bluuebunny/crossref_metadata_2025_split huggingface dataset:
Involvement of the NMDA Receptor in a Non–cholinergic Action of Acetylcholinesterase in Guinea–pig Substantia Nigra Pars Compacta Neurons
Authors: Webb C. P. , Nedergaard S. , Giles K. , Greenfield S. A. 
Published: April 2006

AbstractEvidence is accumulating that a soluble, secretory form of acetylcholinesterase may have novel, non–cholinergic functions in certain brain regions, such as the substantia nigra. In this study, application of human recombinant acetylcholinesterase (rhAChE) to pars compacta neurons in the rostral substantia nigra resulted in a sustained hyperpolarization that was not only mimicked by application of N‐methyl–D–aSpartate (NMDA) but also blocked by the NMDA receptor antagonists MK801 and 2–amino–5phosphonopentanoic acid. Neither the rhAChE–nor the NMDA–induced hyperpolarization was seen when the calcium chelator BAPTA was injected into the neuron; hence the effect is mediated by accumulation of intracellular calcium. This intracellular calcium appears sufficient to compromise neuronal metabolism since the rhAChE–induced hyperpolarization was reversed by application of the K–ATP channel antagonist tolbutamide. Butyrylcholinesterase, a protein of similar molecular weight to acetylcholinesterase, which also hydrolyses acetylcholine, had no effect whatsoever. The results suggest that, independent of its normal catalytic function, acetylcholinesterase can act via the NMDA receptor complex to enhance calcium entry into nigral neurons and jeopardize cell metabolism. This non–classical action of acetylcholinesterase might thus be an important factor in the mechanisms underlying parkinsonian neurodegeneration.
Transience of Astrocytes In the Newborn Macaque Monkey Retina
Authors: Distler C. , Kirby M.A. 
Published: April 2006

AbstractWe investigated the morphology and spatial distribution of retinal astrocytes in newborn and early postnatal macaque monkeys. As in adults, retinal astrocytes in neonatal animals were closely associated with ganglion cell axons and blood vessels. However, in contrast with adults, astrocytes transiently occupied the fovea and perifoveal region in newborns and, to a lesser degree, also in early postnatal animals. The density of the perifoveal astrocytes rapidly declined during the first 2‐3 months of life. The results are discussed in relationship to foveal development.
Immunocytochemical Visualization of the mG1uR1 a Metabotropic Glutamate Receptor at Synapses of Corticothalamic Terminals Originating from Area 17 of the Rat
Authors: Vidnyánszky Zoltán , Görcs Tamás J. , Négyessy László , Borostyánköi Zsolt , Kuhn Rainer , Knöpfel Thomas , Hámori József 
Published: April 2006

AbstractPre‐embedding immunogold histochemistry was combined with Phaseolus vulgaris leucoagglutinin anterograde tract tracing in order to analyse the relationship between the subcellular localization of the mGluR1a metabotropic glutamate receptors and the distribution of corticothalamic synapses in the dorsal lateral geniculate nucleus (dLGN) and the lateral posterior nucleus (LP) of the rat. The injection of the tracer into area 17 labelled two types of corticothalamic terminals: (i) the small boutons constituting the majority of the labelled fibres which form asymmetrical synapses both in the dLGN and LP; and (ii) the giant terminals typically participating in glomerulus‐like synaptic arrangements and found exclusively in the lateral posterior nucleus. The small corticothalamic terminals often established synapses with mGluR1a‐immunopositive dendrites, with immunometal particles concentrated at the periphery of their postsynaptic membranes. In contrast, the synapses formed by giant boutons in the lateral posterior nucleus were always mGluR1a‐immunonegative. We conclude that the corticothalamic fibres forming the small synaptic terminals are the most likely candidates for the postulated mGluR‐mediated modulation of visual information flow by corticothalamic feedback mechanisms.
A Cholecystokinin‐B Receptor Antagonist Potentiates GABAergic and Glycinergic Inhibition in the Nucleus of the Solitary Tract of the Rat
Authors: McLean H. A. , Champagnat J. , Denavit‐Saubié M. 
Published: April 2006

