bluuebunny/crossref_metadata_2025_split huggingface dataset:
Synaptic Plasticity in an In Vitro Slice Preparation of the Rat Nucleus Accumbens
Authors: Pennartz C. M. A. , Ameerun R. F. , Groenewegen H. J. , Lopes da Silva F. H. 
Published: April 2006

AbstractExtra‐ and intracellular recordings in slices were used to examine what types of synaptic plasticity can be found in the core of the nucleus accumbens, and how these forms of plasticity may be modulated by dopamine. Stimulus electrodes were placed at the rostral border of the nucleus accumbens in order to excite primarily infralimbic and prelimbic afferents, as was confirmed by injections of the retrograde tracer fluoro‐gold. In extracellular recordings, tetanization induced long‐term potentiation (LTP) of the population spike in 20 out of 53 slices. The presynaptic compound action potential did not change following LTP induction. For the intracellularly recorded excitatory postsynaptic potential, three types of synaptic plasticity were noted: long‐term potentiation (16 out of 54 cells), decremental potentiation (eight cells) and long‐term depression (LTD; six cells). No correlation was found between the occurrence of potentiation or depression and various parameters of the tetanic depolarization (e.g. peak voltage, integral under the curve). The N‐methyl‐d‐aspartate receptor antagonist d(–)‐2‐amino‐5‐phosphonopentanoic acid (50 μM; d‐AP5) reduced, but did not completely prevent, the induction of LTP. The incidence of LTD was not markedly affected by d‐AP5. No difference in LTP was found when comparing slices bathed in dopamine (10 μM) and controls. Likewise, slices treated with a mixture of the D1 receptor antagonist Sch 23390 (1 μM) and the D2 antagonist S(–)‐sulpiride (1 μM) generated a similar amount of LTP as controls. In conclusion, both LTP and LTD can be induced in a key structure of the limbic‐innervated basal ganglia. LTP in the nucleus accumbens strongly depends on N‐methyl‐d‐aspartate receptor activity, but is not significantly affected by dopamine.
Intrastriatal Transplants of Embryonic Dopaminergic Neurons Counteract the Increase of Striatal Enkephalin Immunostaining but not Serotoninergic Sprouting Elicited by a Neonatal Lesion of the Nigrostriatal Dopaminergic Pathway
Authors: Abrous D. N. , Manier M. , Mennicken F. , Feuerstein C. , Moal M. Le , Herman J. P. 
Published: April 2006

AbstractThe aim of the our experiment was to compare the ability of intrastriatal implants of embryonic dopaminergic neurons to reverse two kinds of postlesion modification in the host brain: the change in the activity level of neurons in the denervated area and morphological modifications, e.g. collateral sprouting. The ascending dopaminergic system of 3‐day‐old rat pups was unilaterally lesioned by an intrahypothalamic injection of the neurotoxin 6‐hydroxydopamine. This lesion has been described previously to induce an increase in the level of activity of striatal enkephalinergic neurons. The same lesion leads also to sprouting of the serotoninergic afferents in the striatum, leading to hyperinnervation of this structure. The existence of these modifications thus offers the possibility of testing the influence of grafts in one structure of the same animal on two lesion‐induced reactions of different nature. A cell suspension obtained from mesencephali of embryonic day 14 rats and containing dopaminergic neurons was implanted into the denervated striatum of lesioned animals 5 days after the lesion. Nine months later the animals were killed and immunohistochemistry was performed on striatal sections using antibodies directed against tyrosine hydroxylase, methionine enkephalin and serotonin. Intensity of immunostaining (methionine enkephalin and serotonin) as well as innervation density (serotonin) was quantified through the use of a computer‐assisted image analyser. The lesion led to the disappearance of striatal dopaminergic innervation. Implanted dopaminergic neurons were found scattered in the striatum and restored a dopaminergic innervation in a large portion of this structure. There was a marked increase in striatal methionine enkephalin immunostaining in lesioned animals, which was most pronounced in the dorsolateral part of the striatum (+ 150% compared to control values), while in the ventral part it was slight or non‐existent. The density of striatal serotoninergic innervation was also increased by ∼250% relative to control values. In grafted animals striatal enkephalin immunostaining was similar to that observed in control animals. On the other hand, the serotoninergic hyperinnervation was still present in the graft‐bearing striata. These results suggest that while intrastriatal implants of embryonic dopaminergic neurons are able to counteract modifications in the functioning of local striatal neuronal systems such as the increase in enkephalinergic activity or receptor hypersensitivity occurring as a result of the lesion, they might be unable to reverse postlesion morphological modifications.
Mediation of Thalamic Sensory Responses In Vivo by ACPD‐activated Excitatory Amino Acid Receptors
Authors: Eaton S. A. , Birse E. F. , Wharton B. , Sunter D. C. , Udvarhelyi P. M. , Watkins J. C. , Salt T. E. 
Published: April 2006

