bluuebunny/crossref_metadata_2025_split huggingface dataset:
Axonal Growth on Solubilized and Reconstituted Matrix from the Embryonic Chicken Retina Inner Limiting Membrane
Authors: Halfter W. , Von Boxberg Y. 
Published: April 2006

AbstractBasal laminae, thin sheets of extracellular matrix covering the basal side of all neuroepithelia, are strongly supportive for neurite outgrowth in vitro and may provide a permissive environment for growing neurites in vivo. To gain information about the biological activity and composition of in situ‐derived basal laminae the inner limiting membranes from embryonic day (E) 7 to E11 chick and quail retinae were isolated. The basal laminae were solubilized with high‐molar guanidine hydrochloride or urea, and the solubilized proteins reconstituted by dialysis. The matrix proteins were spotted or dried onto nitrocellulose or polylysine‐coated dishes. When explants from retina or from dorsal root ganglia were incubated on the protein spots, neurite extension was very robust, at a level as high as on authentic basal lamina. Extracts from the pigment epithelial basement membrane did not support neurite extension. Western blot analysis showed that the explant from the retinal inner limiting membrane contained predominantly basal lamina‐type proteins, such as laminin, collagen type IV and heparan sulphate proteoglycan, whereas the matrix extract from the pigment epithelium contained predominantly mesenchymal‐type proteins, like collagen type I and tenascin. JG22, a β1 integrin antibody that inhibited neurite extension on EHS tumour laminin substrate, had no effect on neurite outgrowth on retinal basal lamina matrix, indicating that embryonic basal laminae contain other or additional growth promoting substrate molecules.
GABAergic Interneurons are the Major Postsynaptic Targets of Median Raphe Afferents in the Rat Dentate Gyrus
Authors: Halasy K. , Miettinen R. , Szabat E. , Freund T. F. 
Published: April 2006

AbstractThe termination pattern of median raphe axons was studied in the rat dentate gyrus using Phaseolus vulgaris leucoagglutinin as an anterograde tracer, in combination with postembedding immunostaining for γ‐amino‐butyric acid (GABA), and pre‐embedding immunostaining for calbindin D28k, parvalbumin and GABA. Postembedding immunogold staining for GABA revealed that the majority (73.7%) of anterogradely labelled median raphe boutons make synaptic contacts with GABA‐immunoreactive postsynaptic targets, mainly with dendritic shafts and perikarya. Pre‐embedding immunocytochemical double staining for the anterograde tracer and GABA confirmed the electron microscopic results and showed that varicose median raphe axons establish multiple contacts with fusiform interneurons in the hilus and different types of basket cells in the granule cell layer. Some of the innervated cells were shown to contain calbindin D28k, whereas GABAergic interneurons containing another calcium‐binding protein, parvalbumin, were never seen to receive multiple contacts from axons of raphe origin. Our results suggest that serotonergic median raphe fibres influence the firing of dentate granule cells via local inhibitory interneurons. The mechanism of using these interneurons with extensive local connections as monosynaptic targets may explain the great efficacy of this pathway in the control of hippocampal electrical activity.
Learning of Sequential Finger Movements in Man: A Combined Kinematic and Positron Emission Tomography (PET) Study
Authors: Seitz Rüdiger J. , Roland Per E. 
Published: April 2006

AbstractThe cerebral structures participating in learning of a manual skill were mapped with regional cerebral blood flow (rCBF) measurements and positron emission tomography in nine healthy volunteers. The task was a complicated right‐hand finger movement sequence. The subjects were examined at three stages: during initial practice of the finger movement sequence, in an advanced stage of learning, and after they had learnt the finger movement sequence. Quantitative evaluation of video tapes and electromyographic records of the right forearm and hand muscles demonstrated that the finger movements significantly accelerated and became more regular. Significant mean rCBF increases were induced in the left motor hand area, the left premotor cortex, the left supplementary motor area, the left sensory hand area, the left supplementary sensory area and the right anterior lobe of the cerebellum. During the learning process significant depressions of the mean rCBF occurred bilaterally in the superior parietal lobule, the anterior parietal cortex and the pars triangularis of the right inferior frontal cortex. The mean rCBF increases in these structures during the initial stage of learning were related to somatosensory feedback processing and internal language for the guidance of the finger movements. These activations disappeared when the subjects had learnt the finger movement sequence. Conversely, the mean rCBF significantly rose during the course of learning in the midsector of the putamen and globus pallidus on the left side. It is suggested that during the learning phase of this movement sequence, the basal ganglia were critically involved in the establishment of the final motor programme.
Widespread Horizontal Connections Arising from Layer 5/6 Border Inverted Cells in Rabbit Visual Cortex
Authors: Reblet Conceptión , López‐Medina Antonio , Gómez‐Urquijo Sonia M. , Bueno‐López José L. 
Published: April 2006

