bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prostaglandin E2 release from isolated bladder strips in rats with spinal cord injury
Authors: MASUNAGA KOICHI , YOSHIDA MASAKI , INADOME AKITO , IWASHITA HITOSHI , MIYAMAE KOICHI , UEDA SHOICHI 
Published: April 2006

Aim:  Recent studies have shown that various factors contribute to the increased excitability into the bladder afferent nerves in spinal cord injury (SCI) rats. It has been reported that prostaglandins (PG) act as local modulators of reflex micturition in pathological conditions. In the present study, we measured the amount of PGE2 release from the bladder of chronic SCI rats.Methods:  Spinal cord was transected at the level of T8–9 in adult female Sprague‐Dawley rats. After 10 weeks, specimens of the urinary bladder were obtained from SCI rats and sham‐injured control rats, and bladder strips were dissected from the bladder. Using an muscle‐bath technique and a microdialysis procedure, the dialysate, containing substance released from bladder strips, was collected. Then the amount of PGE2 in the dialysate was measured by radioimmunoassay.Results:  Excretion of urinary PGE2 was significantly higher in SCI rats than in control rats. PGE2 release from bladder strips was significantly higher in SCI rats than in control rats. Removal of urothelium caused significant decreases in PGE2 release in both control and SCI rats. Stretches of the bladder strips caused significant resting tension‐dependent increases in PGE2 release from the strips with urothelium.Conclusions:  The present data suggest that bladder urothelium partly contributes to the increase in PGE2 release from the bladder, and that bladder distension may cause increases in PGE2 release in SCI rats.
Prostaglandin E2 Receptors in the Chicken Spinal Cord:
Authors: Pralong E. , Vesin M.‐F. , Droz B. 
Published: April 2006

AbstractProstaglandins (PGs) are neuroactive substances which act in the vicinity of their site of synthesis through receptors coupled to G‐proteins. Since large amounts of PGE2 can be synthesized by chicken spinal cord, binding sites for PGE2 were looked for in various cell fractions of spinal cord. In the 17 000 g pellet incubated with 0.3 nM [3H]PGE2, 70% of ligand was specifically bound. Two types of PGE2 binding site were characterized (i) high affinity, low capacity binding sites (KD1 1.34 nM, Bmax1 34.5 fmol/mg prot); (ii) low affinity, high capacity binding sites (KD2 2.23 μM, Bmax2 13.2 pmol/mg prot). The high affinity binding sites fulfil several requirements for being receptors to PGE2: (i) since the KD1 is increased in the presence of the GTP analogue, Gpp(NH)p, these binding sites would be regulated by a G‐protein; (ii) a desensitization was obtained by an excess of unlabelled PGE2 and reversed by Gpp(NH)p; (iii) the competition experiments between PGE2 and various prostanoids pointed to PGE2 receptors such as EP2 or EP3. The receptor characteristics of the low‐affinity binding sites were not investigated. Hence, our results support the presence of two types of PGE2 binding site in the chicken spinal cord; a high affinity site, which corresponds to a PGE2 receptor responding to nanomolar concentrations and a low affinity site sensitive to micromolar concentrations of PGE2.
Fibroblast Growth Factor Enhances Long‐term Potentiation in the Hippocampal Slice
Authors: Terlau Heinrich , Seifert Wilfried 
Published: April 2006

AbstractRecently we reported that perfusion of hippocampal slices with epidermal growth factor (EGF) lead to enhancement of potentiated responses after tetanic stimulation. In the present study we report that basic fibroblast growth factor (FGF) can also lead to an enhancement of potentiated responses. FGF is a mitogen for several cell types and exhibits neurotrophic effects on neurons of the central nervous system (CNS). Rat hippocampal slices were perfused with FGF at a concentration of 10−9 M. During extra‐ and intracellular recordings in the CA1 ‐region, the addition of FGF to the perfusing medium produced no change in evoked responses if single pulse or paired pulse stimulation was used. Furthermore FGF had no influence on the resting membrane potential and input resistance. However, after tetanic stimulation, FGF‐treated slices showed an increase in the magnitude of potentiation compared to control slices. Taken together with the EGF data these results support the hypothesis that growth factors like FGF with neurotrophic potential on CNS‐neurons can influence synaptic efficacy. Furthermore these results show that factors which are able to modulate developmental plasticity and regenerative plasticity can also modulate synaptic plasticity.
Prechiasmatic Reordering of Fibre Diameter Classes in the Retinofugal Pathway of Ferrets
Authors: Baker G. E. 
Published: April 2006

