The expression of D1 mRNA in striatal neurons, as investigated by in situ hybridization, displays a similar pattern during this period. Substance P mRNA is also preferentially expressed in the patch compartment during the same period. D1 immunoreactivity appears at G17 in the substantia nigra as clusters of fibres and increases subsequently until reaching its adult form during the first postnatal week. These results demonstrate that the two compartments of the developing striatum display differential transcriptional and translational activity for the D1 gene and consequently two different and successive patterns of expression of D1 protein: patch neurons first express D1 receptor intensely while matrix neurons express it later and in smaller amounts so that D1 receptor appears transiently during the perinatal period as a marker of the patch compartment.
Axonal Target Choice and Dendritic Development of Ferret Beta Retinal Ganglion Cells
Authors: Wingate Richard J. T. , Thompson Ian D. 
Published: April 2006

AbstractWe have investigated the relationship between axon targeting and dendritic morphology in beta retinal ganglion cells in the postnatal ferret. Axonal projections were assessed by making separate injections of different fluorescent retrograde tracers into either the superior colliculus or lateral geniculate nucleus in viva The dendritic morphology of retrogradely labelled cells was revealed by the in vitro intracellular injection of Lucifer yellow in fixed retina. In this way, 405 retinal ganglion cells were triple‐ or double‐labelled and characterized by their dendritic branching styles. Both the distinct dendritic morphology of beta cells and the characteristic restriction of their adult axonal terminals to the lateral geniculate nucleus emerge postnatally. Beta cell dendritic morphology is established between postnatal days 5 and 9. As in the cat (Ramoa et al, 1989), beta cells extend and then retract a projection to the superior colliculus as part of their normal development. Transient beta axonal collaterals to the superior colliculus persist beyond the period of cell death, but nearly all are withdrawn by postnatal day 15. No dendritically distinct beta cell projects to the superior colliculus alone, at any age.Heterochronic injections of different colours of retrograde tracer into the superior colliculus were used to study changes in the complement of the retinocollicular projection over time. A significant proportion of cells (58%) labelled at postnatal day O from the superior colliculus, which subsequently survived the period of cell death, were found to be beta cells that could no longer be demonstrated to have a retinocollicular axon. Neonatal decortication, which reduced the volume of the adult lateral geniculate nucleus by 36–86%, resulted in the limited stabilization of this normally transient beta cell projection to the superior colliculus. The fundamental dendritic branching style of beta ganglion cells is unchanged in decorticate ferrets, suggesting that it develops independently of their ultimate axonal target choice.
Development and Pharmacological Suppression of Secondary Afterdischarges in the Hippocampus of Amygdala‐kindled Rats
Authors: Ebert Ulrich , Rundfeldt Chris , Löscher Wolfgang 
Published: April 2006

AbstractThe development and spread of afterdischarges in the ipsilateral limbic system during amygdala kindling, a model of complex partial seizures, was studied in male and female rats. Kindling stimulation was performed in the basolateral amygdala, and afterdischarges were recorded from the stimulation electrode and electrodes in the nucleus accumbens, the posterior piriform cortex and the ventral hippocampus, all implanted on the right side of the brain. All structures showed primary afterdischarges already after the first stimulation, indicating a close anatomical and physiological connection to the epileptogenic focus. The development of robust secondary afterdischarges, which occurred after the end of the primary afterdischarges in the amygdala and which always originated in the hippocampus but also spread to one or more of the other recording sites, is described. The secondary afterdischarges initially occurred after about nine kindling stimulations in both male and female rats, and were associated with an increase in primary afterdischarge duration and a progression from focal to motor seizures. In order to test the effect of common antiepileptic drugs on the secondary afterdischarges, a group of female rats were treated with valproate, carbamazepine or phenytoin. All drugs suppressed the secondary afterdischarges, although they had a different anticonvulsant efficacy on motor seizures and afterdischarge duration after amygdala stimulation. While valproate and carbamazepine dose‐dependently reduced all parameters of the kindled seizure, including the secondary afterdischarges in the hippocampus, phenytoin suppressed the secondary afterdischarges also in the absence of any anticonvulsant effect, suggesting that recurrent hippocampal activation is not crucial for the kindled state. Recording of secondary afterdischarges in the hippocampus may offer the possibility of studying the conditions for development and pharmacological suppression of recurrent hippocampal activation in amygdala‐kindled rats.
Expression of the Homeobox‐containing Gene En‐2 During the Development of the Chick Central Nervous System
Authors: Millet Sandrine , Alvarado‐Mallart Rosa‐Magda 
Published: April 2006