AbstractHerein we describe the inverted cells [defined as those projection neurons having a major dendritic shaft abpially oriented (Bueno‐López et al., Eur. J. Neurosci., 3, 415, 1991)] originating a unique set of cortical connections characterized by extraordinarily widespread horizontal distribution. Single and multiple injections of wheatgerm agglutinin ‐ horseradish peroxidase were made in areas 17 and 18 and the resulting retrograde labelling in the cortex was analysed. The findings were assessed in independent control experiments in which Fluoro‐Gold was used as retrograde tracer. Following single injections in area 17 several separate patches of labelled cells comprising layers 2–6 were consistently found in area 18. In addition to these associational cells a number of labelled cells appeared at the layer 5/6 border but were distributed over most of the tangential extent of the visual occipital cortex. This widespread pattern was particularly striking in brains after multiple injections. In these brains a conspicuous band of labelled cells at the 5/6 border radiated from the injection sites, making up an apparently continuous horizontal sheet that intersected the striate ‐ extrastriate boundary and merged with the patches of labelled cells in area 18 and beyond. Most of the cells in the 5/6 border band were inverted cells (82%; n= 2081). Injections in area 18 failed to produce such a widespread set of labelled cells in area 17. The functional significance of these connections furnished by the 5/6 border inverted cells remains to be determined, but their distribution would allow for convergent/divergent binding interactions both intra‐areally (within area 17) and inter‐areally (from area 18 to area 17).
Increase in GABAergic Cells and GABA Levels in the Spinal Cord in Unilateral Inflammation of the Hindlimb in the Rat
Authors: Castro‐Lopes J. M. , Tavares Isaura , Tölle T. R. , Coito Ana , Coimbra A. 
Published: April 2006

AbstractThe effects of chronic peripheral inflammation on spinal cord γ‐aminobutyric acid (GABA) were examined in the rat. Following the injection of complete Freund's adjuvant in the left hindlimb footpad an increased number of immunoreactive cells occurred in ipsilateral laminae I‐III of the dorsal horn from L3 to L5. GABA‐immunoreactive cells were more numerous than contralaterally 1 week after the onset of the inflammation, reached maximal numbers after 3–4 weeks, and declined thereafter. Differences from control sides were statistically significant except at week 6. GABA levels in homogenates of the ipsilateral lumbar enlargement were increased significantly at 4 weeks. Since increases in GABA occurred in the spinal cord zone of projection of the nerves supplying the inflamed foot, the central response is surmised to result from the increased nociceptive input arriving from the periphery. However, the transmission from primary axons to GABA interneurons is not likely to be monosynaptic since profiles containing glutamate decarboxylase or GABA immunoreactivity are known to be predominantly presynaptic, and rarely postsynaptic, to primary afferent endings in electron micrographs in the rat. The findings support the function attributed to spinal GABA in modulating nociceptive input at segmental level.
Antagonists of the Platelet‐activating Factor Receptor Block Long‐term Potentiation in Hippocampal Slices
Authors: Arai Amy , Lynch Gary 
Published: April 2006

