bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induction of MMP9 (92 kDa Gelatinase) Activity and Expression of Tissue In hibitor of Metalloproteinase‐2 mRNA (TIMP‐2) in Primitive Neuroectodermal Cells Infected with Retrovirus HTLV‐I
Authors: Giraudon P. , Thomasset N. , Bernard A. , Verrier B. , Belin M. F. 
Published: April 2006

AbstractMatrix‐degrading proteases, including metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), are involved in modulation of the extracellular matrix, which participates in neural cell differentiation, brain morphogenesis and tissue integrity. Metalloproteinases and TlMPs are associated with inflammatory and degenerative processes in the central nervous system and are regulated by cytokines. Human retroviral infections are frequently associated with neurological disturbances. In the present paper, we have studied the changes occurring in human primitive neuroectodermal cells following infection with human T cell lymphotropic virus type 1 (HTLV‐I), a retrovirus responsible for HTLV‐I‐associated myelopathy. Infected neural cells were found to have high metalloproteinase 9 (MMP9–92 kDa gelatinase) activity. MMP9 induction is dependent on HTLV‐I infection of neural cells. In addition, soluble factors, especially tumour necrosis factor α, secreted by infected cells, act as mediators of induction. HTLV‐I infection also induces expression of RNA coding for tissue inhibitor of metalloproteinase 2. These observations indicate that HTLV‐I infection selectively modulates the expression of molecules involved in the dynamic equilibrium between the synthesis and degradation of the neural cell matrix and leads to its remodelling, which modifies cell‐cell interactions and cellular function.
Physiological Characterization of Pretectal Neurons Projecting to the Lateral Posterior‐Pulvinar Complex in the Cat
Authors: Sudkamp S. , Schmidt M. 
Published: April 2006

AbstractPretectal neurons projecting to the lateral posterior‐pulvinar complex (LP‐P) in cats were electrophysiologically identified by their antidromic activation from the LP‐P. Their responses to various visual stimuli and to electrical stimulation of the optic chiasm and the lateral geniculate nucleus (LGN) were characterized. In retrograde double‐labelling experiments, the pretectal projections to the LP‐P and to the LGN were tested for possible overlap. Forty‐five neurons were antidromically activated from the LP‐P; 55 % of them could also be activated orthodromically from the optic chiasm. Most antidromically activated neurons responded to rapid movements of large textured visual stimuli as well as to ‘on’ or ‘off’ visual stimulation with short bursts. When stimulated with a slowly moving, large, structured visual stimulus, most cells showed a slight but significant activity increase. None of the neurons projecting to the LP‐P was also activated antidromically from the LGN. Thus, the two populations are separate. This is supported by the results from the retrograde double‐labelling experiments. None of the LP‐P projecting neurons showed any directional selectivity to slow movements of large visual stimuli, a property by which pretectal neurons projecting to the inferior olive are characterized. Thus, neurons projecting to the LP‐P do not bifurcate to the inferior olive. Response properties of neurons projecting to the LP‐P were very similar to those of the ‘jerk’ neurons described by Schweigart and Hoffmann (Exp. Brain Res., 91, 273–283, 1992); therefore we believe them to be identical. Jerk neurons are known to react not only to rapid image shifts with short high‐frequency bursts, but also to saccadic eye movements in the light. As a possible function of LP‐P projecting neurons, the transfer of information about image displacement during saccades or fast‐moving objects in the visual scene is discussed.
The Extracellular Matrix Molecule Tenascin: Expression in the Developing Chick Retinotectal System and Substrate Properties for Retinal Ganglion Cell Neurites In vitro
Authors: Bartsch Susanne , Husmann Knut , Schachner Melitta , Bartsch Udo 
Published: April 2006

