bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modulation of Responses of Four Types of Feline Ascending Tract Neurons by Serotonin and Noradrenaline
Authors: Jankowska E. , Hammar I. , Djouhri L. , Hedén C. , Läckberg Z. Szabo , Yin X.‐K. 
Published: April 2006

AbstractModulation of responses of four types of ascending tract cells by noradrenaline and serotonin was compared in order to investigate how information forwarded by these cells may be gated by monoaminergic tract neurons. Spinocervical tract, postsynaptic dorsal column and dorsal spinocerebellar tract neurons located in Clarke's column and in the dorsal horn were identified by their axonal projections. Noradrenaline and serotonin were applied ionophoretically close to a selected neuron, and their effects were tested on extracellularly recorded responses of this neuron to electrical stimulation of low‐threshold skin afferents and group II muscle spindle afferents. The modulatory actions of noradrenaline and serotonin were estimated from changes in the number of responses evoked by 30 successive stimuli, the minimal latencies of these responses, and their firing frequency. All four populations of ascending tract neurons investigated were modulated by serotonin and noradrenaline, but not in the same way. The responses were most often depressed by noradrenaline and facilitated by serotonin, but in some types of neuron they were affected in the same direction. Transmission from low‐threshold skin and group II muscle afferents changed in the same direction in some types of neuron but in the opposite direction in other types. The results indicate that transfer of information from skin and group II muscle afferents to supraspinal centres may be gated by descending monoaminergic pathways in a highly differentiated manner, and is adjusted to the requirements of various behavioural situations.
Differential Regulation of mRNAs for GDNF and its Receptors Ret and GDNFRα After Sciatic Nerve Lesion in the Mouse
Authors: Naveilhan Philippe , ElShamy Wael M. , Ernfors Patrik 
Published: April 2006

AbstractGlial cell line‐derived neurotrophic factor (GDNF), first characterized for its effect on dopamine uptake in central dopaminergic neurons, appears to be a powerful neurotrophic factor for motor neurons. GDNF has recently been shown to signal through a multisubunit receptor. This receptor is composed of a ligand‐binding subunit, called GDNF receptor α (GDNFRα), and a signalling tyrosine kinase subunit, Ret. To gain further insight into GDNF function, we investigated the expression of GDNF and its receptors after nerve lesion in adult mice. Analysis of expression in muscle, nerve and spinal cord by RNase protection assay and in situ hydridization revealed that, in adult non‐lesioned mice, GDNF mRNA was expressed in the nerve and GDNFRα mRNA in the nerve and the spinal cord, while the expression of Ret was restricted to spinal cord motor neurons. After a sciatic nerve crush a rapid increase in GDNF mRNA was observed in the distal part of the nerve and a delayed elevation in the muscle, while GDNFRα mRNA was up‐regulated in the distal part of the sciatic nerve but not in proximal nerve or spinal cord. The lesion also induced a rapid increase in Ret mRNA expression, but the increase was observed only in spinal cord motor neurons and in dorsal root ganglion neurons. A pattern of expression of GDNF and its receptors similar to that seen after lesion in the adult was detected during embryonic development. Administration of GDNF enhanced sciatic nerve regeneration measured by the nerve pinch test. Taken together, these results suggest that GDNF has an important role during regeneration after nerve damage in the adult.
Modulation of Sensory and Excitatory Amino Acid Responses by Nitric Oxide Donors and Glutathione in the Ventrobasal Thalamus of the Rat
Authors: Shaw P. J. , Salt T. E. 
Published: April 2006

AbstractNitric oxide has been identified as having a role in synaptic transmission in the central nervous system. In the ventrobasal complex of the thalamus (VB), the precursor of nitric oxide synthesis, L‐arginine, causes enhancement of excitatory amino acid responses and somatosensory transmission. In this study, the nitric oxide donors sodium nitroprusside, 3‐morpholinosydnonimine and S‐nitrosoglutathione were applied to VB relay neurons by iontophoresis and responses of single neurons were recorded extracellularly. Sodium nitroprusside caused selective inhibition of responses to NMDA, probably mediated by a by‐product, ferrocyanide, as described in previous studies. 3‐Morpholinosydnonimine and S‐nitrosoglutathione, however, caused potentiation of responses to sensory stimuli and to excitatory amino acids. In contrast, glutathione in both its reduced and oxidized forms reduced such responses, and this suggests that the potentiating effect of S‐nitrosoglutathione could be due to nitric oxide production. These results are consistent with the hypothesis that nitric oxide may have a local modulatory role in the thalamus. Data are presented which suggest that glutathione may have a negative modulatory influence on neurotransmission and excitatory amino acid responses in the ventrobasal thalamus.
Metabotropic Glutamate Receptors in the Rat Nucleus Accumbens
Authors: Manzoni Olivier , Michel Jean‐Marie , Bockaert Joél 
Published: April 2006