AbstractThe existence of the so‐called metabotropic excitatory amino acid receptor has been known for some years. Various functions have been suggested for this receptor, but the lack of selective antagonists for (IS, 3R)‐aminocyclopentane dicarboxylic acid (ACPD) has precluded the direct demonstration of a functional role for this receptor in synaptic processes. We describe here a specific antagonism of the excitatory responses of thalamic neurons to ACPD by two novel antagonists, and a parallel antagonism by these compounds of sensory synaptic responses to noxious stimuli of the same neurons. This provides the first direct pharmacological evidence for a functional role of ACPD‐sensitive receptors in central neurotransmission, and indicates that these receptors may play an important part in central sensory processes.
Differential Expression of Immediate Early Genes in Rubrospinal Neurons Following Axotomy in Rat
Authors: Jenkins R. , Tetzlaff W. , Hunt S. P. 
Published: April 2006

AbstractMany immediate early genes are rapidly and transiently expressed in the central nervous system following a variety of stimuli. Damage to the axons of peripheral and certain central neurons has been shown to result in a long‐term increase in expression of c‐Jun in the parent cell bodies. In the peripheral nervous system this increased expression of c‐Jun protein and mRNA develops over 24 h following sciatic nerve section and is maintained if the damaged nerve is ligated, but returns to basal levels if the peripheral nerve is allowed to regenerate. Here, we report on the response of rubrospinal neurons to spinal cord hemisection at levels C3 and T10. c‐Jun expression was first seen at 12 h post‐lesion in a limited number of rubral neurons. The number of positively stained neurons increased up to 10 days post‐lesion and then declined over the following weeks. By 7 weeks post‐lesion there was still evidence of c‐Jun immunoreactivity in both large and other clearly atrophic rubrospinal neurons. c‐Fos immunoreactivity was seen only at 12–48 h in a small number of rubrospinal neurons. Evidence from retrograde tracing experiments following fluorogold application to the hemisected cord suggested that all c‐Jun‐positive neurons projected into the spinal cord. No c‐Jun response was seen following a lesion at T10. These observations on the rubrospinal tract contrast with previous results of immediate early gene expression studies in neurons of the substantia nigra, pars compacta following axotomy with 6‐hydroxydopamine, where c‐Fos immunoreactivity was not seen and the increased expression of c‐Jun declined to basal levels within 21 days. These results suggest that the immediate early gene response of different central neuronal pathways to damage may vary. This may have important implications for any experimental intervention designed to facilitate the repair of damaged neuronal pathways in the adult brain.
Cytochemical Redistribution of 5′‐Nucleotidase in the Developing Cat Visual Cortex
Authors: Schoen S. W. , Kreutzberg G. W. , Singer W. 
Published: April 2006

AbstractThe adenosine‐producing ectoenzyme 5′‐nucleotidase has recently been shown to undergo a marked redistribution during development of the cat visual cortex and to be involved in the remodelling of ocular dominance columns (Schoen et al., J. Comp. Neurol., 296, 379 – 392, 1990). Using an enzyme‐cytochemical technique, we now investigate the developmental redistribution of 5′‐nucleotidase activity in area 17 of kittens at the ultrastructural level. Between postnatal days 35 and 42, when 5′‐nucleotidase is concentrated in layer IV, enzyme reaction product occupies the clefts of asymmetrical synapses within the neuropil. During later development (9th and 13th postnatal weeks), when 5′‐nucleotidase spreads over all cortical laminae, the enzyme disappears from its synaptic localization and becomes increasingly associated with astrocytic membranes. The transient appearance of 5′‐nucleotidase at synapses parallels the time‐course and laminar profile of the synaptic remodelling which takes place during the critical period of visual cortex development. This suggests that synapse‐bound 5′‐nucleotidase activity plays a role in synaptic malleability, whereas its later association with glial profiles is likely to reflect other functions of the enzyme.
Long‐term Effects of Selective Target Removal on Brainstem Premotor Neurons in the Adult Cat
Authors: de La Cruz Rosa R. , Pastor Angel M. , Delgado‐García José M. 
Published: April 2006