AbstractTo investigate the molecular mechanisms involved in the outgrowth of retinal ganglion cell axons in the tectum, the expression of the extracellular matrix molecule tenascin was analysed in the tectum and retina of chickens by immunocytochemistry and in situ hybridization. Tissue was analysed between embryonic days 4 and 12, just before and during the period when retinal ganglion cell axons innervate their target region, the optic tectum. In the tectum, tenascin immunoreactivity becomes detectable at the anterior pole at embryonic day 4, 2 days before retinal ganglion cell axons arrive, and spreads caudally with increasing age. At early stages, tenascin is predominantly accumulated in the stratum opticum, the zone of ingrowing retinal ganglion cell axons, and along their prospective pathway. In the stratum opticum, the molecule is associated with radial glial fibres, glial endfeet and retinal ganglion cell axons located in the immediate neighbourhood of radial glial fibres. At all ages investigated, tenascin mRNA is mainly restricted to cells located in the periventricular region, suggesting that the molecule is synthesized by radial glial cells. In the retina, tenascin is expressed by amacrine, displaced amacrine and horizontal cells but not by retinal ganglion cells. To investigate whether the accumulation of tenascin in the developing and prospective pathway of retinal ganglion cell axons may affect their rate of growth we assayed the substrate properties of tenascin for retinal ganglion cell neurites in vitro. When retinal ganglion cell suspensions from 6–day‐old chick embryos were maintained on homogeneous mouse or chick tenascin/ polyornithine substrates, neurite length was significantly increased when compared to polyornithine substrates at coating concentrations of 10 or 20 μg/ml. Higher coating concentrations (35 or 70 μg/ml) resulted in neurite lengths comparable to control values. Together, these observations suggest that tenascin in the developing and prospective stratum opticum might serve as a preformed pathway to support growth of retinal ganglion cell axons in the tectum.
A Combined Retrograde Tracer and GABA‐immunocytochemical Study of the Projection from Nucleus Interpositus Posterior to the Posterior Lobe c2 Zone of the Cat Cerebellum
Authors: Kolston Jacqueline , Apps Richard , Trott Judy R. 
Published: April 2006

AbstractThe extent to which the cells of origin of the cerebellar nucleocortical pathway are immunopositive for γ‐aminobutyric acid (GABA) was investigated in four cats using retrograde labelling of nucleocortical neurons in combination with immunocytochemistry. Neurons were retrogradely labelled by injection of fluorescent (coumarin)‐tagged latex microspheres into the c2 zone in the rostral part of the paramedian lobule. The zone was identified electrophysiologically by the characteristics of the climbing fibre responses evoked on the cerebellar surface by percutaneous stimulation applied to the left and right forepaws in pentobarbitone‐anaesthetized animals. Sections of the cerebellum containing the retrogradely labelled neurons were processed for GABA immunocytochemistty using a fluorescent (rhodamine)‐tagged immunoglobulin. When viewed with epifluorescence microscopy and appropriate filter blocks the retrogradely labelled nucleocortical neurons could be visualized in the same sections as the GABA‐immunopositive neurons. Almost all of a total of 254 labelled nucleocortical neurons were located in nucleus interpositus posterior, where a total of 711 GABAergic neurons were also found. None of these cells contained coumarin‐tagged beads and displayed immunoreactivity for GABA (i.e. none was double‐labelled). When compared by area of their cell body, the nucleocortical and GABA‐immunopositive neurons appeared to form two partially overlapping populations. The mean cell area of the nucleocortical neurons was 620 ± 233 pm2 (SD), whereas the GABA‐immunopositive neurons were much smaller, with a mean cell area of 220 ± 115 pm2. The results suggest that GABA does not play a major role in the nucleocortical pathway to the c2 zone of the rostral paramedian lobule of the cat cerebellum.
Marginal Cells in the Spinal Cord of Four Elasmobranchs (Torpedo marmorata, T. torpedo, Raja undulata and Scyliorhinus canicula): Evidence for Homology with Lamprey lntraspinal Stretch Receptor Neurons
Authors: Anadón Ramon , Molist Pilar , Pombal Manuel Angel , Rodríguez‐Moldes Isabel , Rodicio Maria Celina 
Published: April 2006

AbstractThis study reports for the first time the presence of marginal cells, probably with stretch receptor function, in the spinal cord of four elasmobranch species, two electric rays, Torpedo marmorata and T. torpedo, the skate Raja undulata and the dogfish Scyliorhinus canicula. In all four species, the marginal cells were located close to the lateroventral surface of the cord and possessed thick dendrites which formed part of characteristic glomerular structures. In vitro retrograde labelling of the spinal cord of the dogfish with horseradish peroxidase (HRP) showed that some of these cells have contralateral projections. Ultrastructural study of normal and retrograde HRP‐labelled material showed that the glomerular dendrites of marginal cells give rise to numerous fingerlike structures and are associated with a rich plexus of nerve terminals. Characteristically, these dendrites contain numerous mitochondria. Immunocytochemical studies revealed a rich plexus of somatostatin‐ and GABA‐immunoreactive fibres in the glomeruli. These results strongly suggest that the marginal cells of the elasmobranch spinal cord are stretch receptors homologous to lamprey edge cells and to the marginal nucleus cells of the spinal cord of urodeles and snakes. We discuss the possible role of these cells in the modulation of swimming movements.
Gene Expression and In Vitro Release of Galanin in Rat Hypothalamus During Development
Authors: Giorgi S. , Forloni G. , Baldi G. , Consolo S. 
Published: April 2006