This study examines the distribution of fibre diameter classes at various sites along the retinofugal pathway of adult ferrets. Light microscopic observations were made on semi‐thin sections, and regional fibre diameter spectra were constructed from diameter measurements taken from electron micrographs of thin sections of the intraorbital optic nerve (2.5 mm from the optic disc), the intracranial optic nerve (1 mm rostral to the fusion of the nerves), and the optic tract (just caudal to the optic chiasm).Whereas diameter types are relatively evenly distributed behind the eye in the postoptic nerve, they begin to segregate along its prechiasmatic course. Within this prechiasmatic region, coarse and fine calibre fibres are confined increasingly to more ventral locations in the nerve, leaving a dorsal band populated predominantly by intermediate calibre fibres. In conjunction with this redistribution of axon size classes, the fascicular arrangement of axons which is present distally, changes to a non‐fascicular organization. The prechiasmatic organization of fibre types approximates that found in the optic tract where the coarse and fine calibre fibres lie further ventrally towards the pial surface.The prechiasmatic region can be viewed as a region of transition where the order of fibres in the nerve (retinotopic) starts to change to that present in the optic tract (chronotopic), resulting in the first‐born beta cell axons becoming segregated dorsally, and rostral to the coarse and fine calibre classes which segregate at further caudal locations. Further, since the sorting of fibres according to diameter appears before the fibres reach the optic chiasm, the segregation of diameter classes is not dependent on the chiasmatic sorting of fibres according to their crossed or uncrossed course.
Immunocytochemistry of cGMP in the Cerebellum of the Immature, Adult, and Aged Rat: the Involvement of Nitric Oxide. A Micropharmacological Study
Authors: de Vente J. , Bol J. G. J. M. , Berkelmans H. S. , Schipper J. , Steinbusch H. M. W. 
Published: April 2006

AbstractIn this study we describe the localization of formaldehyde‐fixed cGMP‐immunoreactivity (cGMP‐IR) in rat cerebellar tissue slices incubated in vitro. In the absence of phosphodiesterase inhibition, cGMP‐immunofluorescence was of low intensity in tissue slices prepared from immature cerebella. Addition of isobutylmethylxanthine (IBMX) to the incubation medium resulted in the appearance of cGMP‐IR in clusters of astrocytes in the internal granular layer. Addition of N‐methyl‐D‐aspartate (NMDA), kainic acid, atrial natriuretic factor (ANF), or sodium nitroprusside (SNP) gave an intense cGMP‐IR in Bergmann fibres, Bergmann cell bodies, and astrocytes in the internal granular layer. Astrocytes in the white matter showed cGMP‐IR after incubation of the slice in the presence of ANF or nitroprusside, but not after NMDA or kainic acid. In addition, after SNP stimulation of cGMP production, cGMP‐IR was found in fibres which were not positive for glial fibrillary acidic protein (GFAP). In the adult cerebellar slice, intense basal cGMP‐immunostaining was observed in Bergmann fibres, Bergmann cell bodies, and astrocytes in the granular layer. No cGMP‐IR was observed in Purkinje cells. Stimulation of the cGMP‐content in the glial structures by NMDA, ANF, or SNP, was suggested by the immunocytochemical results. However, when measured biochemically, only the effect of SNP was statistically significant, and immunocytochemistry showed that SNP clearly stimulated cGMP synthesis in neuronal cell structures. In the cerebellum of the aged rat a reduced cGMP‐IR was found compared to the adult, in the same structures which showed cGMP‐IR in the adult. Basal cGMP‐immunostaining was reduced in the presence of haemoglobin, methylene blue, by inhibiting nitric oxide synthesis with NG‐monomethyl‐L‐arginine (NGMAr), or by depletion of external Ca2+. Also the stimulatory effect of NMDA and of ANF (partly) on the cGMP‐IR was inhibited by these compounds. cGMP‐IR after stimulation of guanylate cyclase by SNP was reduced by the concomitant presence of haemoglobin or methylene blue, but not by NGMAr, or by omission of Ca2+. Our results point to an important role for cGMP in the functioning of glial tissue in the cerebellum and also suggest a role for nitric oxide as an intercellular mediator in the functioning of glutamate and ANF in the cerebellum.
Pharmacological and Biochemical Properties of Nicotinic Receptors from Chick Retina
Authors: Loring Ralph H. , Zigmond Richard E. 
Published: April 2006