AbstractThe expression of the homeobox‐containing gene En‐2 was analysed with the monoclonal antibody 4D9 in the chick central nervous system throughout embryogenesis. Confirming previous studies, early expression of the En‐2 protein [beginning at stage 9 of Hamburger and Hamilton (HH9)] is restricted to a portion of the neural tube containing the primordia of the cerebellum, the isthmic region and the mesencephalic grisea, and forms a double gradient decreasing both caudally and rostrally from a high point located around the midbrain‐hindbrain constriction. This mes‐isthmo‐cerebellar region contains all the En‐2‐positive germinative cells and the great majority of the En‐2‐positive postmitotic neurons throughout embryogenesis. Nevertheless, as the postmitotic neurons appear, En‐2 expression also occurs outside this region: in two columns of non‐motoneuron cells in rhombomeres two to four (between HH20 and HH30) and, from HH24 onwards, throughout the grey matter of the lumbar and thoracic spinal cord, with the exception of the ventral motoneuron columns. Here, a detailed description of En‐2 expression is provided for the mes‐isthmo‐cerebellar region at stages HH30–32 [embryonic day (E) 71, HH37 (E11) and HH46 (E21, hatching). This allows the visualization of cellular groups with heterogeneous patterns of En‐2 expression, which are specific for each group in the intensity of En‐2 expression, the distribution of the labelled cells and the temporal regulation of the gene. The use of tyrosine hydroxylase antiserum shows coexpression of the tyrosine hydroxylase enzyme and En‐2 protein in the caudal part of the nuclei tegmenti pedunculo‐pontinus, the area ventralis of Tsai and the substantia grisea centralis, but not in the locus coeruleus. In the cerebellum, the first expression, which is located in the deep nuclei and parasagittal bands of Purkinje cells, is down‐regulated when the molecular layer interneurons and the granular cells begin to express the gene, at the end of embryogenesis. Finally, at hatching, En‐2 expression permits the visualization in the cerebellum of a population of small En‐2‐negative cells located around the Purkinje cells that may correspond to those described in chick/quail chimaeras as having an origin different from that of the bulk of granular neurons.
Antibodies to Postsynaptic PKC Substrate Neurogranin Prevent Long‐term Potentiation in Hippocampal CA1 Neurons
Authors: Fedorov N. B. , Pasinelli P. , Oestreicher A. B. , DeGraan P. N. E. , Reymann K. G. 
Published: April 2006

AbstractBoth pre‐ and postsynaptic protein kinase C have been implicated in long‐term potentiation. Neurogranin (also known as BICKs and RC3) is a neuronal postsynaptic protein kinase C substrate. In the present study we injected monoclonal IgGs that recognize the protein kinase C phosphorylation site in neurogranin and B‐50 (GAP‐43), and that have been shown to inhibit protein kinase C‐mediated B‐50 phosphorylation, through a whole‐cell clamp pipette into CA1 pyramidal neurons in rat hippocampal slices. Injection of neurogranin IgGs, but not of control IgGs, prevented the induction of tetanus‐induced long‐term potentiation without affecting posttetanic potentiation. Our results suggest that neurogranin is involved in mechanisms of activity‐dependent synaptic plasticity.
Laufband Therapy Based on‘Rules of Spinal Locomotion’is Effective in Spinal Cord Injured Persons
Authors: Wernig A. , Müller S. , Nanassy A. , Cagol E. 
Published: April 2006