AbstractThe expression and distribution of the mRNA coding for galanin precursor, preprogalanin (ppGAL), were analysed in several rat hypothalamic nuclei (periventricular, paraventricular, supraoptic, dorsomedial and arcuate nuclei and the lateral hypothalamic area) during development by an in situ hybridization technique and computer‐assisted grain counting over individual cells. ppGAL mRNA (expressed as number of grains/100 pm2) was detectable from postnatal day (PD) 1 in all the nuclei considered, and the amount of transcript per cell was 6–11 times less than in the adult. ppGAL mRNA progressively increased from PD8 to 14 to 21. The level of ppGAL mRNA in all the nuclei at PD21 was about half that in adulthood, except in the dorsomedial nucleus, where the difference was no more than 20%. As an index of the activity of galanin‐containing neurons, we measured the basal and K+‐evoked in vitro release of galanin‐like immunoreactivity from hypothalamic slices of PD14, 21 and 90 rats by radioimmunoassay. Basal release of galanin‐like immunoreactivity remained at the same level from PD14 to PD90, but the response to KCI (50 mM) stimulation was lower at PD14 (‐90%) and PD21 (>200%) than at PD90 (350%). Basal and K+‐evoked release was sensitive to tetrodotoxin, indicating a neuronal origin. This study provides the first evidence that the increase in ppGAL mRNA during the ontogeny of hypothalamic nuclei is associated with an increase in galaninergic neuronal function.
Expression of Endopeptidase‐24.11 (Common Acute Lymphoblastic Leukaemia Antigen CDI0) in the Sciatic Nerve of the Adult Rat After Lesion and During Regeneration
Authors: Kioussi Chrissa , Mamalaki Avgi , Jesse Kristjan , Mirsky Rhona , Hersh Louis B. , Matsas Rebecca 
Published: April 2006

AbstractEndopeptidase‐24.11, which is identical with the common acute lymphoblastic leukaemia antigen CD1O (CALLA), is a cell surface Zn2+ metalloprotease that regulates peptide‐induced responses in different tissues, including the nervous and immune systems. In the peripheral nervous system, high levels of the enzyme are present in all neonatal and early postnatal Schwann cells, while as myelination proceeds it is gradually suppressed in the majority of cells that form myelin but retained in non‐myelin‐forming cells in the adult animal. In the present study we have investigated the effects of transection, crush and regeneration of the adult rat sciatic nerve on the expression of the endopeptidase by Schwann cells in situ. Endopeptidase‐24.11 was monitored by immunocytochemistry using the monoclonal anti‐endopeptidase antibody 23811. For comparison, a parallel study was carried out with a monoclonal antibody directed against the rat nerve growth factor receptor. We found that (i) all Schwann cells of the distal segment re‐expressed endopeptidase‐24.11 as early as 4 days after axotomy, the level of immunostaining reaching a maximum after 2 weeks, (ii) axonal regeneration repressed Schwann cell expression of endopeptidase‐24.11, and (iii) the induction of the nerve growth factor receptor followed a similar pattern to that of endopeptidase‐24.11 in the transected and crushed nerve. Enzymatic amplification of endopeptidase‐24.11 cDNA from normal and axotomized adult rat sciatic nerve confirmed the expression of endopeptidase‐24.11 in these tissues. Our results show that the expression of endopeptidase‐24.11 in Schwann cells, as is the case with the nerve growth factor receptor, is induced by the loss of the normal axon‐Schwann cell contact. The significant increase in the expression of endopeptidase‐24.11 by Schwann cells after axonal damage suggests that the enzyme could play a role in axonal regeneration.
Cholecystokinin Octapeptide In Vitro and Ex Vivo Strongly Modulates Striatal Dopamine D2 Receptors in Rat Forebrain Sections
Authors: Li X.‐M. , Hedlund P. B. , Fuxe K. 
Published: April 2006