AbstractThe effects of glutamate metabotropic receptors (mGluRs) on excitatory transmission in the nucleus accumbens were investigated using electrophysiological techniques in rat nucleus accumbens slices. The broad‐spectrum mGluR agonist (1S,3R)‐1‐aminocyclopentyl‐1,3‐dicarboxylate, the mGluR group 2 selective agonists (S)‐4‐carboxy‐3‐hydroxyphenylglycine, (1S,3S)‐ACPD) and (2S,1′S,2′S)‐2‐(2′‐carboxycyclopropyl)glycine (L‐CCG1), and the mGluR group 3 specific agonist L‐2‐amino‐4‐phosphonobutyrate (L‐AP4) all reversibly inhibited evoked excitatory synaptic responses. The specific group 1 mGluR agonist (R,S)‐3,5‐dihydroxyphenylglycine [(R,S)‐DHPG] did not depress transmission. Dose‐response curves showed that the rank order of agonist potencies was: L‐CCGI > L‐AP4 > (1 S,3S)‐ACPD. Group 2 and 3 mGluRs inhibited transmission via a presynaptic mechanism, as they increased paired‐pulse facilitation, decreased the frequency of miniature excitatory postsynaptic currents and had no effect on their amplitude. The mGluRs did not inhibit transmitter release by reducing voltage‐dependent Ca2+ currents through N‐ or P‐type Ca2+ channels, as inhibition persisted in the presence of a‐conotoxin‐GVIA or Aga‐IVA. The depression induced by mGluRs was not affected by specific antagonists of dopamine D1, GABA‐B or adenosine A1 receptors, indicating direct effects. Finally, (13,s)‐DHPG specifically blocked the postsynaptic afterhyperpolarization current (Iahp). Our results represent the first direct demonstration of functional mGluRs in the nucleus accumbens of the rat.
Evidence that Blue‐on Cells are Part of the Third Geniculocortical Pathway in Primates
Authors: Martin Paul R. , White Andrew J. R. , Goodchild Ann K. , Wilder Heath D. , Sefton Ann E. 
Published: April 2006

AbstractColour vision in primates is mediated by cone opponent ganglion cells in the retina, whose axons project to the dorsal lateral geniculate nucleus in the visual thalamus. It has long been assumed that cone opponent ganglion cells project to the parvocellular layers of the geniculate. Here, we examine the role of a third subdivision of the geniculocortical pathway: the interlaminar or koniocellular geniculate relay cells. We made extracellular recordings in the dorsal lateral geniculate nucleus of the common marmoset Callithrix jacchus, a New World monkey in which the interlaminar cells are well segregated from the parvocellular layers. We found that one group of colour opponent cells, the blue‐on cells, was largely segregated to the interlaminar zone. This segregation was common to dichromatic (‘red‐green colour‐blind’) and trichromatic marmosets. The result calls into question the traditional notion that all colour information passes through the parvocellular division of the retino‐geniculo‐cortical pathway in primates.
Modulation of NCAM Polvsialvlation is Associated with Morphofunctional Modifkations in the Hypothalamo‐neurohypophysial System During Lactation
Authors: Nothias Fatiha , Vernier Philippe , von Boxberg Ysander , Mirman Simone , Vincent Jean‐Didier 
Published: April 2006

AbstractPost‐transcriptional modification of the neural cell adhesion molecule (NCAM) by polysialic acid significantly decreases NCAM adhesiveness and more generally modifies cell‐cell interactions. Polysialic acid‐NCAM (PSA‐NCAM) is mainly expressed in the developing nervous system. In the adult, its expression is restricted to regions that retain morphological plasticity, such as the hypothalamo‐neurohypophysial system during lactation in rats. Since cell‐cell interactions and synaptic contacts in the hypothalamo‐neurohypophysial system are greatly increased during lactation, we examined whether PSA‐NCAM expression is modified during this period. lmmunohistochemistry and immunoblotting showed that, compared with virgin rats, PSA‐NCAM dramatically decreased during lactation in both the supraoptic nuclei and the neurohypophysis, and returned to its initial level only after weaning. This decrease was progressive and became significant only at the end of the first week of lactation. By contrast, modifications in the level of NCAM protein or changes in the splicing pattern of NCAM mRNAs could not be detected. The decline in polysialic acid on the NCAM molecule could strengthen membrane appositions, thereby stabilizing the newly established synapses and neurohaemal contacts in the hypothalamo‐neurohypophysial system that accompany the increased neuronal activity that occurs during lactation. We also studied the regulation of the phosphorylated microtubule‐associated protein‐1B (MAP1B‐P), whose distribution pattern largely overlaps with that of PSA‐NCAM in the adult brain. Expression of MAP1B‐P was greatly increased during lactation in the hypothalamic axons projecting into the neurohypophysis. Thus, the expression patterns of both PSA‐NCAM and MAP1B‐P may reflect the permanent structural plasticity characterizing the hypothalamo‐neurohypophysial system in the adult.
Interneuron‐specific Ca2+ Responses Linked to Metabotropic ‐and lonotropic Glutamate Receptors in Rat Hippocampal Slices
Authors: Carmant Lionel , Woodhall Gavin , Ouardouz Mohamed , Robitaille Richard , Lacaille Jean‐Claude 
Published: April 2006