AbstractIn both rodent and primate in vivo models, cholecystokininB (CCKB) antagonists such as PD134,308 have anxiolytic effects that may involve the potentiation of GABAergic transmission. We have investigated this interaction using exogenous application of GABA and whole cell patch recording techniques in neurons of the nucleus of the solitary tract (NTS) in brainstem slice preparations. In the presence of PD134, 308 the magnitude of the GABA‐evoked decrease in membrane input resistance was enhanced by 41.2 ± 3.1% and the duration of the response was prolonged by 34.8 ± 2.2%. Also, PD134, 308 potentiated glycine‐evoked decreases in membrane input resistance, increasing the amplitude of the response by 62.8 ± 4.8% and prolonging the duration of the response by 23.5 ± 3.6%. The effect of PD134, 308 persisted in the presence of tetrodotoxin, after reversal of the transmembrane gradient to chloride ions and under conditions of exaggerated GABAA receptor desensitization. Our results demonstrate that at least part of the functional link between PD134,308 and the GABAA response occurs postsynaptically.
Synergistic Neurite‐outgrowth Promoting Activity of Two Related Axonal Proteins, Bravo/Nr‐CAM and G4/Ng‐CAM in Chicken Retinal Explants
Authors: Morales Gracia , Sánhez‐Puelles Jose Maria , Schwarz Uli , de la Rosa Enrique J. 
Published: April 2006

AbstractIn the developing chicken retina, optic fibres migrating to the tectum express on their surfaces several cell adhesion molecules, including Bravo/Nr‐CAM and G4/Ng‐CAM. We have previously described differential distribution along the retinotectal projection and differential modulation by environmental cues for Bravo and G4 and here we further compare the characteristics of these immunoglobulin superfamily molecules. From day 6 of embryonic development (E6) to day 20 (E20), Bravo and G4 were found to coexist in the retinal optic fibre layer. However, while G4 staining was confined to that layer, as development proceeded Bravo staining spread to the plexiform layers and some radial structures of the retina. G4 displayed a dose‐dependent neurite‐outgrowth promoting activity for E6 retinal explants, while Bravo did not support neurite growth. Surprisingly, when the retinal explants were grown on mixtures of the two molecules, a much more vigorous growth of neurites was seen, revealing a synergistic effect. We propose that Bravo and G4, as well as other axonal surface molecules, affect axonal growth in different ways when they are present in combination than when they are alone.
Peripheral, but not Central, Nervous System Abnormalities are Reversed by Pancreatic Islet Transplantation in Diabetic Lewis Rats
Authors: Morano S. , Sensi M. , Di Gregorio S. , Pozzessere G. , Petrucci A. F. G. , Valle E. , Pugliese G. , Caltabiano V. , Vetri M. , Di Mario U. , Purrello F. 
Published: April 2006

AbstractNeuroelectrophysiological recordings represent a non‐invasive and reproducible method of detecting central and peripheral nervous system alterations in diabetes mellitus. In order to evaluate whether the normalization of metabolic control obtained by pancreatic islet transplantation could reverse diabetic neuroelectrophysiological alterations, or prevent further deterioration, we used an experimental model in which pancreatic islets (n= 1200) were injected into the portal vein of inbred Lewis rats (used as islet donors as well as recipients). Islets were injected 4 months after diabetes induction, since previous work had shown functional but not morphological damage at the nervous tissue level at this stage of the disease. Visual (V), brainstem auditory (BA) and somatosensory (S) evoked potentials (EPs) were measured in streptozotocin‐induced, islet‐recipient diabetic rats (n= 7), streptozotocin‐induced diabetic rats (n= 16) and non‐diabetic control rats (n= 12). Metabolic parameters and electrophysiological recordings were evaluated before diabetes induction, before transplantation and 4 months later. After transplantation, glycaemic levels returned to normal values within 1 week and remained so until the end of the study, as confirmed by a normal oral glucose tolerance test and by an increase in body weight. Electrophysiological recordings were altered in diabetic animals before transplantation. Four months after transplantation EP recordings improved, with a detectable gradient from the peripheral to the central structures. SEPs were significantly improved in the peripheral tarsus‐16 tract and the L6‐cortex tract (P < 0.005 and P < 0.01 versus diabetic rats) and were ameliorated without achieving statistical significance in the central T6‐cortex tract. BAEP latency values tended to improve in transplanted rats, but the differences versus non‐transplanted diabetic animals failed to reach significance. VEP values remained clearly pathological and even deteriorated after transplantation. These results show that normalization of metabolic control by pancreatic islet transplantation can reverse some of the already established neuroelectrophysiological alterations at the peripheral nervous system level, but does not affect other alterations at the central nervous system level.
Potentiated cAMP Rise in Metabotropically Stimulated Rat Cultured Astrocytes by a Ca2+‐related Al/k2 Adenosine Receptor Cooperation
Authors: Ogata Tadanori , Nakamura Yoichi , Schubert Peter 
Published: April 2006

