bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acetylcholinesterase Adaptation to Voluntary Wheel Running is Proportional to the Volume of Activity in Fast, but not Slow, Rat Hindlimb Muscles
Authors: Gisiger Victor , Bélisle Manon , Gardiner Phillip F. 
Published: April 2006

AbstractChronic enhancement of neuromuscular activity by forced exercise training programmes results in selective adaptation of the G4 acetylcholinesterase (AChE) molecular form in hindlimb fast muscles of the rat, with only minor and non‐selective AChE changes in the soleus. In order to shed further light on the physiological significance of this G4 adaptation to training, we turned to a voluntary exercise model. The impact of 5 days and 4 weeks of voluntary wheel cage running on AChE molecular forms was examined in four hindlimb fast muscles and the slow‐twitch soleus from two rat strains. Inbred Fisher and Sprague– Dawley rats, placed in live‐in wheel cages, exercised spontaneously for distances which progressively increased up to an average of ∼3 and 18 km/day, respectively, by the end of week 4. Fast muscles responded to this voluntary activity by massive G4 increases (up to 420%) with almost no changes in A12, so that by week 4 the tetramer became the main AChE component of these muscles. The additional G4 was composed primarily of amphiphilic molecules, suggesting a membrane‐bound state. The G4 content of fast muscles was highly correlated with the distance covered by the rats during the 5 days before they were killed (r= 0.850‐0.879, P < 0.001 in three muscles). The soleus muscle, in turn, responded to wheel cage activity by a marked selective reduction of its asymmetric forms—up to 45% for A12. This A12 decline, already maximal by day 5 of wheel cage running, showed no relationship with the distance covered. The present results constitute strong new evidence suggesting that the role of AChE in neuromuscular transmission is not limited solely to the rapid inactivation of just‐released acetylcholine.
Nerve Growth Factor and Basic Fibroblast Growth Factor Protect Cholinergic Neurons Against Quinolinic Acid Excitotoxicity in Rat Neostriatum
Authors: Pérez‐Navarro Esther , Alberch Jordi , Arenas Ernest , Calvo Nancy , Marsal Jordi 
Published: April 2006

AbstractIn the present work we have characterized a possible mechanism leading to the early survival of neostriatal cholinergic neurons after quinolinic acid injection. Different doses of quinolinic acid were injected in rat neostriatum and two different parameters were analysed 7 days after the lesion: choline acetyltransferase (ChAT) activity and nerve growth factor (NGF) levels. We have observed that ChAT activity decreased (until 68 nmol quinolinic acid) and NGF levels increased (until 34 nmol quinolinic acid) in a dose‐dependent manner. In order to characterize the time‐course of the lesion on NGF levels and ChAT activity, and the possible protective effect of NGF and basic fibroblast growth factor (bFGF) on cholinergic neurons, we have used the quinolinic acid dose (68 nmol) at which the first decrease of ChAT activity was observed. ChAT activity and NGF levels showed different patterns of response to quinolinic acid injection, since the maximal effect was reached at 1 day for ChAT activity and at 2 days for NGF levels. NGF or bFGF simultaneously injected with quinolinic acid (68 nmol) completely prevented the decrease in ChAT activity in a dose‐dependent manner but NGF was more effective than bFGF. Furthermore, differences observed in ChAT activity after NGF but not bFGF treatment were correlated with changes in the number of ChAT immunoreactive cells. Finally, we have also observed that, although bFGF alone was not able to modify NGF levels, bFGF simultaneously injected with quinolinic acid produced an increase of NGF levels higher than that observed after quinolinic acid injection alone. Our results show that NGF and bFGF protect striatal cholinergic neurons against quinolinic acid injury, and bFGF is able to potentiate the increase of NGF after the lesion, suggesting a cooperative action between different trophic factors in neuronal protection after excitotoxic injury. Thus, administration of trophic factors may be relevant in the prevention and treatment of neurodegenerative disorders, such as Huntington's disease.
Secondary Cell Death and the Inflammatory Reaction After Dorsal Hemisection of the Rat Spinal Cord
Authors: Dusart I. , Schwab M. E. 
Published: April 2006