AbstractGlutamate‐mediated regulation of intracellular Ca2+ levels was examined in different populations of CA1 interneurons, using confocal microscopy and the Ca2+ indicator fluo 3‐AM in rat hippocampal slices. Interneurons in basal [stratum oriendalveus (OA)] and apical [strata radiatum and lacunosum‐moleculare (R/LM)] dendritic layers responded heterogeneously to glutamate. In control medium, OA interneurons responded mostly with oscillatory Ca2+ responses, which consisted of a large Ca2+ transient and successive smaller elevations. R/LM interneurons responded mostly with biphasic responses, characterized by an initial large transient and a secondary prolonged elevation. Other interneurons in both R/LM and OA responded with transient elevations in Ca2+ levels. lonotropic glutamate receptor antagonists (±)2‐amino‐5‐phosphonopentanoic acid and 6‐cyano‐7‐nitro‐quinoxaline‐2,3‐dione reduced peak Ca2+ responses in OA and R/LM cells, and blocked biphasic responses in R/LM interneurons. The metabotropic glutamate receptor antagonist (RS)‐α‐methyl‐4‐carboxyphenylglycine reduced peak Ca2+ responses only in OA interneurons, and prevented oscillatory responses. In low Ca2+ medium, peak responses were reduced in R/LM but not in OA interneurons, and oscillatory responses were absent. Combination of ionotropic and metabotropic receptor antagonists blocked all glutamate‐evoked Ca2+ responses. Activation of different types of glutamate receptors may thus produce heterogeneous Ca2+ signals in subpopulations of CA1 interneurons. lonotropic receptors may generate biphasic responses in interneurons in apical dendritic layers, whereas combined activation of metabotropic and ionotropic receptors may trigger oscillatory responses in interneurons of basal dendritic layers. These heterogeneous Ca2+ responses indicate that glutamate‐mediated Ca2+ processes and second messenger systems differ in subpopulations of hippocampal interneurons and suggest possible postsynaptic functional specialization of interneurons.
Epidermal Growth Factor is a Motility Factor for Microglial Cells In Vitro: Evidence for EGF Receptor Expression
Authors: Nolte Christiané , Kirchhoff Frank , Kettenmann Helmut 
Published: April 2006

AbstractEpidermal growth factor (EGF) and its receptor are present in the central nervous system and modulate a variety of neural functions. Here we show that microglial cells, the brain‐intrinsic macrophages, express the receptor for EGF and migrate in response to EGF. Transcripts encoding the EGF receptor could be detected in purified microglial cultures obtained from newborn mouse cortex. More specifically, cDNA fragments derived from EGF receptor mRNA could be amplified from 21% of electrophysiologically characterized microglial cells by the use of a single‐cell reverse transcription‐polymerase chain reaction method. Expression of the protein was confirmed on rat microglia by flow cytometty. EGF dose‐dependently stimulated chemotactic migration, as revealed with a microchemotaxis assay. The dose‐response curve peaked at 10 ng/ml EGF, reaching a 3‐fold increase in migration over the unstimulated control; migration was about half of that induced by complement 5a (10 nM), a previously described microglial chemoattractant. Chequerboard analysis showed that EGF‐induced motility was composed of both chemotaxis and chemokinesis. In contrast to its pronounced effect on cell motility, EGF (0.01–10 ng/ml) was not a mitotic signal for microglia, as shown by lack of bromodeoxyuridine incorporation. Acute and chronic pathological processes within the brain stimulate the synthesis and release of immunoregulators and growth factors (including EGF) that play a major role in the brain's response to injury. EGF may serve as a paracrine factor to direct microglial cells to the lesion site. Moreover, since EGF is secreted by activated microglia themselves in vivo, it may act as an autocrine modulator of microglial cell function.
Distinct Effects of Clostridial Toxins on Activity‐dependent Modulation of Autaptic Responses in Cultured Hippocampal Neurons
Authors: Owe‐Larsson Björn , Kristensson Krister , Hill Russell H. , Brodin Lennart 
Published: April 2006