AbstractRehabilitation of locomotion in spinal cord (s.c.) injured patients is unsatisfactory. Here we report the effects of a novel ‘Laufband (LB; treadmill) therapy’ based on ‘rules of spinal locomotion’ derived from lower vertebrates. Eighty‐nine incompletely paralysed (44 chronic and 45 acute) para‐ and tetraplegics underwent this therapy, then were compared with 64 patients (24 chronic and 40 acute) treated conventionally. The programme consisted of daily upright walking on a motor driven LB initially with body weight support (BWS) provided by a harness and assisted limb movements by the therapists when necessary. Forty‐four chronic patients with different degrees of paralysis undertook the programme for 3‐20 weeks (median = 10.5), 0.5–18 years after S.C. damage. At the onset of LB therapy 33/44 patients were wheelchair‐bound (no standing and/or walking without help by others) compared with 25 at completion of LB therapy, i.e. 76% had learned to walk independently, 7 patients with help. Only 1 subject did not improve. It was striking that voluntary muscle activity in the resting position was still low in several patients who had gained walking capability. Eleven patients who could already walk before LB therapy improved in speed and endurance. Of the 44 patients, six were capable of staircase walking before LB therapy compared with 34 afterwards. In order to validate the apparent superiority of LB therapy two types of comparisons were performed. In a ‘temporal’ control 12 spastic paretic patients, still wheelchair‐bound after the period of postacute conventional therapy, performed LB immediately thereafter. After completion of LB therapy nine of these patients had learned to walk without help from others. In another control, two groups of chronic patients, matched in type of injury, time after injury (1 or more years) and history of previous rehabilitation (one or several periods of conventional therapy), were compared. One group underwent LB therapy (n= 29), the other conventional therapy (n= 24) for similar periods of time. From 18 wheelchair‐bound patients, 14 became independent walkers after LB, but only 1/14 after conventional therapy. From 45 acute patients 92% (33/36) of those wheelchair‐bound at the onset of LB therapy became independent, but only 50% (12/24) after conventional therapy (n= 40). It is noteworthy that voluntary muscle activity at rest was similar in both groups. The presumed underlying mechanisms are discussed in the light of the absence of any apparent effects in seven functionally completely paralysed paraplegic persons.
Electron Microscopic Observation of Substance P‐like Immunoreactive Nerve Fibres and Innervation in the Anterior Pituitary of Macaques
Authors: Liu Shaojun 
Published: April 2006

AbstractThe anterior pituitary has recently been confirmed to be innervated by substance P‐immunoreactive nerve fibres in the monkey and human. The present study investigated the morphology of the nerve fibres and their relationship with anterior pituitary gland cells in the macaque by means of immunoelectron microscopy. Many substance P‐immunoreactive and unlabelled nerve fibres were distributed among the gland cells or formed nerve fibre bundles. These nerve fibres were unmyelinated and varicose, and contained a great many clear and/or large dense‐cored vesicles. Substance P‐immunoreactive cells were seen in the pars distalis of the anterior pituitary. Direct contacts between these nerve fibres and every cell type of the gland could be ascertained, including substance P‐immunoreactive cells. Synaptoid contacts were seen among the substance P‐immunoreactive varicosities and somatotropes, opiocortico‐melanotropes and folliculostellate cells. Typical synapses were identified in somatotropes and opiocortico‐melanotropes.
Vulnerability of Medium Spiny Striatal Neurons to Glutamate: Role of Na+/K+ ATPase
Authors: Calabresi Paolo , De Murtas Marco , Pisani Antonio , Stefani Alessandro , Sancesario Giuseppe , Mercuri Nicola B. , Bernardi Giorgio 
Published: April 2006

AbstractIn Huntington's disease neuronal degeneration mainly involves medium‐sized spiny neurons. It has been postulated that both excitotoxic mechanisms and energy metabolism failure are implicated in the neuronal degeneration observed in Huntington's disease. In central neurons, >40% of the energy released by respiration is used by Na+/K+ ATPase to maintain ionic gradients. Considering that impairment of Na+/K+ ATPase activity might alter postsynaptic responsivity to excitatory amino acids (EAAs), we investigated the effects of the Na+/K+ ATPase inhibitors, ouabain and strophanthidin, on the responses to different agonists of EAA receptors in identified medium‐sized spiny neurons electrophysiologically recorded in the current‐ and voltage‐clamp modes. In most of the cells both ouabain and strophanthidin (1–3 μM) did not cause significant change in the membrane properties of the recorded neurons. Higher doses of either ouabain (30 μM) or strophanthidin (30 μM) induced, per se, an irreversible inward current coupled to an increase in conductance, leading to cell deterioration. Moreover, both ouabain (1–10 μM) and strophanthidin (1–10 μM) dramatically increased the membrane depolarization and the inward current produced by subcritical concentrations of glutamate, AMPA and NMDA. These concentrations of Na+/K+ ATPase inhibitors also increased the membrane responses induced by repetitive cortical activation. In addition, since it had previously been proposed that dopamine mimics the effects of Na+/K+ ATPase inhibitors and that dopamine agonists differentially regulate the postsynaptic responses to EAAs, we tested the possible modulation of EAA‐induced membrane depolarization and inward current by dopamine agonists. Neither dopamine nor selective dopamine agonists or antagonists affected the postsynaptic responses to EAAs. Our experiments show that impairment of the activity of Na+/K+ ATPase may render striatal neurons more sensitive to the action of glutamate, lowering the threshold for the excitotoxic events. Our data support neither the role of dopamine as an ouabain‐like agent nor the differential modulatory action of dopamine receptors on the EAA‐induced responses in the striatum.
Properties of the Ryanodine‐sensitive Release Channels that Underlie Caffeine‐induced Ca2+Mobilization from Intracellular Stores in Mammalian Sympathetic Neurons
Authors: Hernández‐Cruz A. , Díaz‐Muñoz M. , Gómez‐Chavarín M. , Canñedo‐Merino R. , Protti D. A. , Escobar A. L. , Sierralta J. , Suárez‐Isla B. A. 
Published: April 2006