AbstractReceptor autoradiographic experiments together with the filter wipe‐off technique were performed to investigate the effects of cholecystokinin octapeptide (CCK‐8) on dopamine D2 receptors. In vitro studies showed that 1 nM CCK‐8 significantly increased the KD value of binding sites for the D2 agonist [3H]N‐propylnorapomorphine (NPA) in the rostral and caudal parts of the nucleus accumbens by 48 and 148% respectively. In contrast, 1 nM CCK‐8 significantly decreased the IC50 value of dopamine for binding sites for the D2 antagonist [125I]iodosulpride in the rostral and caudal parts of the caudate‐putamen by 46 and 56% respectively, and in the rostral and caudal parts of the nucleus accumbens (areas of CCK‐dopamine coexistence) by 57 and 75% respectively. Ex vivo studies demonstrated that 30 min after an intraventricular injection of 1 nmol/rat CCK‐8 the KD value of [3H]NPA binding sites in the caudal part of the forebrain and the IC50 value of dopamine for [125I]iodosulpride binding sites in the caudal part of the nucleus accumbens were significantly increased by 160% and decreased by 77% respectively. These results indicate for the first time that in sections CCK‐8 in vitro and ex vivo can strongly regulate D2 receptor affinity in the striatum. The present studies also provide evidence for stronger modulation of D2 receptors by CCK‐8 in the area of CCW‐dopamine coexistence in the nucleus accumbens than in other basal ganglion areas, supporting the existence of CCWD2 receptor interactions in cotransmission. The stronger interactions found in sections than in membrane preparations may indicate the requirement of intracellular mechanisms and/or a more intact membrane structure for optimal receptor‐receptor interactions.
Evidence for Cis Interaction and Cooperative Signalling by the Heat‐stable Antigen Nectadrin (murine CD24) and the Cell Adhesion Molecule L1 in Neurons
Authors: Kadmon Guni , von Bohlen und Halbach Friedrich , Horstkorte Rüdiger , Eckert Marion , Altevogt Peter , Schachner Melitta 
Published: April 2006

AbstractL1 is a transmembranal hornophilic cell adhesion molecule of the immunoglobulin superfamily expressed by neural and lymphoid cells. The heat‐stable antigen (HSA, murine CD24) nectadrin is a highly and heterogeneously glycosylated glycophosphatidylinositol‐linked differentiation antigen of haematopoietic and neural cells. L1 and nectadrin have been shown to mediate cell adhesion and intracellular Ca2+ signals in neurons and B lymphoblasts, respectively. Here we show that nectadrin is co‐expressed with L1 in murine cerebellar granule cell neurons and neuroblastoma N2A cells. Purified nectadrin bound to L1 with an apparent binding ratio of five nectadrin molecules to one L1 molecule at saturation. Binding between nectadrin and purified N‐CAM was not observed. In co‐capping experiments nectadrin co‐redistributed with L1 and N‐CAM. Since in these cells N‐CAM and L1 cohere by cis binding nectadrin appears to join the L1‐N‐CAM complex through binding to L1. Antibodies to each L1 and nectadrin evoked small increases in the intracellular Ca2+ concentration. However, when both antibodies were added together or in tandem to the cells, a strong intracellular Ca2+ signal was measured that was at least 6‐ and 10‐fold stronger than the signal separately induced by L1 and nectadrin antibodies respectively. Such a cooperative effect was not observed in B lymphoblasts, using the same antibodies, or in neurons, using a combination of L1 and Thy‐1 antibodies. Both the weak Ca2+ signal mediated by L1 alone and the enhanced signal jointly triggered by antibodies to L1 and nectadrin were inhibited by phorbol 12‐myristate 13‐acetate and were not significantly affected by Ni2+ and Cd2+ cations, suggesting that they are related to one another and involve recruitment of intracellular Ca2+. Nectadrin therefore appears to join a functional complex of neuronal adhesion molecules and to potentiate the signal transduction pathway of L1, possibly in response to neuron‐neuron contact formation.
AMPA‐induced Lesions of the Basal Forebrain Differentially Affect Cholinergic and Non‐cholinergic Neurons: Lesion Assessment Using Quantitative In Situ Hybridization Histochemistry
Authors: Page Keith J. , Sirinathsinghji D. J. S. , Everitt Barry J. 
Published: April 2006