AbstractPrevious work has established that functional nicotinic receptors in the chick retina are blocked by neuronal bungarotoxin (NBT), and that the binding of radio‐iodinated NBT to retinal homogenates is displaced by nicotinic ligands. In the present study, we examined the desensitizing effects of agonists on nicotinically‐mediated depolarizations recorded from chick retina. The concentrations of five agonists necessary to reduce the amplitude of these depolarizations by 50% were found to correlate closely with the concentrations of these same agonists previously found necessary to displace 50% of NBT binding. In addition, bromoacetylcholine (BAC), a selective affinity alkylating agent for the agonist binding site, irreversibly inactivated the functional responses of intact chick retina with an inhibiting concentration for 50% block (IC50) near 10‐6 M, the same concentration of BAC that displaced 50% of labelled NBT binding from alkylated retinal homogenates. These data suggest that NBT acts at the receptor agonist binding site. Furthermore, this binding site has a relatively low affinity for agonists, in the micromolar range, even in the desensitized state. Multiple subtypes of nicotinic receptors are known to exist in neuronal tissue, and receptors that bind agonists in the nanomolar range have been detergent‐solubilized and purified using monoclonal antibodies. Under similar conditions, detergent‐solubilization of chick retinal homogenates interfere with the interaction between NBT and the low‐affinity neuronal nicotinic receptors. These data suggest that the conditions used to purify high‐affinity neuronal nicotinic receptors may denature the subtype(s) of neuronal receptors recognized by NBT.
The Microtubular Pattern Changes at the Spinal Cord‐Root Junction and Reverts at the Root‐Peripheral Nerve Junction in Sensory and Motor Fibres of the Rat
Authors: López José Manuel A. , Alvarez Jaime 
Published: April 2006

AbstractIn the rat, we studied the microtubular content of central nervous system (CNS) axons (pyramidal tract, dorsal funiculus, and intracord domain of motor axons), of radicular axons (ventral and dorsal roots), and of peripheral axons (sural and lateral gastrocnemius nerves). The microtubular density had an inverse relationship with the size of the axon. Within the CNS, values ranged from over 120 microtubules/μm2 for axons smaller than 0.1 μm2 of the pyramidal tract and dorsal funiculus to 24 for 3‐μm motor axons (area, 7 μm2) in their spinal cord domain. Peripheral nerve and CNS axons of the same size had comparable microtubular densities. In contrast, the microtubular density of dorsal and ventral root axons was one half that of CNS or peripheral nerve axons of equal calibre. Considered along the axon, the microtubular density of motor and sensory fibres is high in the CNS domain, low in the root, and high again in the peripheral nerve domain. These observations are inconsistent with the notion that the cytoskeleton moves coherently away from the perikaryon. We conclude that the axonal microtubular content accords with the calibre of the fibre and with the anatomical region where it courses. We propose that axonal microtubules are regulated by local cues.
Accumulation of N‐CAM 180 at Contact Sites Between Neuroblastoma Cells and Latex Beads Coated with Extracellular Matrix Molecules
Authors: Pollerberg G. Elisabeth , Nolte Christiane , Schachner Melitta 
Published: April 2006

AbstractNeuronal cells expressing neural cell adhesion molecule (N‐CAM) accumulate the largest N‐CAM component (N‐CAM 180) at cell — cell contact sites. To test whether this accumulation is induced by interactions at the surface membrane, latex beads coated with several purified adhesion molecules or extracellular matrix (ECM) components were co‐cultured with neuroblastoma cells. Beads coated with L1, N‐CAM, the L2/HNK‐1 carbohydrate epitope‐carrying molecules from adult mouse brain or laminin from Engelbreth‐Holm‐Swarm (EHS) sarcoma did not induce an accumulation of N‐CAM 180 or L1 at sites of contact suggesting that these molecules are not directly involved in N‐CAM 180 accumulation or that their mobility is required for this process. Beads coated with ECM components of the PF‐HR9 cell line induced accumulation of N‐CAM 180 at sites of contact with neuroblastoma cells. Accumulation was seen at cell bodies of undifferentiated and differentiated neuroblastoma cells, as well as on neurites and growth cones of differentiated neuroblastoma cells. Accumulation of the neural adhesion molecule L1 was also seen, but less prominently and reproducibly. These observations suggest that molecules of the ECM can directly or indirectly, e.g. via molecules linked to N‐CAM 180 on the cell surface, induce accumulation of N‐CAM 180.
Electrophysiology and Pharmacology of the Corticothalamic Input to Lateral Thalamic Nuclei: an Intracellular Study in the Cat
Authors: Deschênes Martin , Hu Bin 
Published: April 2006