AbstractThe effects of antagonists and agonists of the platelet‐activating factor (PAF) receptor on the formation of long‐term potentiation (LTP) were examined in slices of rat hippocampus. The antagonist trans‐BTD (trans‐2,5‐bis‐(3,4,5‐trimethoxyphenyl)‐1,3‐dioxolane) at concentrations of 8–16 μM blocked LTP in field CA1 while the same concentration of a stereo isomer (cis‐BTD) with low affinity for PAF receptors was without effect. CV3988, an antagonist structurally related to PAF, also attenuated LTP. The blockade of LTP by trans‐BTD was partially reversed by simultaneous application of the non‐metabolizable receptor agonist carbamyl‐PAF. Trans‐BTD did not change the following physiological measures: (i) paired‐pulse facilitation, (ii) responses occurring during the short bursts given to induce LTP, (iii) N‐methyl‐d‐aspartate receptor‐mediated responses, and (iv) potentiation measured during the first minute after high‐frequency stimulation. It thus appears that trans‐BTD interferes with LTP at some step after induction and initial expression. These results suggest that activation of PAF receptors contributes to the stabilization of LTP, possibly via an effect on intracellular calcium levels.
A Role for Nitric Oxide in Long‐term Potentiation
Authors: Bon Christelle , Böhme Georg Andrees , Doble Adam , Stutzmann Jean‐Marie , Blanchard Jean‐Charles 
Published: April 2006

AbstractNitric oxide production in the cerebellum and induction of long‐term potentiation (LTP) in the hippocampus have some characteristics in common: both phenomena are induced by activation of N‐methyl‐D‐aspartate receptors and both are highly dependent on calcium‐mediated processes. Here we provide evidence that endogenous nitric oxide production is necessary for synaptic plasticity in the CA1 hippocampus of the rat. LTP recorded in slices was blocked in a concentration‐dependent manner by the nitric oxide synthase inhibitors L‐NG‐nitroarginine and L‐NG‐nitroarginine methyl ester, but L‐NG‐monomethylarginine was only marginally active. Bathing the slices with haemoglobin, a protein that scavenges nitric oxide, also resulted in a concentration‐dependent blockade of LTP. Nitric oxide released locally from hydroxylamine produced a stable potentiation of synaptic transmission that was not additive with LTP induced by high‐frequency stimulation. These results are fully consistent with the presumed retrograde messenger role of nitric oxide in LTP.
The Role of Ca2+ in the Elimination of Polyneuronal Innervation of Rat Soleus Muscle Fibres
Authors: Zhu Pei‐Hong , Vrbová G. 
Published: April 2006

AbstractThe mechanism by which nerve ‐ muscle contacts are reduced during postnatal development of the rat soleus muscle was investigated using electrophysiological methods. Between days 7 and 9 after birth, soleus muscle fibres lose 0.19–0.24 terminals per muscle fibre within 24 h. A much more rapid loss of contacts is seen when muscles are exposed in vitro to acetylcholine (10−3 g/ml). In this case 0.67–0.87 terminals per muscle fibre lose contact within 2 h. The loss of neuromuscular contacts induced by acetylcholine can be reduced by preincubating the muscles in solutions containing acetoxymethyl ester of 1,2‐bis(2‐amino‐phenoxylethane‐N,N1;N1‐tetraacetic acid (BAPTA‐AM), a Ca2+ chelating agent that enters cells and reduces the Ca2+ transients inside the cell. Treatment of muscles with nifedipine, which blocks dihydropyridine‐sensitive (L‐type) Ca2+ channels, also reduced the acetylcholinesterase‐induced loss of neuromuscular contacts. The results indicate that transient increases in Ca2+ inside nerve terminals contribute to loss of neuromuscular contacts, and that these increases occur by Ca2+ entry through L‐type channels.
Heterogeneity in the Membrane Current Pattern of Identified Glial Cells in the Hippocampal Slice
Authors: Steinhaüser C. , Berger T. , Frotscher M. , Kettenmann H. 
Published: April 2006

AbstractGlial cells, acutely isolated or in tissue culture, have previously been shown to express a variety of voltage‐gated channels. To resolve the question whether such channels are also expressed by glial cells in their normal cellular environment, we have applied the patch‐clamp technique to study glial cells in hippocampal slices of 10–12‐day‐old mice. Based on the membrane current pattern, we distinguished four glial cell types. One was characterized by passive, symmetrical K+ currents activated in depolarizing and hyperpolarizing directions. A second population showed a similar current pattern, but with a marked decay of the current during the 50‐ms voltage jumps. In a third population, the decaying passive currents were superimposed with a delayed rectifier outward current and, in some cases, with a slow inward current activated by depolarization. The fourth population expressed delayed rectifying outward currents, an inward rectifier K+ current and fast inward currents activated by depolarization. To unequivocally identify the glial cells we combined electrophysiological and ultrastructural characterizations. Therefore, cells were filled with the fluorescent dye lucifer yellow during characterization of their membrane currents, the fluorescence of the dye was used to convert diaminobenzidine to an electron‐dense material, and subsequently slices were inspected in the electron microscope. Recordings were obtained from cells in the stratum radiatum and were identified as glial by their size, the characteristic chromatin distribution, and the lack of synaptic membrane specializations.
Characterization of L‐2‐Amino‐4‐Phosphonobutanoate Action Following Sensitization by Quisqualate in Rat Hippocampal Slice Cultures
Authors: Charpak Serge , Thompson Scott M. , Gähwiler Beat H. , Gerber Urs 
Published: April 2006