AbstractLocal spinal cord lesions are often greatly enlarged by secondary damage, a process which leads to massive additional cell death. This process is poorly understood. In order to investigate which types of cells could play a role in increasing the size of the lesion, we have analysed the events occurring at rat spinal cord lesion sites from 1 h to 3 months after partial transection using cell type‐specific markers. One hour after transection, the lesion site was small and corresponded to the zone of primary mechanical damage. Extravasation of blood and an opening of the blood – brain barrier occurred. Rapidly thereafter, at 3 and 6 h, an area of secondary cell death developed around the zone of the primary lesion. This secondary cell death, which was probably largely of the necrotic type, affected neurons, macroglia and microglial cells indiscriminately. It was virtually complete at 12 h. Recruitment of inflammatory cells followed a time course which lagged behind that of secondary cell death. Adhesion of neutrophils to the inside of blood vessels was observed at 3 h. They appeared in large numbers at 6 h at the site of the primary lesion, but not yet in the area of secondary cell death. They were numerous throughout the lesion site at 24 h and then disappeared rapidly. Proliferation and recruitment of macrophages and microglial cells became predominant 2 days after injury. Their density was highest within the lesion site between 4 and 8 days. Very few astrocytes were present in the lesion site during the first week. In contrast, the surrounding area contained numerous activated astrocytes, which began to delineate the lesion site. After 2 weeks, the microglial cells and macrophages progressively disappeared from the lesion site, and a cavity formed. A glial scar surrounded this cavity and consisted of reactive astrocytes and activated microglial cells. The time course of the cellular reactions observed here suggests that secondary damage is not primarily due to destructive effects of neutrophils and macrophages. The inflammatory process after spinal cord transection is qualitatively similar to that observed outside the CNS. Inflammatory cells, which can release cytokines and growth factors, could play important roles in protective reactions of the tissue and glial scar formation.
Life‐spanning Behavioural and Adrenal Dysfunction Induced by Prenatal Hypoxia in the Rat is Prevented by the Calcium Antagonist Nimodipine
Authors: Nyakas Csaba , Buwalda Bauke , Markel Éva , Korte S. Mechiel , Luiten Paul G. M. 
Published: April 2006

AbstractThe long‐term behavioural effects of prenatal chronic anaemic hypoxia were investigated in young (5 months old), late adult (19 months) and aged Wistar rats (23–26 months). Sodium nitrite (2 g/l) offered in the drinking water during the second half of pregnancy served to evoke prenatal hypoxia. In parallel to nitrite treatment the Ca2+ channel blocker nimodipine (10 mg/kg) or vehicle alone was administered intragastrically once daily. Open‐field activity, intermale social behaviour, learning ability in a black–white discrimination paradigm and fear‐induced emotionality were assessed at different ages. Plasma corticosterone response to novelty stress was measured by blood sampling through chronic venous canulas at the age of 28 months. The nitrite‐exposed 5‐month‐old offspring started exploration in a novel open‐field with considerable delay. This delayed start‐latency was augmented in 19‐ and 23‐month‐old rats, pointing to exaggerated suppression of behavioural arousal. Nitrite‐induced hypoxia decreased the duration of social interactions during ageing. Aged rats exposed to nitrite were unable to learn a black–white discrimination but showed a normal generalized conditioned fear response (immobility) to the test situation as a whole. The conditioned fear‐induced vocalization was more frequent among hypoxic aged animals. The aged hypoxic rats displayed a prolonged plasma corticosterone stress response and had higher adrenal weight than their controls. The abnormal open‐field, social, learning and emotional behaviours, as well as the altered plasma corticosterone response, were prevented by prenatal nimodipine treatment.
Alterations in GAP‐43 and Synapsin Immunoreactivity Provide Evidence for Synaptic Reorganization in Adult Cat Dorsal Lateral Geniculate Nucleus following Retinal Lesions
Authors: Baekelandt V. , Arckens L. , Annaert W. , Eysel U. T. , Orban G. A. , Vandesande F. 
Published: April 2006

