bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neurodegenerative Effects Induced by Chronic Infusion of Quinolinic Acid in Rat Striatum and Hippocampus
Authors: Vezzani A. , Forloni G. L. , Serafini R. , Rizzi M. , Samanin R. 
Published: April 2006

AbstractIn this study we examined whether the potency of quinolinic acid (Quin) in inducing neurodegeneration in vivo was dependent on the exposure time of the tissue to the excitotoxin. The effect of chronic infusion of Quin into rat striatum and hippocampus was examined at the light microscopic level and by cell count on 40 μm Cresyl violet stained brain sections. Continuous infusion was at a constant speed (0.5 μl/h) for various times (15 h–2 weeks) by osmotic minipumps (Alzet 2002). No build up of [3H]Quin occurred in the tissue during infusion; this was assessed by measuring the radioactivity 3–14 days after minipump placement. Intrastriatal infusion of 6 and 10 nmol/h Quin, but not of nicotinic acid, for 1 week induced a dose‐dependent neurodegeneration (70 and 90% loss of neurons, respectively, compared to the contralateral striatum) extending 1.2–2 mm from the centre of the injection. The onset of the neurotoxicity caused by 10 nmol/h Quin was >24 h. One week's infusion of 4 nmol/h Quin did not induce neurotoxicity, but a 40% drop of neurons, compared to the contralateral side, occurred after 2 weeks. One week's intrahippocampal infusion of 2.4 and 6 nmol/h Quin, but not of nicotinic acid, caused a dose‐dependent neurodegeneration with a radius of ∼1–1.5 mm around the injection track. The onset of the neurotoxicity induced by 2.4 nmol/h Quin was <15 h. The pattern of nerve cell loss induced by 1.2 nmol/h Quin after 1 week (CA4 cells lost in 50% of the rats) did not differ from that observed after 2 weeks of infusion. Nerve cell loss caused by Quin in the striatum and in the hippocampus was restricted to the injected area and antagonized by coinfusion with d(–)‐2‐amino‐7‐phosphonoheptanoic and kynurenic acids in molar ratios of 1:0.1 and 1:3, respectively. These data show that Quin's potency in inducing neurodegeneration in the striatum, but not in the hippocampus, depends on the exposure time of the tissue to the excitotoxin. In addition, neurodegeneration is induced faster by Quin in the hippocampus than in the striatum. The usefulness of this model to study the sequelae of the neurotoxic process in vivo will be discussed.
Evidence of a Monosynaptic Pathway Between Cells of the Ventromedial Medulla and the Motoneuron Pool of the Thoracic Spinal Cord in Rat: Electron Microscopic Analysis of Synaptic Contacts
Authors: Zagon A. , Bacon S. J. 
Published: April 2006

AbstractPrevious electrophysiological and anatomical data have suggested the existence of a descending pathway from the ventromedial medulla into the thoracic motoneuron pool. However, systematic light and electron microscopic analysis have not yet been done to reveal such a projection. In the present study, the anterograde tracer, Phaseolus vulgaris leucoagglutinin (PHA‐L) was injected into several discrete regions of the medioventral medulla and descending PHA‐L‐labelled axons were investigated in the thoracic ventral horn using both light and electron microscopy. Light microscopic analysis of descending projections from 20 distinct areas of the medioventral medulla showed that neurons that project predominantly to the intermediate and ventral regions of the thoracic spinal grey matter are located caudal to the facial nucleus. Monosynaptic contacts were found between axons originating from five distinct regions of the medioventral medulla (containing raphé and/or gigantocellular reticular neurons) and cells in the thoracic motoneuron pool. PHA‐L‐labelled boutons formed synaptic contacts with large calibre dendrites and with somata. Seventy‐two per cent of the investigated 32 boutons appeared to have symmetrical synaptic membrane specializations. The majority of the boutons contained only small, pleomorphic vesicles. Our findings show the existence of a direct monosynaptic pathway between the neurons of the ventromedial medulla and thoracic motor nuclei, providing anatomical support for previous physiological data.
Very Slow Retrograde and Wallerian Degeneration in the CNS of C57BL/Ola Mice
Authors: Perry V. H. , Brown M. C. , Lunn E. R. 
Published: April 2006

AbstractWallerian degeneration following peripheral nerve transection in C57BL/Ola mice is very slow in comparison to other strains of mice. We show that following optic nerve transection, the axons of retinal ganglion cells in C57BL/Ola mice undergo very slow Wallerian degeneration and that retrograde degeneration of the ganglion cell bodies is much slower than in other strains of mice. The results suggest that the gene product affecting Wallerian degeneration in the peripheral nervous system (PNS) also confers a greater resistance to degeneration on central nervous system (CNS) neurons.
Modulation of GABA‐mediated Synaptic Potentials by Glutamatergic Agonists in Neonatal CA3 Rat Hippocampal Neurons
Authors: Gaiarsa Jean‐Luc , Corradetti Renato , Cherubini Enrico , Ben‐Ari Yehezkel 
Published: April 2006

AbstractIntracellular recordings were made from slices of adult and neonatal hippocampal neurons. During the first 2 weeks of life the majority of pyramidal cells exhibited spontaneous gamma‐aminobutyric acid (GABA)‐mediated synaptic potentials, which were depolarizing at birth and became hyperpolarizing by the end of the first postnatal week. These synaptic potentials were reduced in frequency or blocked by the N‐methyl‐d‐aspartate (NMDA) receptor antagonist d(‐)2‐amino‐5‐phosphonovalerate (AP‐5, 50 μM) (13/15 cells). The non‐NMDA antagonist, 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX, 5–10μM) abolished the GABA‐mediated synaptic potentials in all the cells tested (n= 12), Superfusion of l‐glutamate (up to 100 μM) increased the frequency of both depolarizing and hyperpolarizing GABA‐mediated synaptic potentials. This effect was reduced by AP‐5 or dl‐2‐amino‐7‐phosphonoheptanoate (AP‐7, 50 μM) and fully blocked by concomitant application of AP‐5 (50 μM) and CNQX (5–10 μM). NMDA (0.5–2 μM) increased the frequency of the GABA‐mediated synaptic potentials. These effects were blocked by AP‐5 (50 μM) and by bicuculline (10 μM). Quisqualate (100–300 nM), (RS)‐alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐izopropionate (AMPA, 100–300 nM) and kainate (100 nM) also increased the frequency of the GABA‐mediated synaptic potentials. These effects were blocked by CNQX (5–10 μM) and by bicuculline (10 μM) but not by AP‐5 (50 μM). In the presence of tetrodotoxin (TTX, 1 μM), quisqualate (up to 300 nM), AMPA (up to 500 nM) and kainate (100 nM) had no effect on membrane potential or input resistance. In conclusion, our experiments suggest that, in early postnatal life, NMDA and non‐NMDA receptors located on GABAergic interneurons modulate GABAergic synaptic potentials.
Expression and Developmental Regulation of a GABAA Receptor in Cultured Murine Cells of the Oligodendrocyte Lineage
Authors: von Blankenfeld G. , Trotter J. , Kettenmann H. 
Published: April 2006

AbstractThe inhibitory neurotransmitter GABA activated Cl− currents in oligodendrocytes and their precursor cells. Most of the pharmacological features of these GABA‐evoked currents matched those described for the neuronal GABAA/benzodiazepine receptor complex, such as the blockade by picrotoxin and bicuculline and the enhancement by barbiturates and benzodiazepines. In contrast to the astrocytic GABA receptor, but similar to the neuronal GABAA receptor, the inverse benzodiazepine agonist DMCM decreased GABA‐induced current responses. A further similarity to the neuronal receptor is the strong run‐down of the current in the absence of ATP in the pipette. A difference between oligodendroglial receptors and receptors expressed on neurons and astrocytes was revealed by the dose ‐ response curve, which indicated only one binding site for GABA or weak allosterical interactions between two putative binding sites. Thus, GABAA receptors of precursor cells and oligodendrocytes might represent a third class of GABAA receptors, in addition to those expressed by neurons and astrocytes. The density of these receptors in the membrane, as calculated on the basis of whole cell currents and membrane capacitance, decreased by a factor of 100 when cells matured along the oligodendrocyte lineage, indicating a developmental regulation of the expression of the GABA receptor.
Afferent and Efferent Connections of Temporal Association Cortex in the Rat: A Horseradish Peroxidase Study
Authors: Vaudano E. , Legg C. R. , Glickstein M. 
Published: April 2006

AbstractWe studied the afferent and efferent connections of the caudal temporal cortex in rat using the tracer wheat germ agglutinin – horseradish peroxidase (WGA–HRP). This area is reciprocally connected with primary and secondary visual and auditory areas of cortex. The connections with primary visual cortex are restricted to the ventral and caudal parts of the caudal temporal area. Caudal temporal cortex has reciprocal connections with the perirhinal cortex and projects to the caudate ‐ putamen and lateral and basolateral nuclei of the amygdala. It also has reciprocal connections with the nucleus lateral is posterior, the dorsal and medial divisions of the medial geniculate nucleus and the caudal part of the posterior nucleus of the thalamus. It projects to the deep layers of the superior colliculus, the pericentral nucleus of the inferior colliculus and to the ventral nucleus of the basilar pons. Our results suggest that the rat caudal temporal cortex forms part of a pathway that connects visual and auditory cortex with the limbic system, by the way of the amygdala and perirhinal cortex.
Peptide‐containing Neurons Projecting to the Tongue of the Rat: Retrograde Tracing and Immunocytochemistry
Authors: Luts Anders , Uddman Rolf , Grunditz Torsten , Montavon Phillippe , Lindstrand Kaj , Sundler Frank 
Published: April 2006

AbstractThe origin and neuropeptide content of nerve fibres in the rat circumvallate papilla was studied by retrograde tracing in combination with immunocytochemistry. An injection of the retrograde tracer True Blue into the circumvallate papilla resulted in the appearance of labelled nerve cell bodies in the superior cervical, the stellate, the thyroid, the nodose, the jugular, the petrosal, the otic, the trigeminal and the dorsal root ganglia at level C2. Most of the True Blue‐labelled nerve cells in the superior cervical ganglia contained neuropeptide Y. The majority of labelled cell bodies in the thyroid ganglia contained vasoactive intestinal peptide. In the jugular and trigeminal ganglia, the majority of the labelled nerve cell bodies stored calcitonin gene‐related peptide. A small number of neurons in the medial reticular formation of the central nervous system was labelled. Tracer injections deep into the tongue tissue beneath the circumvallate papilla gave rise to True Blue‐labelled neurons in the hypoglossal nucleus.
Differential Regulation of Calcitonin Gene‐related Peptide (CGRP) in Regenerating Rat Facial Nucleus and Dorsal Root Ganglion
Authors: Dumoulin F. L. , Raivich G. , Streit W. J. , Kreutzberg G. W. 
Published: April 2006

AbstractThe content of calcitonin gene‐related peptide (CGRP) and CGRP‐mRNA were determined in axotomized rat facial motor nucleus and sensory fifth lumbar dorsal root ganglion (L5 DRG) using radioimmunoassay and Northern blot analysis. After facial nerve transection CGRP levels in the facial nucleus showed a biphasic, five‐fold increase. A first peak occurred at postoperative day 3 and, after a transient decrease to normal levels at day 9, another increase was observed reaching a peak around the time of reinnervation (postoperative day 21). CGRP‐mRNA showed a similar, biphasic increase. The first peak in CGRP mRNA preceded the peptide peak by 2 days, the second peak was day 21. In contrast, a decrease in CGRP levels is seen in L5 DRG after sciatic nerve section, reaching minimal levels of 45% of control during the second postoperative week. CGRP‐mRNA in axotomized DRG also decreases preceding the decrease in peptide levels. No recovery to normal levels is seen for either peptide or mRNA levels in regenerating DRG up to 45 days after injury. Thus, axotomy leads to a differential regulation of both CGRP and CGRP‐mRNA in regenerating facial motor nucleus and sensory L5 DRG. This difference may be due to different regulating factors present in both the respective target tissues and the CNS regions and could reflect different functions of CGRP in regenerating motor and sensory neurons.
Climbing Fibre Responses in Olivo‐cerebellar Slice Cultures. II. Dynamics of Cytosolic Calcium in Purkinje Cells
Authors: Knöpfel T. , Vranesic I. , Staub C. , Gähwiler B. H. 
Published: April 2006

AbstractThe generation of climbing fibre responses in cerebellar Purkinje cells has been analysed in co‐cultured slices of rat cerebellum and inferior olive. Complex spikes were evoked in Purkinje cells by climbing fibre activation or by intrasomatic injection of depolarizing current pulses. Microfluorometric measurements of cytosolic free calcium ([Ca2+]i) by means of intracellularly injected fura‐2 combined with intracellular recordings revealed that both types of complex spikes were accompanied by a transient rise in [Ca2]i, which was most prominent at dendritic locations. Synaptically induced Ca2+ transients were completely and reversibly abolished by 6‐cyano‐7‐nitroquinoxaline‐2–3‐dione (CNQX, 5 μM), an antagonist of the ionotropic action mediated by non‐N‐methyl‐d‐aspartate excitatory amino acid receptors. Ca2+ transients evoked by injections of depolarizing current pulses were not affected by CNQX. These observations indicate that Ca2+ transients induced by climbing fibre activity are generated by voltage‐gated Ca2+ channels, which are activated by a CNQX‐sensitive synaptic depolarization.
Endothelin Opens Potassium Channels in Glial Cells
Authors: Supattapone Surachai , Ashley Christopher C. 
Published: April 2006

AbstractEndothelin‐1 (ET‐1), an autocrine hormone synthesized by astrocytes, and endothelin‐3 (ET‐3), a highly homologous peptide produced by neurons, have both been shown previously to cause proliferation of these astrocytes in culture [Supattapone et al. (1989) Biochem. Biophys. Res. Commun., 165, 1115–1122; MacCumber et al. (1990) Proc. Natl. Acad. Sci. USA, 87, 2359–2363]. We now demonstrate, using 86Rb+ influx assays and single channel patch‐clamp recording, that both endothelins–ET‐3 and ET‐1–can also open a charybdotoxin‐sensitive, calcium‐activated K+ channel of 15–40 pS in glial cells. The opening of this channel may be important for the regulation of [K+] in the brain microenvironment. Thus, the endothelins may be a general mediator of astroglial response to neuronal injury.
Divalent Cations Modulate the Inhibitory Substrate Properties of Murine Glia‐derived J1‐160 and J1‐180 Extracellular Matrix Glycoproteins for Neuronal Adhesion
Authors: Pesheva Penka , Probstmeier Rainer , Spiess Eberhard , Schachner Melitta 
Published: April 2006

AbstractJ1–160 and J1–180 are developmentally late appearing J1 extracellular matrix glycoproteins derived from oligodendrocytes. They prevent adhesion of neurons (but not of astrocytes or fibroblasts) when offered as a substrate in mixture with laminin (Pesheva et al., J. Cell Biol., 109, 1765–1778, 1989). In the present study we have examined the influence of divalent cations on the inhibitory substrate properties of J1‐160/180 glycoproteins towards adhesion of neurons. By metal chelate affinity chromatography, we show that J1‐180, but not J1‐160, binds Ca2+, while both J1 components are capable of binding Zn2+ and other divalent metal ions. Divalent cation binding was observed by gel filtration, aggregation assays with coated latex beads and electron microscopic examination to elicit aggregation of the molecules. Divalent cation binding also affects their non‐permissive substrate properties towards neurons from early postnatal mouse cerebellum. Without divalent cations, J1–160 and J1–180 are inhibitory for substrate adhesion of neurons independently of the adhesive substrate present (laminin or poly‐l‐lysine). This effect is neutralized when J1–180 is preincubated with Ca2+ or Zn2+ prior to coating as substrate. In contrast, preincubation with Ca2+ ions does not affect the inhibitory substrate properties of J1–160 under these conditions. These observations show that J1‐160/180 molecules may undergo self‐aggregation in a divalent cation‐dependent mechanism, which correlates with the neutralization of their inhibitory effect on neuronal adhesion. The aggregation state of the molecules may thus influence the process of myelination by a homophilic binding mechanism and determine the effectiveness of neurite extension during central nervous system development and under traumatic conditions in the adult.
Climbing Fibres as a Source of Nitric Oxide in the Cerebellum
Authors: Southam Eric , Garthwaite John 
Published: April 2006

AbstractExposure of adult rat cerebellar slices to a moderately raised K+ concentration (15 mM) caused a large (30‐fold) rise in the levels of cyclic GMP. Excitatory amino acid antagonists failed to inhibit this response, nor could it be mimicked by agonists active at a number of other transmitter receptors. It was, however, inhibited by the nitric oxide (NO) synthase antagonist, l‐methylarginine (lC50= 10 μM), and also by tetrodotoxin (1 μM) implying that underlying the cyclic GMP response was an action potential‐dependent formation of NO. Prelesioning of climbing fibres resulted in a loss of ∼50% of the response to K+ but failed to influence the effects of glutamate receptor agonists or the NO‐donor, nitroprusside. These findings point to a new mechanism for the formation of NO in the central nervous system and suggest that, in the cerebellum, climbing fibres are a source of NO.
Catecholamine Metabolism in Locus Coeruleus Neurons: A Study of its Activation by Sciatic Nerve Stimulation in the Rat
Authors: Brun P. , Suaud‐Chagny M. F. , Lachuer J. , Gonon F. , Buda M. 
Published: April 2006

AbstractSciatic nerve stimulation, which strongly activates noradrenergic locus coeruleus (NA‐LC) neurons, was used in anaesthetized rats as a model to study the transneuronal control of catechol metabolism in this nucleus. We show, using in vivo electrochemistry and biochemical post‐mortem assays, that a prolonged (20 min) unilateral sciatic nerve electrical stimulation led to a reversible enhancement (80 – 130%) of both endogenous and in vivo extracellular levels of 3,4‐dihydroxyphenylacetic acid (DOPAC) within the contralateral LC region. An elevation in DOPAC levels was also observed in the ipsilateral nucleus but was always significantly lower. The response was abolished by a pretreatment with kynurenic acid, a non‐selective excitatory amino acid (EAA) antagonist known to block footshock‐induced excitations of NA‐LC neurons: in antagonist‐treated rats, the stimulation induced a non‐significant effect (+ 30%) on endogenous DOPAC levels, which contrasted with the highly significant effect (+ 113%) observed in vehicle‐treated animals. As the major source of EAA afferents to the LC originates in the nucleus paragigantocellularis, we made an attempt to suppress activation by a section of these fibres. An incision performed obliquely (45°) between LC and PGi greatly and significantly attenuated, but did not totally suppress, the increase in DOPAC endogenous content due to the stimulation. These experiments indicate that a peripheral stimulus provokes an activation of catecholamine metabolism within the soma ‐ dendritic region of the NA‐LC cells. They suggest that this effect may be mediated, at least in part, by afferent pathways originating from the medulla which utilize an EAA as transmitter.
Taste Buds and Neuromasts of Astyanax jordani: Distribution and Immunochemical Demonstration of Co‐localized Substance P and Enkephalins
Authors: Bensouilah M. , Denizot J.‐P. 
Published: April 2006

AbstractThe distribution and some immunohistochemical aspects of the taste buds and free neuromasts of the blind cave fish Astyanax jordani were investigated using serial sections of whole fish. Taste buds are restricted to the skin of the lips and the lower jaw. Neuromasts are widely distributed over the whole epidermis except the lips and are particularly numerous in the opercular region and the caudal fin; they are absent from all other fins. The histological structure of the taste buds and the free neuromasts is similar to that described in other fish. The former are composed of two types of cells. The free neuromast, as seen under the electron microscope, is also constituted by two types of cell: dark supporting cells and clear sensory cells whose basal cytoplasm contains presynaptic bodies. Immunohistochemical results obtained with the peroxidase antiperoxidase method revealed the presence of different peptides in the taste buds and the free neuromasts. The former contain substance P (SP) and enkephalins (leu‐ and metenkephalin); the latter contain SP and leuenkephalin, but no metenkephalin. These peptides are localized in the cytoplasm of the accessory and sensory cells but not in the nervous fibres. None of these peptides occur in the olfactory epithelium of A.jordani. These immunohistochemical results raise the question of whether SP, leuenkephalin or metenkephalin play a role in transmission between the sensory cells and the afferent fibre.
Targets and Laminar Distribution of Projection Neurons with ‘Inverted’ Morphology in Rabbit Cortex
Authors: Bueno‐López José L. , Reblet Concepción , López‐Medina Antonio , Gómez‐Urquijo Sonia M. , Grandes Pedro , Gondra Juan , Hennequet Leonor 
Published: April 2006

AbstractThis study examines the axonal projections of so‐called inverted pyramids and other neurons with their major dendritic shaft oriented in the direction of the white matter (‘inverted cells’) in the adult rabbit cortex. Single injections of horseradish peroxidase wheat germ agglutinin were made into cortical or subcortical sites. The resulting retrograde labelling in the cortex was analysed and the distribution across areas and layers of inverted cells contributing to each of these projections was estimated. In addition, the radial distribution of inverted cells was independently determined from rapid Golgi‐impregnated and Nissl‐stained material. All three procedures revealed that inverted cells lay overwhelmingly in infragranular layers, but congregated at the border between layers 5 and 6. Inverted cells, identified by retrograde labelling, seldom furnished non‐telencephalic centres; in contrast, these cells constituted a major source for the projections to the ipsi‐ or the contralateral cortex, the claustrum or the nucleus caudatus. In general, each set of inverted cells (when defined by its specific destination as a group) was located below the typically oriented cells whose axons were aimed at the same target. Thus, the inverted cells of the rabbit cortex are characterized not only by their unique morphology and their corticocortical, corticoclaustral and corticostriatal projections, but also by their distinctive radial locations. These findings suggest that inverted cells, even though possibly composed of different cell types, are a specific class of projection neurons.