AbstractAn excitatory action of l‐2‐amino‐4‐phosphonobutanoate (l‐AP4), a glutamate analogue, is observed following pre‐exposure of tissue to quisqualate. We have studied the mechanism of sensitization of l‐AP4 responses by quisqualate in voltage‐clamped CA3 pyramidal cells in rat hippocampal slice cultures in the presence of tetrodotoxin. Prior to quisqualate addition, CA3 cells did not respond to l‐AP4 (50–1000μM). Following brief application of quisqualate (500 nM for 30 s), l‐AP4 (50–200 μM) induced a complex excitatory response which could be obtained for >1 h. l‐AP4 caused an ionotropic inward current associated with a conductance increase. This response was in part sensitive to 6‐cyano‐7‐nitro‐quinoxaline‐2,3‐dione (CNQX) and in part sensitive to d‐2‐amino‐5‐phosphonovalerate (d‐AP5) and Mg2+ ions. At depolarizing potentials, in the presence of CNQX and d‐AP5, l‐AP4 caused excitation by depressing K+ currents, mimicking the metabotropic action of glutamate. This indicates that the action of l‐AP4 is mediated by three different receptor types: N‐methyl‐D‐aspartate (NMDA) receptors, α‐amino‐3‐hydroxy‐5‐methyl‐isoxazole‐4‐propionate (AMPA) receptors, and glutamatergic metabotropic receptors. The l‐AP4 response persisted in solutions containing low Ca2+ and high Mg2+ concentrations or 100–200 μM Cd2+, suggesting that it is independent of extracellular Ca2+. We were unable to identify any substance other than quisqualate capable of sensitizing the l‐AP4 action. This effect also occurred when quisqualate was applied in Ca2+‐free solution or in solutions containing low concentrations of Na+ or Cl−. Sensitization of l‐AP4 responses by quisqualate was not observed in acutely dissociated pyramidal cells recorded by means of the whole‐cell recording mode, although ionotropic quisqualate responses were present. Sensitization was readily reversed by short applications of the endogenous excitatory amino acids glutamate, aspartate and homocysteate at concentrations of 10–100 μM. Our data are consistent with the hypothesis that the excitatory action of l‐AP4 results from a Ca2+‐independent release of endogenous excitatory amino acids from some presynaptic neuronal or glial site.
Quisqualate Metabotropic Receptors Modulate NMDA Currents and Facilitate Induction of Long‐Term Potentiation Through Protein Kinase C
Authors: Aniksztejn Laurent , Otani Satoru , Ben‐Ari Yehezkel 
Published: April 2006

AbstractUsing intracellular and extracellular recordings in rat hippocampal slices, we have investigated the interactions between the quisqualate metabotropic receptor (QP) and currents mediated by N‐methyl‐d‐aspartate (NMDA) and α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA). We found that trans‐ (t)‐1‐amino‐1,3‐cyclopentanedicarboxylic acid (trans‐ACPD) and 1S,3R‐aminocyclopentane‐1,3‐dicarboxylic acid (1S,3R‐ACPD) potentiated NMDA but not AMPA‐mediated currents. Intracellular injections of selective protein kinase C inhibitors prevented the up‐regulation of the NMDA response. The physiological consequence of the up‐regulation by ACPD of the NMDA response on the threshold of long‐term potentiation induction was tested. We found that a subthreshold train of electrical stimulation that produced short‐term potentiation generated long‐term potentiation when coupled with ACPD application, an effect which was not produced by AMPA or NMDA. This effect was blocked by an inhibitor of protein kinase C. These results demonstrate for the first time that one subtype of glutamate receptor (QP) can regulate another subtype of glutamate receptor (NMDA) through the activation of protein kinase C. Our results also suggest that the NMDA receptor is regulated by protein kinase C, and that the intracellular level of protein kinase C may determine the threshold for induction of long‐term potentiation.
Parallel Circuits from Cones to the On‐Beta Ganglion Cell
Authors: Cohen Ethan , Sterling Peter 
Published: April 2006