AbstractThe electrical activity of antidromically identified abducens internuclear neurons selectively deprived of their target motoneurons was recorded in chronic alert cats. Target motoneurons were killed by the injection of the cytotoxic lectin of Ricinus communis into the medial rectus muscle. Following target removal, the discharge pattern of abducens internuclear neurons showed an overall decrease in firing rate, a significant reduction in their sensitivity to eye position and velocity, and the presence of anomalous responses such as bursts of spikes associated with off‐directed saccades. The decreased excitability of abducens internuclear neurons correlated well with a marked reduction in the synaptic efficacy of their inputs. Thus, both excitatory and inhibitory synaptic potentials of vestibular origin showed a noticeable decrease in amplitude. The alterations in firing properties and synaptic transmission were only observed during an initial period of 3 weeks following ricin injection. Within 1 month the electrophysiological parameters returned to control values and remained unaltered for 1 year. Retrograde labelling of abducens internuclear neurons revealed that no cell death occurred after target loss. The anterograde axonal labelling of these neurons showed a progressive decrease in the density of their axonal terminals, and no sign of redistribution to other areas was found. These findings indicate that abducens internuclear neurons are not dependent on the presence of their natural target cells, either for the survival or for the maintenance of appropriate physiological signals.
Cholecystokinin in Mammalian Primary Sensory Neurons and Spinal Cord: In Situ Hybridization Studies in Rat and Monkey
Authors: Verge V. M. K. , Wiesenfeld‐Hallin Z. , Hökfelt T. 
Published: April 2006

AbstractThe peptide cholecystokinin (CCK) has been suggested to be involved in nociception, but its exact localization at the level of the spinal cord and in spinal ganglia has been a controversial issue. Therefore the distribution of messenger RNA (mRNA) for CCK was studied by in situ hybridization using oligonucleotide probes on sections of adult rat lumbar dorsal root ganglia following unilateral section of the sciatic nerve and on sections of untreated monkey trigeminal ganglia, spinal cord and spinal ganglia from all levels. For comparison, calcitonin gene‐related peptide (CGRP) mRNA was also studied in the monkey tissue using the same techniques. Peripheral sectioning of the sciatic nerve in the rat resulted in the appearance of detectable CCK mRNA in up to 30% of remaining ipsilateral L4 and L5 dorsal root ganglion neurons 3 weeks after surgery, with a distinct but more limited appearance also in the contralateral ganglia. No cells, or only single cells, could be seen in normal control rat ganglia. In contrast, in the normal monkey, ∼20% of dorsal root ganglion neurons, regardless of spinal level, and 10% of trigeminal ganglia neurons expressed mRNA for CCK. CGRP mRNA was expressed at detectable levels in ∼80% of these monkey dorsal root ganglion neurons. In the monkey spinal cord, CCK mRNA was detected in the dorsal horn and in motoneurons, whereas CGRP mRNA was only seen in motoneurons. The present results suggest that CCK peptides can be involved in sensory processing in the dorsal horn of the spinal cord in normal monkeys and in rats after peripheral nerve injury, adding one more possible excitatory peptide to the group of mediators in the dorsal horn.
The glia‐derived protease nexin 1 persists for over 1 year in rat brain areas selectively lesioned by transient global ischaemia
Authors: Nitsch C. , Scotti A. L. , Monard D. , Heim C. , Sontag K.‐H. 
Published: April 2006

AbstractThe re‐expression of the developmentally regulated serine protease inhibitor glia‐derived nexin (GDN) was investigated 1 year after transient global ischaemia induced by the four‐vessel occlusion technique in rats. The CA1 sector of the hippocampus was severely shrunken due to the absence of pyramidal cells, but still clearly discernible due to the continued presence of the parvalbumin‐containing GABAergic neurons. In this partially neuron‐depleted hippocampus, GDN immunoreactivity was found in reactive astrocytes containing glial fibrillary acidic protein. GDN‐positive astrocytes were also found in other lesioned areas, the reticular thalamic nucleus and the cerebellar cortex. Thus, the re‐expression of GDN in the adult excitotoxically lesioned brain described previously in the gerbil model of ischaemia persists. The continued presence of the protease inhibitor might disturb the proteolytic balance and lead to the deposition of pathological breakdown products of proteins, e.g. β‐amyloid.
Localization of Janusin mRNA in the Central Nervous System of the Developing and Adult Mouse
Authors: Wintergerst Eva Sabine , Fuss Babette , Bartsch Udo 
Published: April 2006