AbstractThough most experimental evidence indicates that the corticothalamic (CT) pathway would exert a direct excitatory action on thalamic relay neurons, the electrophysiological features of this excitation have never been clearly described. A methodological problem in previous electrophysiological studies was that direct corticofugal effects on relay cells could not be separated from those mediated by collateral activation of reticular thalamic neurons. In the present study, the reticular complex was lesioned by kainic acid and the CT response of relay neurons of the ventral lateral nucleus was recorded intracellularly in cats under pentobarbital or urethane anaesthesia.Following reticular thalamic lesions, a prominent depolarization was triggered in thalamic relay cells by stimulation of the CT pathway. This depolarization strongly drove spike discharges, and its amplitude augmented when the stimulation rate exceeded 2 Hz. Tetanizing the CT input with short trains (100–200 Hz for 200–300 ms) produced a similar augmentation to test volleys for 15–30 s after the tetanos. The CT excitation and its frequency‐dependent augmentation were depressed by ketamine injection or by local application of N‐methyl‐D‐aspartate (NMDA) antagonists. The augmenting phenomenon appeared strictly homosynaptic. For instance, it did not appear during repetitive stimulation of the cerebellar input, nor did the CT input potentiate subthreshold synaptic potentials of cerebellar origin during a conditioning procedure. Conversely, the cerebellar excitation was depressed when it occurred during the CT depolarization.It is concluded that the direct synaptic responses induced by CT fibres in relay neurons are mediated at least partly by the activation of NMDA receptors. Moreover, the marked non‐linear additivity of cerebellar and CT synaptic potentials raises questions concerning the presumed improvement of thalamic transmission of peripheral informations ensured by the CT input. Instead, both inputs could compete for control of the firing of thalamic neurons. The numerical importance of CT fibres and the strong augmenting mechanism operating at synaptic sites in the thalamus suggest that the role of the thalamus is not only to transfer peripheral informations toward the cortex, but also and mainly to feed back to the cortex a modified copy of its own neuronal constructs.
Complex Expression Patterns for Na+,K+ ‐ATPase Isoforms in Retina and Optic Nerve
Authors: McGrail Kevin M. , Sweadner Kathleen J. 
Published: April 2006

AbstractThree genetically distinct isozymes of the catalytic subunit of the Na,K‐ATPase have been detected and have been designated α1, α2, and α3. To determine whether their expression is restricted to identifiable neurons and glia, specific monoclonal antibodies were used for immunofluorescent localization in the rat retina and optic nerve. The patterns of staining were markedly different, suggesting differences in cellular localization. Photoreceptor inner segments and optic nerve fibers expressed predominantly α3. Müller glia in the retina and astrocytes in the optic nerve expressed α1 and α2. Isolated, dissociated bipolar, horizontal, and Müller cells expressed different isozymes separately or in combination. The complexity of staining of neurons and their axons and dendrites suggested that Na,K‐ATPase isozyme expression is not stereotyped, but is tailored to the ion transport needs of individual cell types, and targeted to specified membrane domains.
Effect of Prior Dopamine Denervation on Survival and Fiber Outgrowth from Intrastriatal Fetal Mesencephalic Grafts
Authors: Doucet G. , Brundin P. , Descarries L. , Björklund A. 
Published: April 2006

Abstract[3H]Dopamine (DA) uptake radioautography and tyrosine hydroxylase (TH) immunocytochemistry were used to assess quantitatively the effects of the presence or absence of host mesostriatal DA afferents on the survival and fiber outgrowth from fetal ventral mesencephalic DA neurons grafted into the neostriatum of adult recipient rats. Rats received bilateral intrastriatal transplants of fetal ventral mesencephalic tissue 1 month after a unilateral injection of 6‐hydroxydopamine (6‐OHDA) into the right nigrostriatal bundle (denervated side). Five to six months later, some of the grafted rats received a second 6‐OHDA injection in the left nigrostriatal bundle (acutely denervated or ‘intact’side). After a further 7 days, slices of each hemisphere from the latter rats were incubated with [3H]DA and processed for film and high resolution radioautography. The density of the film radioautographs was measured with a computerized image analysis system and calibrated by silver grain cluster (i.e. DA terminal) counting over selected areas of the same sections in light microscope radioautographs. The brains of the remaining grafted rats were processed for TH immunoreactivity 6–12 months after graft surgery. Neither the size of the grafts, nor the number of surviving TH‐positive graft neurons showed any significant difference between the nondenervated and the denervated sides. However, the size of the TH‐positive cell bodies was significantly greater in the grafts on the denervated side. In the [3H]DA uptake radioautographs, considerable outgrowth of DA fibers was evident in the neostriatum on the ‘intact’side in spite of the presence of an intact host DA innervation until 7 days before sacrifice. The overall DA fiber outgrowth was nevertheless almost two‐fold greater on the denervated side, and extended deeper into the host neostriatum than on the ‘intact’side; only 7% of the total neostriatal area, on average, was at background level compared to 30% on the ‘intact’side, and the overall density of neostriatal DA innervation amounted to 36% of normal as compared to 20% on the ‘intact’side. The correlation between the overall density of graft‐derived DA innervation and the size of the grafts was linear on the ‘intact’side, but reached a plateau with relatively small grafts on the denervated side. However, the ventral striatum on both sides was very poorly innervated by these grafts. These findings demonstrate that the mature neostriatal tissue can support axonal growth and innervation from grafted fetal DA neurons even in the presence of a normal complement of endogenous DA fibers. Prior removal of the host striatal DA innervation does not influence the overall size of the grafts nor the number of surviving DA neurons, but induces an increase in the cell body size and fiber outgrowth of the grafted DA neurons.
7‐Chlorokynurenate Blocks NMDA Receptor‐Mediated Neurotoxicity in Murine Cortical Culture
Authors: Hartley D. M. , Monyer H. , Colamarino S. A. , Choi D. W. 
Published: April 2006

AbstractWe examined the neuroprotective actions of the glycine site N‐methyl‐D‐aspartate (NMDA) antagonist, 7‐chlorokynurenate, in murine neocortical cell cultures. Cultures exposed for 5 min to 100–500 μM NMDA in the absence of added glycine developed substantial neuronal degeneration over the next 24 h. The addition of 10 μM glycine did not increase submaximal NMDA‐induced neuronal injury, suggesting that endogenous glycine levels were sufficient to saturate its receptor sites on NMDA receptor complexes. Addition of 3–300 μM 7‐chlorokynurenate produced concentration‐dependent reduction in this neuronal damage with an IC50 of approximately 30 μM. Some injury reduction was seen even if the drug was added after completion of the NMDA exposure. The protective effect of 100 μM 7‐chlorokynurenate could be overcome by adding 10–1000 μM glycine (glycine median effective concentration (EC50) approximately 100 μM) or 1 mM D‐serine. As predicted by its ability to block NMDA receptor‐mediated injury, 10–300 μM 7‐chlorokynurenate also produced concentration‐dependent reduction in the neuronal loss induced by 50–60 min exposure to combined glucose and oxygen deprivation. These data support the suggestion that pharmacologic interference with the binding of glycine to the NMDA receptor complex represents a potentially effective approach to blocking NMDA receptor‐induced neurotoxicity in ischemia.
Targets and Quantitative Distribution of GABAergic Synapses in the Visual Cortex of the Cat
Authors: Beaulieu C. , Somogyi P. 
Published: April 2006

AbstractThe morphology and postsynaptic targets of GABA‐containing boutons were determined in the striate cortex of cat, using a postembedding immunocytochemical technique at the electron microscopic level. Two types of terminals, both making symmetrical synaptic contacts, were GABA‐positive. The first type (95% of all GABA‐positive boutons) contained small pleomorphic vesicles, the second type (5%) contained larger ovoid vesicles. Furthermore, 99% of all cortical boutons containing pleomorphic vesicles were GABA positive, and all boutons with pleomorphic vesicles made symmetrical synaptic contacts. These results together with previously published stereological data (Beaulieu and Colonnier, 1985, 1987) were used to estimate the density of GABA‐containing synapses, which is about 48 million/mm3 in the striate cortex. The postsynaptic targets of GABA positive boutons were also identified and the distribution was calculated to be as follows: 58% dendritic shafts, 26.4% dendritic spines, 13.1% somata and 2.5% axon initial segments. A total of 11% of the postsynaptic targets were GABA immunoreactive and therefore originated from GABAergic neurons. The results demonstrate that the majority of GABAergic synapses exert their action on the membrane of dendrites and spines rather than on the somata and axons of neurons.