AbstractAdenosine agonists favoured an intracellular Ca2+ rise in cultured type 1 astrocytes if the metabotropic glutamate receptors were concomitantly stimulated by (2S,1′s, 2′s)‐2‐(carboxycyclopropyl) glycine (l‐CCG‐I; group II agonist), quisqualate (group I agonist) or 1 ‐aminocyclopentane‐trans‐1,3‐dicarboxylic acid (t‐ACPD; group VII agonist). Since the generation of a Ca2+ signal reflected a newly adopted adenosine A1 receptor action, we tested the possible consequence that the established opposing control of the cellular cAMP content by inhibitory A1 and stimulatory A2 receptor activation was also altered. During metabotropic receptor stimulation by L‐CCG‐I, quisqualate or t‐ACPD, the non‐selective adenosine agonist 2‐chloroadenosine (CI‐adenosine) caused a potentiated cAMP increase which markedly exceeded that produced by CI‐adenosine alone. This cAMP potentiation resulted from altered and Ca2+‐dependent A1/A2 receptor cooperation. It was abolished by A1 receptor blockade and could not be achieved in the presence of t‐ACPD by the A1 agonist R(‐)N6‐(2‐phenylisopropyl)‐adenosine or by the A2 agonist 5′‐N‐ethyl carboxyamidoadenosine alone, but was obtained using their combination. The cAMP potentiation was blocked by intracellular Ca2+ chelation and the required A1 receptor action could be mimicked by a Ca2+ signal generated by the P2y receptor agonist adenosine 5β‐(β‐thio) diphosphate. The results support the conclusion that nanomolar concentrations of adenosine may influence astrocyte reactions by stimulating the Ca2+ and cAMP‐dependent signalling cascade.
Growth of Callosal Terminal Arbors in Primary Visual Areas of the Cat
Authors: Aggoun‐Zouaoui Djamila , Kiper Daniel C. , Innocenti Giorgio M. 
Published: April 2006

AbstractIn kittens ranging in age between postnatal day (P) 5 and P150, callosal axons originating near the 17/18 border were anterogradely labelled with biocytin and reconstructed from serial sections. At the end of the first postnatal week most of the axons begin to invade the cortex near the 17/18 border with multiple branches; some axons already span the grey matter up to layer I. Branches tend to grow into the grey matter in loose bundles ≤l00 μm in diameter, separated by empty spaces of comparable width. In the following weeks additional branches are produced in the grey matter; this appears to blur the initial bundled distribution, although by the end of the first postnatal month the branches are distributed in discrete patches similar to the adult terminal columns. Although a few boutons (presumably synaptic boutons) are found in the white matter/subplate region at earlier ages, they appear in the grey matter from P12 onwards. Their number per axon increases with age, reaching adult values about the end of the first month. Subsequently the number of boutons continues to increase and remains above adult values at P50, P65 and P80; it then decreases, reaching adult levels by P150. During the first month boutons tend to be more numerous in the infragranular layers, but then the trend reverses in favour of the supragranular layers. In most cases, the distribution of boutons spares layer IV partially or completely. From the onset boutons are distributed in radial‘columns’whose diameter increases with age. They maintain selective laminar and columnar distributions through the period of rapid and exuberant increase. These distributions do not appear to be sharpened further by the reduction in the number of boutons to adult levels. On the whole, callosal terminal arbors differentiate through stages of exuberant, albeit progressively constrained, growth involving both progressive and regressive events. Comparisons with previous work suggest that visual activity might finely shape the arbor, from the onset of synaptogenesis onwards.
Activation of Nucleotide Receptors Inhibits High‐threshold Calcium Currents in NG108‐15 Neuronal Hybrid Cells
Authors: Filippov A. K. , Brown D. A. 
Published: April 2006