AbstractJanusin (formerly termed J1‐160/180) is an oligodendrocyte‐derived extracellular matrix molecule which is restricted to the central nervous system and which is expressed late during development (Pesheva et al., J. Cell Biol., 1765 – 1778, 1989). To gain insights into the molecule's morphogenetic functions and to identify its cellular source in vivo, we have studied the localization of janusin messenger RNA in the optic nerve, retina and spinal cord and the expression of janusin protein in the spinal cord of developing and adult mice. Moreover, we have analysed optic nerve cell cultures and retinal cell suspensions in double‐labelling experiments using a janusin‐specific anti‐sense complementary RNA probe and cell type‐specific antibodies to identify the cell types containing janusin transcripts. In developing animals, oligodendrocytes were strongly labelled with the janusin anti‐sense cRNA probe during the period of myelination. The number of labelled cells and intensity of the hybridization signal decreased significantly with increasing age. Interestingly, expression of janusin was not confined to oligodendrocytes. Some neuronal cell types and type‐2 astrocytes present in optic nerve cell cultures also contained janusin transcripts. In contrast to oligodendrocytes, the number and labelling intensity of neurons containing janusin transcripts remained constant during postnatal development and into adulthood. Expression of janusin protein in the spinal cord was developmentally regulated, with a peak of expression in 2‐or 3‐week‐old animals. The molecule was visible in the white and grey matter. In myelinated regions, it was associated with myelinated fibres and accumulated at nodes of Ranvier. These observations suggest that janusin may be of functional relevance for myelination.
ME1 and GE1: Basic Helix – Loop – Helix Transcription Factors Expressed at High Levels in the Developing Nervous System and in Morphogenetically Active Regions
Authors: Neuman T. , Keen A. , Knapik E. , Shain D. , Ross M. , Nornes H. O. , Zuber M. X. 
Published: April 2006

AbstractSeveral class A basic helix – loop – helix (bHLH) transcription factors have been cloned from the developing mouse and chick nervous system. The cloned cDNAs (ME1, ME2, ME3, ME4, in the mouse and GE1, GE2 in the chick) have HLH coding regions highly homologous to other known class A bHLH genes. The genes corresponding to ME1 and GE1 are abundantly expressed during development of the central nervous system. ME1 and GE1 are expressed in proliferating neuroblasts and in cells at the initial stages of differentiation (for example in the external granule cell layer of the cerebellum and in the lateral region of the ventricular zone in the developing neural tube and cortex). They are also expressed at high levels in morphogenetically active regions such as limb buds, somites and mesonephric tubules. The expression of ME1 and GE1 decreases once cellular differentiation is over. Based on the expression of ME1 and GE1 in regions of active cellular proliferation and differentiation and on the known role of other bHLH factors in development, we suggest that ME1 and GE1 play important roles during development of the nervous system as well as in other organ systems.
Changes in Nuclear 3,5,3′‐Triiodothyronine Receptor Expression in Rat Dorsal Root Ganglia and Sciatic Nerve During Development: Comparison with Regeneration
Authors: Barakat‐Walter I. , Due C. , Puymirat J. 
Published: April 2006