AbstractGrowth‐associated protein‐43 (GAP‐43) and synapsin were used as molecular markers for synaptic reorganization in the adult cat visual system following sensory deprivation. Small binocular retinal lesions (central 10°) were made with a xenon light photocoagulator in adult cats. One, 3, 5 and 7 weeks after induction of the lesion, the neuropil levels of synapsin and GAP‐43 in the dorsal lateral geniculate nucleus (dLGN) and area 17 were determined by immunocytochemistry. GAP‐43 displayed a moderately low basal level in the dLGN of normal adult cats. The parvocellular C layers and the interlaminar plexi were characterized by higher immunoreactivity for GAP‐43. Lesion‐induced alterations were observed in all layers: GAP‐43 immunoreactivity increased in the part of the dLGN representing central vision. This increase was maximal 3 weeks after the lesion. Under our experimental conditions, sensory deprivation did not significantly alter GAP‐43 levels in the visual cortex. The changes in synapsin immunoreactivity were also restricted to the dLGN. In this nucleus, synapsin immunoreactivity decreased in all layers in the part subserving central vision 1 week after lesion. By 3 weeks after lesion, the level of synapsin had already returned to normal. This study provides evidence for a capacity for structural remodelling in primary sensory brain areas such as the dLGN throughout adult life. The observed changes in GAP‐43 and synapsin in the dLGN suggest that synaptic reorganization is induced by retinal lesions. Normalization of synaptic density and activity could be important for the survival of the partially deafferented geniculate neurons.
The Topography of Tangential Inhibitory Connections in the Postnatally Developing and Mature Striate Cortex of the Cat
Authors: Albus K. , Wahle P. 
Published: April 2006

AbstractClustered intrinsic connections in the striate cortex of kittens originate from an unclustered, diffusely organized pattern prevailing during the first postnatal week. In order to study the participation of inhibitory neurons in this reorganization of the connections, we determined the topography of the inhibitory tangential connections in the striate cortex of cats ranging in age between 7 and 330 days by combining retrograde transport of fluorescent microspheres with GABA immunohistochemistry. After small intracortical injections of tracer, neurons containing either microspheres only (non‐GABAergic neurons) or GABA‐like immunoreactivity in addition to microspheres (GABAergic neurons) are labelled at various horizontal distances from the injection. At the end of the first postnatal week, both GABAergic and non‐GABAergic neurons are distributed in the horizontal plane in an unclustered fashion. During the second postnatal week, the tangential connections rearrange rapidly to form clusters. The tendency of the cells to form clusters is much weaker, however, in GABAergic than in non‐GABAergic neurons. In regions >500 μm distant from the centre of injection ∼90% of the non‐GABAergic neurons (range 87.5‐92.6%) but only 63% (range 57.1 – 72.3%) of the GABAergic neurons reside within the clusters formed by the non‐GABAergic neurons. These proportions do not change systematically with age. In the regions outside the non‐GABAergic clusters, GABAergic neurons appear to be evenly distributed and not to aggregate in clusters. From postnatal day 7 forward GABAergic neurons largely retain their overall distribution and density in the horizontal plane. When considering all cortical layers (including the superficial white matter) the lateral spread of the GABAergic neurons is more restricted than that of the non‐GABAergic neurons. Systematic changes in the lateral spread of inhibitory connections according to postnatal age were not observed. We conclude that, like the non‐GABAergic neurons, the GABAergic neurons have attained an adult‐like topography in the horizontal plane by about the end of the second postnatal week. From that time until adulthood they display much weaker clustering, a higher relative occurrence of short axon collaterals and a more restricted lateral distribution than do the excitatory neurons.
Developmental Changes in Spontaneous GABAA‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons
Authors: Hosokawa Y. , Sciancalepore M. , Stratta F. , Martina M. , Cherubini E. 
Published: April 2006