AbstractThe direct and transynaptic effects of lesions of the basal forebrain induced by α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA) and ibotenic acid were investigated using quantitative in situ hybridization histochemistry. Probes complementary to the sequences of choline acetyltransferase mRNA, glutamate decarboxylase mRNA and preproenkephalin mRNA were used to assess direct lesion effects within the basal forebrain and probes for postsynaptic M‐1 and M‐3 muscarinic receptors were used to assess long‐term changes in neocortical muscarinic receptor mRNA expression following cholinergic deafferentation. AMPA‐induced basal forebrain lesions destroyed significantly more neurons that expressed choline acetyltransferase mRNA than ibotenic acid‐induced lesions (90 versus 60%), but significantly fewer neurons which expressed either glutamate decarboxylase or preproenkephalin mRNA (61 versus 83% reduction in glutamate decarboxylase mRNA and 56 versus 79% reduction in preproenkephalin mRNA). AMPA‐induced lesions did, however, destroy a significant proportion of the neurons which expressed glutamate decarboxylase and preproenkephalin mRNA (‐60%). The neurons spared following AMPA‐induced lesions were typically situated dorsolaterally within the dorsal pallidum, although neurons expressing glutamate decarboxylase or preproenkephalin mRNA were frequently observed within the areas of greatest cholinergic neuronal loss, i.e. the region of the nucleus basalis magnocellularis. These findings suggest that there is a population of non‐cholinergic pallidal neurons which are insensitive to AMPA but not to ibotenic acid, reflecting a possibly heterogeneous distribution of NMDA and non‐NMDA subtypes of glutamate receptors within the rat basal forebrain. AMPA‐induced lesions of the basal forebrain were, however, without significant effect on the levels of expression of M‐1 and M‐3 muscarinic receptor mRNAs in the cerebral neocortex.
The Distribution of Neurons Coexpressing Immunoreactivity to AMPA‐sensitive Glutamate Receptor Subtypes (GluR1‐4) and Nerve Growth Factor Receptor in the Rat Basal Forebrain
Authors: Page Keith J. , Everitt Barry J. 
Published: April 2006

AbstractThe regional distribution of neurons containing a‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA) receptor (GluR1‐4) subunit immunoreactivity, relative to the distribution of cholinergic neurons within the basal forebrain of rats, was assessed using single‐ and dual‐antigen immunocytochemistry. Analysis of serial sections stained with antibodies to nerve growth factor receptor (NGFr) and antibodies against each of the AMPA receptor subunits, GluR1‐4, revealed a regional codistribution between NGFr‐ and GluR1‐ and GluR4‐immunoreactive neurons in the medial septum, diagonal band nuclei and nucleus basalis magnocellularis. Quantitative dual‐labelling immunocytochemistry using NGFr in combination with each of the GluR antibodies revealed >65% colocalization between NGFr and GluR4 in each of the major cholinergic nuclei in the basal forebrain and 10–15% colocalization between NGFr, GluR1 and GluR2‐3. The reticular nucleus of the thalamus, a structure known to be highly susceptible to AMPA‐induced neurotoxicity, expressed GluR4 immunoreactivity exclusively. The observation that cholinergic neurons of the basal forebrain are also highly sensitive to AMPA and express the GluR4 subunit suggests that GluR4 may be important in AMPA receptor‐mediated excitotoxicity.
The Effects of AMPA‐induced Lesions of the Medial Septum and Vertical Limb Nucleus of the Diagonal Band of Broca on Spatial Delayed Non‐matching to Sample and Spatial Learning in the Water Maze
Authors: McAlonan Gráinne M. , Dawson Gerard R. , Wilkinson Lynn O. , Robbins Trevor W. , Everitt Barry J. 
Published: April 2006

AbstractThese experiments investigated in the rat the impact on spatial delayed non‐matching to sample and on acquisition of the Morris water maze of (i) AMPA‐induced lesions of the medial septal nucleus, which produced a marked reduction of hippocampal choline acetyltransferase activity and acetylcholine levels (measured using in vivo dialysis) together with lesser reductions in cholinergic markers in the cingulate cortex and (ii) similar AMPA‐induced lesions of the vertical limb nucleus of the diagonal band of Broca (vDB), which produced more marked reductions in cholinergic markers in the cingulate cortex than in the hippocampus. Medial septal lesions produced a delay‐dependent deficit in spatial working memory, while lesions of the vDB resulted in a delay‐independent performance deficit. In addition, rats with vDB lesions adopted biased response strategies during the imposition of long delays. Neither lesion significantly affected the acquisition of a spatial reference memory task, the Morris water maze. The results are discussed in terms of cholinergic‐ and GABAergic‐dependent functions of the hippocampal formation and cingulate cortex in spatial short‐term and reference memory.