AbstractThe action of the thyroid hormones on responsive cells in the peripheral nervous system requires the presence of nuclear triiodothyronine receptors (NT3R). These nuclear receptors, including both the α and β subtypes of NT3R, were visualized by immunocytochemistry with the specific 2B3 monoclonal antibody. In the dorsal root ganglia (DRG) of rat embryos, NT3R immunoreactivity was first discretely revealed in a few neurons at embryonic day 14 (E14), then strongly expressed by all neurons at E17 and during the first postnatal week; all DRG neurons continued to possess clear NT3R immunostaining, which faded slightly with age. The peripheral glial cells in the DRG displayed a short‐lived NT3R immunoreaction, starting at E17 and disappearing from the satellite and Schwann cells by postnatal days 3 and 7 respectively. In the developing sciatic nerve, Schwann cells also exhibited transient NT3R immunoreactivity restricted to a short period ranging from E17 to postnatal day 10; the NT3R immunostaining of the Schwann cells vanished proximodistally along the sciatic nerve, so that the Schwann cells rapidly became free of detectable NT3R immunostaining. However, after the transection or crushing of an adult sciatic nerve, the NT3R immunoreactivity reappeared in the Schwann cells adjacent to the lesion by 2 days, then along the distal segment in which the axons were degenerating, and finally disappeared by 45 days, when the regenerating axons were allowed to re‐occupy the distal segment. It is concluded that (1) NT3R expression lasts throughout the life of the DRG neurons; (2) NT3R expression by peripheral glia is restricted to the perinatal period but may be transiently reactivated in Schwann cells after a nerve injury; and (3) cell‐cell interaction with axons down‐regulates the expression of NT3R by Schwann cells in both growing and regenerating nerves.
Effect of Thiol Reagents on Phosphoinositide Hydrolysis in Rat Brain Synaptoneurosomes
Authors: Vignes Michel , Guiramand Janique , Sassetti Isabelle , Récasens Max 
Published: April 2006

AbstractSome divalent ions, such as Cd2+ and Zn2+, are able to stimulate phosphoinositide (PI) breakdown and to inhibit receptor‐mediated PI metabolism. These ions are also known to react with the free – SH groups of proteins. This prompted us to investigate the effects of more potent sulphhydryl reagents, Hg2+ and p‐chloromercuric benzosulphonic acid (PCMBS), on the inositol phosphate (IP) accumulation triggered by the neuroactive substances: glutamate, carbachol and K+, using synaptoneurosomes from 8‐day‐old rat forebrains. Hg2+ and PCMBS, depending on their concentration, had two distinct effects on IP accumulation: at low doses, Hg2+ (from 1 to 10 μM) and PCMBS (0.1 mM) by themselves stimulated PI breakdown, inhibited glutamate‐elicited IP accumulation and had additive effects with respect to carbachol‐induced IP stimulation. At higher doses, Hg2+ (from 0.01 to 1 mM) inhibited both basal and neuroactive substance‐stimulated IP accumulation. PCMBS (1 mM), provoked only an inhibition of the agonist‐stimulated IP formation. Monitoring membrane potential and intracellular Ca2+ with the fluorescent dyes diSC2(5) and fura2, respectively, indicated that these mercurials could strongly depolarize the synaptoneurosomal membrane and produce a Ca2+ influx dependent on extracellular Ca2+. The stimulatory effects of low concentrations of mercurials on PI turnover could be linked to the depolarization they provoke and the subsequent Ca2+ rise, which in turn is known to stimulate some phospholipase C enzymes. The inhibitory effects observed at high concentrations might be due to a loss of activity of proteins involved in PI breakdown, as all receptor‐mediated IP accumulations were inhibited.
The Development of Retinal Ganglion Cell Decussation Patterns in Postnatal Pigmented and Albino Ferrets
Authors: Thompson I. D. , Morgan J. E. 
Published: April 2006

AbstractThe decussation patterns of retinal ganglion cells in postnatal pigmented and albino ferrets were examined by using retrograde axonal tracers. Following unilateral injections into the optic pathway of newborn pigmented ferrets, ∼ 13 000 cells were labelled in the ipsilateral retina. The majority (11 500) of these were located in temporal retina. Postnatally, the numbers of cells projecting ipsilaterally from temporal retina fell by 49%. High rates of loss were observed in both the smaller uncrossed projection from nasal retina (92%) and also in the crossed projection from temporal retina (84%). After injections on the day of birth, a decussation line was not obvious in the crossed projection: ≥ 14 000 labelled cells were found in temporal retina. Double tracer studies showed that very few of these cells had axons which projected bilaterally. The numbers of ipsilaterally projecting cells labelled in neonatal albino ferrets was dramatically reduced. Only ∼ 2500 were labelled in temporal retina following injections at birth. As in pigmented ferrets, about half of these cells subsequently died. The reduced uncrossed projection in albino neonates was asociated with an increase in the crossed projection from temporal retina, in which ∼ 21 000 cells were labelled following injections at birth. These results suggest that differential postnatal ganglion cell death establishes the adult decussation pattern in the contralateral retinal projection but merely refines the pattern already established in the uncrossed projection. Postnatal ganglion cell death plays no significant role in generating the abnormal projections found in albino ferrets.