AbstractNeural integration depends critically upon circuit architecture; yet the architecture has never been established quantitatively (numbers of cells and synapses) for any vertebrate local circuit. Here we describe circuits in the cat retina that connect cones to the on‐beta ganglion cell. This cell type is important because on‐ and off‐beta cells contribute about 50% of the optic nerve fibres and the major retinal input to the striate cortex. Three adjacent on‐beta cells in the area centralis and their bipolar connections to cones were reconstructed from electron micrographs of 279 serial sections. The beta dendritic field is 34±2 μm in diameter and encompasses 35 cones. All of these cones connect to the beta cell via 14–17 bipolar cells. These bipolar cells were shown previously by cluster analysis to be of four types (b1‐b4); three of these types (b1′ b2 and b3) provided 97% of the bipolar contacts to the beta cell, in the ratio 4:2:1. On average, bipolar cells nearest the centre of the beta dendritic field contribute more synapses than those towards the edge, but the peaked distribution of bipolar synapses across the dendritic field is only slightly broader than the optical pointspread function of the cat's eye, and is narrower by half than the centre of the ganglion cell receptive field. This implies that the distribution of bipolar synapses across the beta cell dendritic field contributes little to the extent or shape of the receptive field. Since all three bipolar circuits connect to the same set of cones, they must carry the same spatial and chromatic information; they might convey different temporal frequencies. The numbers of bipolar synapses (mean ± SD = 154±8) and amacrine synapses (59±5) converging on three adjacent beta cells are remarkably constant (SD=±5% of the mean). Thus, as the circuits repeat locally, the fundamental design is accurately reproduced.
Expression of the Neural Recognition Molecule L1 by Cultured Neural Cells is influenced by K+ and the Glutamate Receptor Agonist NMDA
Authors: Scherer Martin , Heller Martin , Schachner Melitta 
Published: April 2006

AbstractTo investigate the influence of neuronal activity on the expression of neural recognition molecules, cultures of neural cell lines and dissociated cells of early postnatal mouse cerebellum were maintained in the presence of elevated concentrations of K+ and the glutamate agonist N‐methyl‐D‐aspartate (NMDA). Levels of expression of the neural adhesion molecules L1 and N‐CAM at the cell surface were measured by an enzyme‐linked immunosorbent assay. Expression of L1 was up‐regulated in neuroblastoma N2A cells after 1 day of maintenance in 40 and 60 mM K+, but not in phaeochromocytoma PC12 cells. Expression levels of N‐CAM and antigens recognized by the monoclonal antibody A2B5 or by polyclonal antibodies to crude membrane fractions of liver were not significantly altered by elevated K+ concentrations in these two cell lines. In monolayer cultures of early postnatal mouse cerebellum, an increase of 60% in expression of L1, but not N‐CAM or A2B5, was seen at 20 and 40 mM K+. This increase in L1 expression was specifically inhibitable by the Ca2+ channel blocker nicardipine. NMDA at a concentration of 100 μM increased levels of L1, but not of N‐CAM. This increase was inhibitable by the NMDA antagonists 2‐amino‐5‐phosphonovalerate and MK‐801, but not significantly by the kainate/quisqualate antagonist 6‐cyano‐7‐nitroquinoxaline‐2, 3‐dione. The increase in L1 expression at higher K+ concentrations was not inhibitable by the NMDA antagonists, indicating that the K+‐mediated increase in L1 expression is not due to release of glutamate by cerebellar neurons. These observations indicate that compounds influencing neuronal membrane properties, and thus neuronal excitability, are capable of regulating the expression of L1. In a more general context, these findings suggest that previously observed changes in synaptic connectivity in situ, resulting from activity‐dependent fine tuning of neuronal morphology, may be mediated by alterations in the expression of recognition molecules.