AbstractThe most compelling evidence for a functional role of caffeine‐sensitive intracellular Ca2+reservoirs in nerve cells derives from experiments on peripheral neurons. However, the properties of their ryanodine receptor calcium release channels have not been studied. This work combines single‐cell fura‐2 microfluorometry, [3H]ryanodine binding and recording of Ca2+release channels to examine calcium release from these intracellular stores in rat sympathetic neurons from the superior cervical ganglion. Intracellular Ca2+measurements showed that these cells possess caffeine‐sensitive intracellular Ca2+stores capable of releasing the equivalent of 40% of the calcium that enters through voltage‐gated calcium channels. The efficiency of caffeine in releasing Ca2+showed a complex dependence on [Ca2+]i. Transient elevations of [Ca2+]iby 50–500 nM were facilitatory, but they became less facilitatory or depressing when [Ca2+]ireached higher levels. The caffeine‐induced Ca2+release and its dependence on [Ca2+]iwas further examined by [3H]ryanodine binding to ganglionic microsomal membranes. These membranes showed a high‐affinity binding site for ryanodine with a dissociation constant (KD= 10 nM) similar to that previously reported for brain microsomes. However, the density of [3H]ryanodine binding sites (Bmax= 2.06 pmol/mg protein) was at least three‐fold larger than the highest reported for brain tissue. [3H]Ryanodine binding showed a sigmoidal dependence on [Ca2+] in the range 0.1–10 μM that was further increased by caffeine. Caffeine‐dependent enhancement of [3H]ryanodine binding increased and then decreased as [Ca2+] rose, with an optimum at [Ca2+] between 100 and 500 nM and a 50% decrease between 1 and 10 μM. At 100 μM [Ca2+], caffeine and ATP enhanced [3H]ryanodine binding by 35 and 170% respectively, while binding was reduced by >90% with ruthenium red and MgCl2. High‐conductance (240 pS) Ca2+release channels present in ganglionic microsomal membranes were incorporated into planar phospholipid bilayers. These channels were activated by caffeine and by micromolar concentrations of Ca2+from the cytosolic side, and were blocked by Mg2+and ruthenium red. Ryanodine (2 μM) slowed channel gating and elicited a long‐lasting subconductance state while 10 mM ryanodine closed the channel with infrequent opening to the subconductance level. These results show that the properties of the ryanodine receptor/Ca2+release channels present in mammalian peripheral neurons can account for the properties of caffeine‐induced Ca2+release. Our data also suggest that the release of Ca2+by caffeine has a bell‐shaped dependence on Ca2+in the physiological range of cytoplasmic [Ca2+].
Agonist‐induced Down‐regulation of NMDA Receptors in Cerebellar Granule Cells in Culture
Authors: Resink A. , Villa M. , Boer G. J. , Möhler H. , Balázs R. 
Published: April 2006

AbstractIn contrast to the acute toxic effect of NMDA on mature cerebellar granule cells, chronic treatment with NMDA (140 μM from 1 to 9 days in vitro) did not compromise cell survival. Such treatment markedly suppressed NMDA receptor activity: at 8 days in vitro NMDA‐induced 45Ca2+ influx was reduced by ‐60% and acute exposure to NMDA (highest concentration tested, 1 mM) at 9 days in vitro did not cause detectable toxicity. The reduction in NMDA receptor activity was accompanied by a significant decrease (±80% at 9 days in vitro) in the level of the NR1 and the NR2A NMDA receptor subunit protein, detected using the selective photoaffinity ligand [125I]CGP55802A. It seems, therefore, that the agonist‐induced decrease in NMDA receptor activity is due to receptor down‐regulation. In contrast to the marked influence of chronic NMDA exposure on the cellular content of the NMDA receptor subunit proteins, mRNA levels of the different subunits (NR1, NR2A, NR2B and NR2C) were not significantly affected. It seems, therefore, that agonist‐induced down‐regulation of the NMDA receptor involves critically mRNA translation and/or post‐translational regulation.