AbstractOngoing spontaneous postsynaptic potentials (SPSPs) were intracellularly recorded at 34‐36°C from hippocampal CA3 neurons in slices obtained from postnatal days (P) 0 – 6 and 7 – 31. SPSPs occurred randomly, and their frequency distribution was fitted by a single exponential function. They were little affected by kynurenic acid, but were reversibly blocked by bicuculline, implying that they were mediated by GABAA receptors. The mean amplitude was 4.53 ± 0.89 mV in control conditions and 4.07 ± 0.79 mV in kynurenic acid. In kynurenic acid (with CsCl‐filled microelectrodes), SPSPs reversed polarity at 2.4 ± 2 mV. When tetrodotoxin (1 μM) was added to kynurenic acid solution, GABAA‐mediated miniature postsynaptic potentials (MPSPs) were recorded. Under these conditions large events disappeared. The mean amplitude of MPSPs was 2.51 ± 0.43 mV. The mean frequency decreased from 2.96 ± 1.04 Hz in kynurenic acid to 0.4 ± 0.15 Hz in kynurenic acid plus tetrodotoxin. In contrast with P0 – P6, at P7 – P31 SPSPs were significantly affected by kynurenic acid. The mean amplitude of SPSPs shifted from 4.71 ± 0.82 mV in control conditions to 3.79 ± 0.76 mV in kynurenic acid. At this developmental stage, the reversal potential of GABAA‐mediated SPSPs shifted towards more negative values (‐23.7 ± 1.3 mV). Addition of tetrodotoxin to kynurenic acid solution abolished larger events and revealed GABAergic MPSPs. The mean amplitude of MPSPs was 2.72 ± 0.5 mV, a value very close to that observed at P0 – P6. Synaptic currents were recorded at 22 – 24°C from voltage‐clamped CA3 pyramidal neurons (at P6) using the tight‐seal whole‐cell recording technique. Cells were dialysed with CsCl solution and held at ‐70 mV. Spontaneous GABAA‐mediated miniature postsynaptic currents (MPSCs) were recorded in the presence of kynurenic acid and tetrodotoxin. The decay time of MPSCs was fitted with a single exponential and was 29 ± 3 ms. No correlation was found between the peak amplitude of individual events and their rise or decay time constant. The mean amplitude distribution of MPSCs was 12 ± 4.3 pA. In outside‐out patches from acutely dissociated CA3 hippocampal neurons, GABA (50 μM) activated single‐channel events of 24 and 35 pS conductance. Therefore one quantal current represents the simultaneous opening of five to seven GABAA receptor channels on the postsynaptic cell. These data show also that in the immediate postnatal period spontaneous glutamatergic potentials are poorly developed and start appearing towards the end of the first postnatal week concomitant with the shift of GABA from the depolarizing to the hyperpolarizing direction.
Transplanted Transgenically Marked Oligodendrocytes Survive, Migrate and Myelinate in the Normal Mouse Brain as They Do in the Shiverer Mouse Brain
Authors: Lachapelle F. , Duhamel‐Clerin E. , Gansmüller A. , Evercooren A. Baron‐Van , Villarroya H. , Gumpel M. 
Published: April 2006

AbstractThe dye Hoechst 33342 was combined with an immunodetectable transgene product (chloramphenicol acetyltransferase, CAT) expressed in differentiated oligodendrocytes to trace their fate after transplantation in the normal and the shiverer mouse brain. In the shiverer brain, the technique allowed us to visualize grafted cells inside myelin basic protein‐positive myelin patches. Most of these cells were CAT‐positive/Hoechst 33342‐negative, reinforcing our hypothesis that cell division probably follows migration of grafted oligodendrocytes. Correlation of their morphology and distribution with their location in the host CNS suggested a local effect on the cell division and morphogenesis of the grafted material. When compared with transplantation of fragments of normal newborn donor tissue into the newborn shiverer brain, no difference could be seen between the behaviour of normal and transgenic oligodendrocytes. In the normal brain, transgenic oligodendrocytes survived at least 150 days and successfully myelinated the host axons. The timing of differentiation of grafted cells was similar in both types of recipient brains. