bluuebunny/crossref_metadata_2025_split huggingface dataset:
Post‐translational Processing of the Alternative Neuropeptide Precursor Encoded by the FMRFamide Gene in the Pulmonate Snail Lymnaea stagnalis
Authors: Santama Niovi , Wan Li Ka , Geraerts Wijnand P. M. , Benjamin Paul R. , Burke Julian F. 
Published: April 2006

AbstractThe neuropeptide gene encoding FMRFamide‐like peptides in the pulmonate mollusc Lymnaea is subject to alternative splicing that generates cell‐specific expression of distinct sets of peptides in the CNS. In this paper, we analyse the post‐translational processing of the alternative protein precursor encoded by the exon I, III–V transcript (type 2 transcript). We raised anti‐peptide antisera specific to distinct segments of the precursor in order to address the pattern of endoproteolytic cleavages, specifically around the tetrabasic site RRKR. We first showed that not all peptides predicted by the precursor structure are generated as final steady‐state products. We then identified a novel peptide by biochemical purification, amino acid sequencing and mass spectrometry—the 35 amino acid SDPFFRFGKQQVATDDSGELDDEILSRVSDDDKNI, which we termed the acidic peptide, previously not predicted on the basis of the precursor structure. This novel peptide, abundant in the snail brain (0.7 pmol per central nervous system), includes the N‐terminal sequence SDPFFRF, which was previously considered to be a variant of the known heptapeptide SDPFLRFamide, also encoded within the same protein precursor. We showed by in situ hybridization and immunocytochemistry that the acidic peptide is produced in all cells that transcribe type 2 FMRFamide mRNA. We mapped the expression of this novel peptide in the CNS and localized it mainly in three identifiable neuronal clusters—the E, F and B groups of cells—and some additional neurons, all situated in three of the eleven central ganglia. Immunoreactive neurons included the single identifiable visceral white interneuron (VWI or VD4), a key cell of the cardiorespiratory network.
Emx1 and Emx2 Show Different Patterns of Expression During Proliferation and Differentiation of the Developing Cerebral Cortex in the Mouse
Authors: Gulisano Massimo , Broccoli Vania , Pardini Celia , Boncinelli Edoardo 
Published: April 2006

AbstractInsights into the complex structure of the forebrain and its regulation have recently come from the analysis of the expression of genes that are likely to be involved in regionalization of this structure. We cloned four new homeo box genes, Emx1, Emx2, Otx1 and Otx2, and we showed that in day 10 mouse embryos their expression domains are continuous regions of the developing brain contained within each other in the sequence Emx1 < Emx2 < Otx1 < Otx2. Recently Otx1 has been found to be specifically expressed during neurogenesis of layers 5 and 6 in the developing cerebral cortex. In order to better understand the role of Emx1 and Emx2 in the maturation of the cortex we analysed by in situ hybridization their expression patterns in the developing mouse cerebral cortex, from embryonic day 12.5 to adulthood. We found that Emx2 is expressed exclusively in proliferating cells of the ventricular zone whereas Emx1 is expressed in both proliferating and differentiated neurons, throughout the cortical layers and during all the developmental stages examined. Therefore, Emx2 gene products might control some biological parameters of the proliferation of cortical neuroblasts or of the subsequent cell migration of postmitotic neurons, leaving the cortical germinal zone. Conversely, Emx1 expression, which is confined exclusively to the dorsal telencephalon, characterizes most cortical neurons during proliferation, differentiation, migration and postnatal development and maturation.
Topographically Organized Climbing Fibre Sprouting in the Adult Rat Cerebellum
Authors: Zagrebelsky Marta , Rossi Ferdinando , Hawkes Richard , Strata Piergiorgio 
Published: April 2006

AbstractAdaptive recovery following brain injury requires the topography of projection maps to be restored. In the adult mammalian brain, the regeneration of severed axons does not normally occur and repair mainly relies on collateral reinnervation from uninjured neurons. Although reinnervation can be target specific at the single cell level, it is not known if the new connections are organized correctly. The normal olivocerebellar projection has a precise topography in which subnuclei of the inferior olive terminate as climbing fibres on chemically defined bands of cerebellar Purkinje cells. This precision has been exploited to determine the topography of climbing fibre sprouting following an inferior olive lesion in the adult rat. Collateral reinnervation was found to respect the boundaries between the Purkinje cell compartments. Thus, topographical cues are available in the adult during post‐lesion plasticity to guide the restoration of the olivocerebellar projection map.
Transient Colocalization of Parvalbumin and Calbindin D28k in the Postnatal Cerebral Cortex: Evidence for a Phenotypic Shift in Developing Nonpyramidal Neurons
Authors: Alcántara Soledad , de Lecea Luis , Del Río Jose. A. , Ferrer Isidro , Soriano Eduardo 
Published: April 2006

AbstractIn the adult rat cerebral cortex the calcium‐binding proteins parvalbumin and calbindin D28k are present in essentially non‐overlapping populations of GABAergic interneurons. These proteins follow different developmental patterns in the cortex: calbindin D28k‐immunoreactive nonpyramidal neurons are abundant until the second postnatal week and decrease markedly thereafter; it is at this time that parvalbumin immunoreactivity develops in cortical nonpyramidal neurons. To determine whether parvalbumin‐immunoreactive neurons derive from calbindin D28k‐positive cells we used double‐immunofluorescence studies for both calcium‐binding proteins, together with combined immunocytochemistry for calbindin D28k and in situ hybridization for parvalbumin mRNA during postnatal development. Double‐labelled cells were found in all cortical layers between P9 and P21, coinciding with the onset of parvalbumin expression. The percentage of colocalization of the two calcium‐binding proteins depended on the age and layer examined. Colocalization reached a peak (80–100%) during the second postnatal week in layers II–IV and VI and decreased thereafter to adult levels by the end of the third postnatal week. Double‐labelled neurons were rare in layer V at all ages studied. The present results indicate a phenotypic shift during the development of some cortical interneurons that halts the expression of calbindin D28k while parvalbumin expression starts. These findings agree with lineage analyses reporting that different types of nonpyramidal neuron arise from a common progenitor.
The Convergence of Axon Terminals from the Mediodorsal Thalamic Nucleus and Ventral Tegmental Area on Pyramidal Cells in Layer V of the Rat Prelimbic Cortex
Authors: Kuroda Masaru , Murakami Kunio , Igarashi Hiroaki , Okada Akiko 
Published: April 2006

AbstractWe investigated the ultrastructural basis of the synaptic convergence of afferent fibres from the mediodorsal thalamic nucleus (MD) and the ventral tegmental area (VTA) on the prefrontal cortical neurons of the rat by examining the synaptic relationships between thalamocortical or tegmentocortical terminals labelled with anterograde markers [lesion‐induced degeneration or transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA—HRP)] and randomly selected unlabelled apical dendrites of layer V pyramidal cells in the prelimbic cortex. WGA—HRP‐labelled terminals from the VTA ranged in diameter from 0.7 to 2.8 μm and established synaptic contacts with large dendritic profiles, i.e. proximal segments of apical dendritic shafts and spines from layer V pyramidal cells. Symmetrical synapses, i.e. inhibitory synapses, were more often seen than asymmetrical ones. Degenerating terminals from the MD formed asymmetrical synapses on dendritic spines or occasionally on small dendritic shafts of apical dendrites from layer V pyramidal cells, which received tegmentocortical synapses, mostly within layer III. Thalamocortical synapses were more distally distributed over common apical dendrites than tegmentocortical synapses, although some of them overlapped. The numerical density of direct synaptic inputs from the MD and VTA was low. These results suggest that fibres from the VTA exert their inhibitory effects directly on pyramidal cells in layer V via synaptic junctions with apical dendrites of these pyramidal cells, and that the tegmentocortical fibres are in an ideal anatomical position to modulate the reverberatory circuits between the MD and the prelimbic cortex.
Evidence for an Anuran Homologue of the Mammalian Spinocervicothalamic System: An In Vitro Tract‐tracing Study in Xenopus laevis
Authors: Muñoz A. , Muñoz M. , González A. , ten Donkelaar H. J. 
Published: April 2006

AbstractEvidence is presented for an anuran homologue of the mammalian spinocervicothalamic system. In vitro tract‐tracing experiments with biotinylated dextran amine in Xenopus laevis show that ascending spinal fibres from all levels of the spinal cord, passing via the dorsolateral funiculus, terminate in a cell area ventrolateral to the dorsal column nucleus. This cell area can be considered a possible homologue of the mammalian lateral cervical nucleus. After tracer applications to the ventral thalamus or to the torus semicircularis (both targets for somatosensory projections), the anuran lateral cervical nucleus was retrogradely labelled contralateral to the application sites. Tracer applications to the dorsolateral funiculus at the obex level and rostral spinal cord resulted in labelling of the cells of origin of the spinocervical tract. These were found, mainly ipsilaterally, in the ventral part of the dorsal horn, and were rather evenly distributed throughout the spinal cord. These data suggest the presence of an anuran homologue of the mammalian spinocervicothalamic system. A brief survey of the literature shows that such a system is much more common in vertebrates than previously thought.
Expression of Heat Shock Protein‐70 and Limbic Seizure‐induced Neuronal Death in the Rat Brain
Authors: Zhang X. , Boulton A. A. , Yu P. H. 
Published: April 2006

AbstractThe effect of MK‐801, a non‐competitive N‐methyl‐D‐aspartate (NMDA) antagonist, on the kainic acid‐induced expression of the inducible heat shock protein 70 kDa (HSP70) and on neuronal death in the rat hippocampus was investigated. HSP70 is expressed in ˜80% of the pyramidal neurons in the CA1 field 1 day after kainic acid injection. The majority of these HSP70‐immunopositive neurons exhibited swelling and a hollow appearance in the perikaryon, indicating that they had been injured following kainic acid‐elicited limbic seizures. Four days after administration of kainic acid, 87% of the pyramidal neurons in the CA1 field were dead. When a single dose of MK‐801 was administered 1 h before kainic acid injection, the number of rats suffering with seizures was reduced, the severity of limbic seizures was attenuated and seizure onset was delayed. Neither HSP70 expression on day 1 nor neuronal loss on day 4 in the CA1 pyramidal cell layer was observed in these animals. A considerable number of HSP70‐immunopositive neurons was detected in the dentate hilus, however, and somewhat fewer in the CA3a and CA3c subfields on day 1. Severe neuronal damage in these regions followed on day 4. Interestingly, little HSP70 expression or neuronal loss was observed in the CA3b subfield in these same animals. When a single dose of MK‐801 was given 4 h after kainic acid treatment, HSP70 expression was partially blocked; 18% of neurons expressed HSP70 on day 1 and 37% on day 4 in CA1 pyramidal neurons in comparison to the kainic acid controls. About 50% neuronal death was detected in the CA1 pyramidal cell layer 4 days after kainic acid treatment followed by MK‐801. When the animals were treated with MK‐801 4 h after kainic acid treatment followed by additional daily administration for 3 days, a negligible number of pyramidal neurons expressed HSP70, and the survival of pyramidal cells was significantly increased in the CA1 field. Limbic seizure‐induced HSP70 expression not only indicates neuronal injury in the pyramidal cell layer of the hippocampus but also predicts delayed neuronal death, at least in the case of the CA1 field of animals that suffered stage IV—V seizures.
Simultaneous Recording of Spontaneous Activities and Nociceptive Responses from Neurons in the Pars Compacta of Substantia Nigra and in the Lateral Habenula
Authors: Gao D. M. , Hoffman D. , Benabid A. L. 
Published: April 2006

AbstractUsing simultaneous extracellular single‐unit recording in the pars compacta of the substantia nigra and in the lateral habenula of rats, 45 pairs of neurons responding to peripheral nociceptive stimulation were recorded. In 41 of these pairs, nigral dopaminergic neurons were inhibited by peripheral nociceptive stimulation, while lateral habenula neurons were excited. Moreover, in 14 pairs, when sweeps were triggered randomly by spontaneous spikes from lateral habenula neurons the spontaneous firing rate of the dopaminergic neurons during the first 250 ms after the sweep was much lower than rates after this time period. In this case, the sweep was often triggered by burst‐firing of lateral habenula neurons. Our results indicate a cross‐correlation between the spontaneous activities of these two nuclei, suggesting that the excitation of lateral habenula neurons induced by peripheral nociceptive stimulation might be directly responsible for inhibition of nigral dopaminergic neurons.
Dissociations in Hippocampal 5‐Hydroxytryptamine Release in the Rat Following Pavlovian Aversive Conditioning to Discrete and Contextual Stimuli
Authors: Wilkinson Lawrence S. , Humby Trevor , Killcross Simon , Robbins Trevor W. , Everitt Barry J. 
Published: April 2006

AbstractThe experiments examined the release of 5‐hydroxytryptamine using in vivo microdialysis methods in the hippocampus of freely moving rats following Pavlovian aversive conditioning to discrete and contextual stimuli. Differential conditioning was achieved by manipulating the interval between the offset of a discrete auditory ‘clicker’stimulus and the onset of a mild foot‐shock reinforcer (0.5 mA, 0.5 s). Foot‐shock occurred either simultaneously with the last second of the discrete auditory stimulus (in short‐trace subjects) or 60 s later (long‐trace subjects). In this way, subjects were preferentially conditioned to the discrete stimulus and background ‘contextual’stimuli respectively. During conditioning subjects also received two identical unpaired visual stimuli. At test, dialysates were collected and behavioural measures taken as all animals experienced (i) the aversive and two other ‘neutral’environments, and (ii) the discrete unconditioned and conditioned stimuli presented in both aversive and neutral environments. Exposure to the aversive environment, but not to either of the two neutral environments, was associated with significantly increased hippocampal 5‐hydroxytryptamine release in long‐trace subjects. There was also a small but non‐significant increase in 5‐hydroxytryptamine release in short‐trace animals. In contrast, hippocampal 5‐hydroxytryptamine release was unaffected by presentation of either of the discrete stimuli under all conditions. The last result was obtained despite robust behavioural responses (freezing) to the discrete conditioned stimulus. These data do not agree with the hypothesis that aversive cues generally activate 5‐hydroxytryptamine function in the hippocampus. Rather, they suggest a degree of specificity whereby 5‐hydroxytryptamine release in the hippocampus was determined primarily by other qualitative properties of the conditioned aversive stimulus, namely whether the aversive cue was discrete or contextual, as well as by the magnitude of conditioning.
Dopamine D1 Receptor‐mediated Facilitation of GABAergic Neurotransmission in the Rat Strioentopeduncular Pathway and its Modulation by Adenosine A1 Receptor‐mediated Mechanisms
Authors: Ferré Sergi , O'Connor William T. , Svenningsson Per , Björklund Lars , Lindberg Jakob , Tinner Barbro , Strömberg Ingrid , Goldstein Menek , Ögren Sven Ove , Ungerstedt Urban , Fredholm Bertil B. , Fuxe Kjell 
Published: April 2006

AbstractBy using in vivo microdialysis it was found that one of the main functions of striatal dopamine D1 receptors is to selectively facilitate GABAergic neurotransmission in the ‘direct’strioentopeduncular pathway. D1 receptors localized in the entopeduncular nucleus were also found to facilitate GABA release. However, results obtained from in vivo microdialysis, in vivo electrochemistry, immunohistochemistry and confocal laser microscopy suggested that entopeduncular D1 receptors could only be activated under pharmacological conditions. Adenosine A1 receptors were found to antagonistically modulate the D1‐mediated regulation of the strioentopeduncular pathway. Furthermore, using in situ hybridization D1 and A1 receptors were shown to be colocalized in medium‐sized striatal neurons. These results show that the strioentopeduncular neuron is a main locus for adenosine‐dopamine interactions in the brain.
Regulation of CD44 in the Regenerating Mouse Facial Motor Nucleus
Authors: Jones Leonard L. , Kreutzberg Georg W. , Raivich Gennadij 
Published: April 2006

AbstractCD44 is a cell adhesion molecule which plays an important role in cell movement and adhesion, e.g. in lymphocyte homing and tumour metastasis. Here we studied the expression of CD44 mRNA and protein immunoreactivity in the facial nucleus after nerve injury and during the ensuing regeneration. Transection of the facial nerve led to a strong up‐regulation of CD44, peaking 4 days after injury on the motoneurons of the axotomized facial nucleus. Use of the polymerase chain reaction confirmed the de novo expression of CD44 and detected only the standard haematopoietic CD44 isoform. Western blotting also detected the 76 kDa protein subtype, in line with the predicted size of the haematopoietic CD44 variant. At the ultrastructural level, CD44 immunoreactivity was restricted to the surface of the neuronal perikarya, their dendrites and axons. It was not seen in the adjacent activated astrocytes, microglia or vascular endothelia. This study shows strong up‐regulation of the cell adhesion molecule CD44 on the regenerating rnotoneurons in the axotomized facial nucleus. These data suggest that CD44 may play a role in neurite outgrowth, in synaptic stripping or in the adhesion of activated glial cells to the perikaryal surface of the axotomized motoneurons.
Intraneuronal Traffickina and Distribution of Amphiphysin and Synaptojanin in thg Rat Peripheral Nervous System and the Spinal Cord
Authors: Li Jia‐Yi , De Camilli Pietro , Dahlström Annica 
Published: April 2006

AbstractAmphiphysin and synaptojanin are two nerve terminal proteins with a putative role in synaptic vesicle endocytosis and recycling. We have investigated the intraneuronal dynamics and distribution of these two proteins, using nerve crush techniques in combination with immunofluorescence, cytofluorimetric scanning (CFS), confocal laser scanning microscopy and immuno‐electron microscopy (EM). Accumulations of amphiphysin and synaptojanin immunoreactivities at the crush site were detected as short as 1 h after the lesion, indicating that a pool of these two partially cytosolic proteins moves along the axon by fast axoplasmic transport. The amount of proximal accumulation increased linearly between 1 and 8 h. CFS analysis demonstrated that only 30% of fast anterogradely transported amphiphysin and synaptojanin was returned by fast retrograde transport, in contrast to the 70% value observed for synaptophysin, a transmembrane protein. This indicates that the majority of amphiphysin and synaptojanin is degraded/metabolized in the nerve terminals. Immuno‐EM showed that both amphiphysin and synaptojanin are primarily associated with heterogeneous membrane profiles in the crushed sciatic nerve and the immunoperoxidase reaction product is concentrated in the nerve terminal cytomatrix of the spinal cord. Both proteins were differentially distributed in subsets of nerve terminals, indicating heterogeneous expression in neurons.
A Role for Neurotrophins in the Survival of Murine Embryonic Thalamic Neurons
Authors: Lotto R. Beau , Clausen Julia A. , Price David J. 
Published: April 2006

AbstractThe mechanisms that determine whether developing CNS neurons live or die are poorly understood. We studied the role of the neurotrophins and fibroblast growth factors in the survival of embryonic thalamic neurons in culture. Dissociated embryonic dorsal thalamic neurons cultured at high density in defined serum‐free medium survived and grew neurites. As in vivo, they expressed all the neurotrophins, fibroblast growth factor‐1 and their high‐affinity tyrosine kinase receptors. The survival of these cells was reduced by the addition of the protein kinase inhibitor K252a at concentrations that block neurotrophin receptor activity but not the activity of other tyrosine kinase receptors. In low‐density cultures, most dorsal thalamic neurons died, but their survival was increased by co‐culture with thalamic explants or with most of the neurotrophins and fibroblast growth factor‐1 added singly. These results indicate that thalamic neurons have remarkably promiscuous trophic responses to a battery of neurotrophins and fibroblast growth factors. They suggest that neurotrophins endogenous to the early embryonic thalamus may be required to promote the survival of its neurons.
BDNF is Expressed at the Crush Site after Spinal Cord Lesion in Newborn Opossum (Monodelphis domestica)
Authors: Vischer Heinrich A. 
Published: April 2006

AbstractBrain‐derived neurotrophic factor (BDNF) supports the regeneration of axotomized motoneurons in vitro. To study the role of BDNF in vivo, a partial cDNA encoding the BDNF of the opossum (Monodelphis dornestica) was cloned by reverse transcription‐polymerase chain reaction. The sequence was highly homologous to the BDNF of several mammals and chick. The spinal cord of newborn opossums was lesioned and allowed to regenerate in its entirety in a culture system for 3 days. In response to lesion, cells within the lesion and the ventrorostral wound margin showed strong expression of opossum BDNF mRNA as detected by in situ hybridization. In contrast, no BDNF mRNA expression was detected in unlesioned CNS preparations. This suggests that BDNF plays a role in the repair of lesioned neonatal spinal cord.
Connexins, Gap Junctions and Cell‐Cell Signalling in the Nervous System
Authors: Bruzzone Roberto , Ressot Catherine 
Published: April 2006

AbstractConnexins form a multigene family of polytopic membrane proteins that, in vertebrates, are the constitutive subunits of intercellular channels and provide the structural basis for electrical coupling. The appearance of electrical coupling in the nervous system is developmentally regulated and restricted to distinct cell types. Electrical coupling between neurons persists after the establishment of chemical transmission, thus suggesting that this form of cell‐cell signalling may be functionally interrelated with, rather than alternative to chemical transmission. Furthermore, evidence for the possible role of gap junctions in human neurological diseases is also mounting, following the discovery that the X‐linked form of Charcot‐Marie‐Tooth syndrome, a demyelinating neuropathy of the peripheral nervous system, is associated with mutations in a connexin gene. These findings raise new questions on the significance of connexin diversity and on their functional role in the nervous system.