AbstractA P2U(UTP‐sensitive) nucleotide receptor has previously been cloned from NG108‐15 neuroblastoma × glioma hybrid cells and it has been shown that activation of this receptor inhibits the M‐type K+‐current. We now report that UTP also inhibits Ca2+‐currents in differentiated NG 108‐15 cells, but probably through a different nucleotide receptor. UTP (100 μM) inhibited the peak of the high‐threshold current by 28.4 ± 3.1% (n= 38) with no effect on the low‐threshold current. Two components of high‐threshold current were identified: one inhibited by 100 nM ω‐conotoxin (CgTx) and one inhibited by 2 μM nifedipine and enhanced by 1 μM BAY K8644. UTP inhibited the former by 31.0 ± 3.1%, with an IC50of 2.8 ± 1.1 μM, and the latter by 34.2 ± 6.1% with an IC50of 1.7 ± 1.3 μM. Pertussis toxin pretreatment prevented inhibition of the CgTx‐sensitive, nifedipine‐resistant but not CgTx‐resistant current. Inhibition was not prevented by intracellular BAPTA (20 mM) or CAMP (1 mM). Effects of UTP on both currents were imitated by UDP, ATP, ADP, AP4A and ATPγS but weakly or not at all by 2‐MeSATP, GTP, AMP‐CPP or ITP. Since the receptors which inhibit Ca2+‐currents are activated by ATP, it is suggested that they might mediate auto‐inhibition of transmitter release by ATP if present on purinergic nerve terminals.
Inability of Rhesus Monkey Area V1 to Discriminate Between Self‐induced and Externally Induced Retinal Image Slip
Authors: IIg Uwe J. , Thier Peter 
Published: April 2006

AbstractRetinal image slip can result from an eye movement across a stationary object or alternatively from motion of the object while the eyes are stationary. The ability to discriminate between these two kinds of retinal image slip is necessary for the perception of a stable visual world. In order to determine if this ability is already present in monkey visual area V1, we asked if single V1 units are able to differentiate between externally and self‐induced retinal image slip. Externally induced retinal image slip was realized in the‘object motion’condition (OMC) by moving a behaviourally irrelevant visual stimulus (‘object’: a bar or a large random dot pattern) across the receptive field while the monkey fixated a small, stationary target. Conversely, self‐induced retinal image slip of comparable size was evoked in the‘ego motion’condition (EMC) by asking the monkey to pursue the target, moving at the speed of the object in the OMC, while the object was kept stationary. We recorded 221 units from visual area V1, 51 (23%) of them directionally selective, and compared their responses to self‐induced and externally induced retinal image slip. Many of them seemed to give some preference to externally induced retinal image slip. However, on closer examination it became clear that this seeming preference could be attributed to the fact that oculomotor performance was less precise in the EMC than in the OMC, causing a larger deviation from the optimal retinal image trajectory in the EMC. We show that the impact of eye position errors can be eliminated by the use of a position‐invariant stimulus, such as large‐field random dot patterns. We then show that the impact of both eye position errors and deviation of eye velocity from target velocity in the EMC can be eliminated by moving the stimulus in a given OMC trial according to an inverted replica of the eye movement trajectory in the preceding EMC trial, guaranteeing identical retinal stimulation in the OMC and the EMC. If identical retinal stimulation was ensured, none of the V1 units tested was able to differentiate between externally and self‐induced retinal image slip. We conclude that V1 does not contribute to the perception of a world which is stable despite eye movements.
BDNF and NT‐3, but not NGF, Prevent Axotomy‐induced Death of Rat Corticospinal Neurons In Vivo
Authors: Giehl Klaus M. , Tetzlaff Wolfram 
Published: April 2006

AbstractBrain‐derived neurotrophic factor (BDNF) and neurotrophin‐3 (NT‐3) have been identified as survival factors for adult axotomized rat corticospinal neurons (CSN) in vivo. Axotomy of corticospinal neurons at the level of the internal capsule induced death of 46% of the CSN within the first week after axotomy. The surviving population of CSN displayed severe atrophy with mean cross‐sectional area 49% of their unlesioned contralateral counterparts 7 days after axotomy. Using in situ hybridization to assess the expression of the receptors for the family of neurotrophins, we found trkB and trkC but not trkA mRNA expression in CSN. Intraparenchymal application of BDNF or NT‐3 at doses of 12 μg/day for 7 days via an osmotic minipump fully prevented the axotomy‐induced death of CSN. Interestingly, no neuronal atrophy was seen after BDNF application while NT‐3 had only a partial effect on the size of the axotomized CSN. Nerve growth factor did not prevent death or cell atrophy, consistent with the lack of trkA mRNA expression in these neurons. These findings show that BDNF and NT‐3 are survival factors for adult rat CSN in vivo, and may contribute to the development of therapeutic strategies aiming at the prevention of CSN degeneration in human motor neuron diseases.
Blockade of A2a Adenosine Receptors Positively Modulates Turning Behaviour and c‐Fos Expression Induced by D1 Agonists in Dopamine‐denervated Rats
Authors: Pinna A. , Di Chiara G. , Wardas J. , Morelli M. 
Published: April 2006