AbstractClostridial neurotoxins proteolyse specific proteins implicated in synaptic vesicle exocytosis, but their actions on the release machinery in functional synapses is not well understood. Here we examine the effects of botulinum toxin A (BoNT/A) and tetanus toxin (TeTx) on autaptic transmission in cultured rat hippocampal neurons using whole‐cell voltage clamp recordings. The proportion of cells responding to stimulation with an excitatory postsynaptic current (EPSC) and the magnitude of the remaining responses decreased gradually with increasing concentration of either toxin. However, the activity‐dependent modulation (5 Hz repetitive stimulation) of EPSCs remaining after toxin inhibition differed markedly between the two toxins. The TeTx inhibition was associated with a persistent activity‐dependent depression similar to that in control cells. In contrast, the BoNT/A inhibition was accompanied by a reversal of the modulation into facilitation, resembling that induced by lowering of the calcium concentration. These results demonstrate a difference between BoNT/A and TeTx in their mode of inhibition of synaptic vesicle exocytosis, which suggests that they exert their preferential actions at distinct steps of the release process.
Changes in the Expression of the Extracellular Matrix Molecules Tenascin‐C and Tenascin‐R after 3–Acetylpyridine‐induced Lesion of the 01ivocerebe1lar System of the Adult Rat
Authors: Wintergerst Eva Sabine , Bartsch Udo , Batin Cesira , Schachner Melitta 
Published: April 2006

AbstractIn the central nervous system of rodents, the extracellular matrix glycoproteins tenascin‐C and tenascin‐R are expressed predominantly by astrocytes and oligodendrocytes respectively. Both molecules support neurite outgrowth from several neuronal cell types when presented as uniform substrates. When offered as a sharp boundary with a permissive substrate, however, both molecules prevent neurite elongation. On the basis of these observations it has been suggested that tenascin‐C and tenascin‐R may be relevant in determining the cellular response after injury in the adult rodent central nervous system. To investigate whether tenascin‐C and tenascin‐R may play important functional roles in the lesioned central nervous system, we have analysed their expression in the olivocerebellar system of the adult rat after 3–acetylpyridine‐induced degeneration of nerve cells in the inferior olivary nucleus. Tenascin‐C mRNA was not detectable at any time in the unlesioned or lesioned inferior olivary nucleus by in situ hybridization. In the cerebellar cortex, tenascin‐C mRNA in Golgi epithelial cells was down‐regulated 3 days after the lesion and returned to control values 80 days after the lesion. Tenascin‐R mRNA was expressed by distinct neural cell types in the unlesioned olivocerebellar system. After a lesion, the density of cells containing tenascin‐R transcripts increased significantly in the inferior olivary nucleus and in the white matter of the cerebellar cortex. Immunohistochemical and immunochemical investigations confirmed these observations at the protein level. Our data thus suggest differential functions of tenascin‐C and tenascin‐R in the injured central nervous system.
Increased Expression of trkB mRNA in Rat Caudate‐Putamen Following 6–OHDA Lesions of the Nigrostriatal Pathway
Authors: Numan S. , Seroogy K. B. 
Published: April 2006

AbstractThe tyrosine kinase receptors trkB and trkC are essential components of the high‐affinity receptors for members of the neurotrophin family, including brain‐derived neurotrophic factor (BDNF) and neurotrophin‐3 (NT‐3). Both neurotrophin receptor mRNAs are broadly distributed throughout the caudate‐putamen. In animal models of Parkinson's disease, loss of the ventral mesencephalic dopamine projection to the striatum has been shown to alter the expression of several striatal peptides, neurotransmitter‐synthesizing enzymes and receptors. To determine if expression of trkB and/or trkC striatal mRNAs is also regulated by the integrity of the dopaminergic afferents, adult rats were given unilateral injections of 6–hydroxydopamine (6–OHDA), selective catecholamine neurotoxin, or vehicle into the right ascending medial forebrain bundle. Following 2 week survival period, in situ hybridization with 35S‐labelled cRNA probes for the kinase‐specific, full‐length form of trkB mRNA and all forms of trkC mRNA was performed in striatal sections. A significant increase in the hybridization density for trkB mRNA was observed in the caudate‐putamen ipsilateral to the 6–OHDA injection, compared with the uninjected control side (P < 0.001). In contrast, no alteration in the hybridization density for trkC mRNA was observed in the striatum of 6–OHDA‐treated rats. No alterations in trkB or trkC mRNA levels were observed in the striata of vehicle‐treated animals. These data suggest that midbrain dopaminergic afferents regulate the expression of trkB mRNA in the caudate‐putamen. Alternatively, since dopaminergic neurons of the ventral mesencephalon express BDNF mRNA, the up‐regulation of striatal trkB mRNA may reflect compensatory response by striatal neurons due to loss of anterogradely and/or retrogradely derived trophic support from the ventral midbrain.
Development of Action Potential‐dependent and Independent Spontaneous GABAA Receptor‐mediated Currents in Granule Cells of Postnatal Rat Cerebellum
Authors: Wall Mark J. , Usowicz Maria M. 
Published: April 2006

AbstractThe postnatal development of spontaneous GABAergic transmission between cerebellar Golgi cells and granule cells was investigated with voltage‐clamp recording from rat cerebellar slices, in symmetrical Cl‐conditions. Between postnatal days 7 and 14 (P7–14), bicuculline‐and TTX (tetrodotoxin)‐sensitive spontaneous inhibitory postsynaptic currents (sIPSCs), occurred at high frequency in 56% of granule cells. Between P10 and P14, sIPSCs were superimposed on tonic current of‐12 ± 1.8 pA at ‐70 mV, that was accompanied by noise with variance of 17 ± 3 pA2. Both the current and noise were inhibited by bicuculline. TTX blocked the bicuculline‐sensitive current and noise by˜60%. Between P18 and P25, sIPSCs were less frequent; all cells showed tonic, bicuculline‐sensitive currents, but these were partially inhibited by TTX (˜35%). Between P40 and P53, slPSCs were rare; tonic, bicuculline‐sensitive currents and noise were greater in amplitude, with mean values of‐17 pA and 22 pA2 at‐70 mV, they were present in all cells but they were not inhibited by TTX. Glycine receptor channels that were expressed in immature, but not adult cells, did not mediate spontaneous currents. Our results indicate that spontaneous transmission onto cerebellar granule cells in immature animals consists primarily of action potential‐dependent, phasic release of vesicular GABA. This generates GABAA receptor‐mediated slPSCs. The effects of GABA transporter blockers suggest that it also produces the TTX‐sensitive current‐noise, as GABA spills out of synapses to activate extrasynaptic receptors or receptors in neighbouring synapses. In older animals, action potential‐independent release of transmitter is predominant and results in tonic activation of GABAA receptors. This does not appear to be spontaneous vesicular release of GABA. Neither does it appear to be reversed uptake of GABA, although further work is required to rule out these possibilities.
High Molecular Weight Protein of Human Central Nervous System Myelin Inhibits Neurite Outgrowth: an Effect which can be Neutralized by the Monoclonal Antibody IN‐1
Authors: Spillmann Adrian A. , Amberger Verena R. , Schwab Martin E. 
Published: April 2006

AbstractNeurite outgrowth of PC12 cells in the presence of nerve growth factor and the spreading of 3T3 fibroblasts were inhibited by human myelin proteins from different areas of the central nervous system (CNS) in a dose‐dependent manner. Application of liposomes containing human CNS myelin proteins induced rapid collapse of PC12 growth cones. When 3T3 fibroblasts were plated on a human CNS myelin protein‐coated substrate the cells remained round, and spreading was inhibited. All these inhibitory effects could be neutralized by the monoclonal antibody IN‐1, which was raised against a 250 kDa neurite growth‐inhibiting protein (NI‐250) of rat CNS myelin. Comparison of the inhibitory properties of human and bovine CNS myelin on PC12 neurite outgrowth showed that human CNS myelin was slightly more inhibitory per unit of myelin protein. Analysis by sodium dodecyl sulphate‐polyacrylamide gel electrophoresis revealed that in human myelin, as in rat and bovine myelin, a high molecular weight protein is responsible for the inhibitory activities on neurite outgrowth and fibroblast spreading.
Organization of Glutamate Receptors at the Synapse
Authors: Ottersen Ole P. , Landsend Alf S. 
Published: April 2006

AbstractGlutamate receptors can be divided in several groups with distinct functional properties. An additional level of complexity has emerged from recent high resolution immunogold analyses which have provided evidence for a differential targeting of glutamate receptors to specific subsynaptic membrane domains. Notably, different types of glutamate receptor may differ in their distance to the release site and in their spatial relation to glutamate transporters. These data imply that the subsynaptic expression of a given glutamate receptor may bias its response to a released quantum of transmitter and suggest that receptor targeting may be implicated in the modulation of glutamatergic neurotransmission.