AbstractIn rats with unilateral 6‐hydroxydopamine lesions of the dopaminergic nigrostriatal pathway, administration of the A2a adenosine antagonist SCH 58261 alone did not induce any motor asymmetry but strongly potentiated the contralateral turning behaviour induced by the dopamine D1 agonist SKF 38393. SCH 58261 also increased the number of Fos‐like positive nuclei induced by SKF 38393 in the 6‐hydroxydopamine‐lesioned striatum. Intense potentiation of D1‐dependent turning behaviour and c‐Fos expression was also observed after administration of the A2a/A1 antagonist CGS 15943. Administration of the A1 adenosine receptor antagonist DPCPX induced a small potentiation of D1‐mediated contralateral turning while c‐Fos expression induced by SKF 38393 was not modified. The results suggest that endogenous adenosine acting on A2a receptors can exert an inhibitory influence on the functional expression of D1‐mediated responses in dopamine‐denervated rats, and propose new possible therapeutic approaches in the treatment of Parkinson's disease.
Differential Long‐lasting Potentiation of the NMDA and Non‐NMDA Synaptic Currents Induced by Metabotropic and NMDA Receptor Coactivation in Cerebellar Granule Cells
Authors: Rossi Paola , D'Angelo Egidio , Taglietti Vanni 
Published: April 2006

AbstractWhole‐cell patch‐clamp recordings in rat cerebellar slices were used to investigate the effect of metabotropic glutamate receptor activation on mossy fibre‐granule cell synaptic transmission. Transient application of 20 μM 1 S, 3R‐1 ‐aminocyclopentane‐1,3‐dicarboxylic acid simultaneously with low‐frequency NMDA receptor activation induced long‐lasting non‐decremental potentiation of both NMDA and non‐NMDA receptor‐mediated synaptic transmission. Potentiation could be prevented by application of the metabotropic glutamate receptor antagonist (+)‐O‐methyl‐4‐carboxyphenyl‐glycine at 500 μM. Characteristically, NMDA potentiation was two to three times as large as non‐NMDA current potentiation, occurred only in a slow subcomponent, and was voltage independent. This result demonstrates a pivotal role of NMDA receptors in the metabotropic potentiation of transmission, which may be important in regulating cerebellar information processing.
Calcium Signalling in Mouse Bergmann Glial Cells Mediated by α1‐adrenoreceptors and H1 Histamine ‐ Receptors
Authors: Kirischuk Sergej , Tuschick Sebastian , Verkhratsky Alexej , Kettenmann Helmut 
Published: April 2006

AbstractThe presence of adrenergic and histaminergic receptors in Bergmann glial cells from cerebellar slices from mice aged 20–25 days was determined using fura‐2 Ca2+ microfluorimetry. To measure the cytoplasmic concentration of Ca2+ ([Ca2+]i), either individual cells were loaded with the Ca2+‐sensitive probe fura‐2 using the whole‐cell patch‐clamp technique or slices were incubated with a membrane‐permeable form of the dye (fura‐2/AM) and the microfluorimetric system was focused on individual cells. The monoamines adrenalin and noradrenalin (0.1‐10 μM) and histamine (10‐100 μM) triggered a transient increase in [Ca2+]i. The involvement of the α1‐adrenoreceptor was inferred from the observations that monoamine‐triggered [Ca2+]i responses were blocked by the selective α1‐adreno‐antagonist prazosin and were mimicked by the α1‐adreno‐agonist phenylephrine. The monoamine‐induced [Ca2+]i signals were not affected by β‐ and α2‐adrenoreceptor antagonists (propranolol and yohimbine), and were not mimicked by β‐ and α2‐adrenoreceptor agonists (isoproterenol and clonidine). Histamine‐induced [Ca2+]i responses demonstrated specific sensitivity to only H1 histamine receptor modulators. [Ca2+]i responses to monoamines and histamine did not require the presence of extracellular Ca2+ and they were blocked by preincubation of slices with thapsigargin (500 nM), indicating that the [Ca2+]i increase is due to release from intracellular pools. No [Ca2+]i responses were recorded after application of aspartate, bradykinin, dopamine, GABA, glycine, oxytocin, serotonin, somatostatin, substance P, taurine or vasopressin. We conclude that cerebellar Bergmann glial cells are endowed with α1 ‐adrenoreceptors and H1 histamine receptors which induce the generation of intracellular [Ca2+]i signals via activation of Ca2+ release from inositol‐l,4,5‐trisphosphate‐sensitive intracellular stores.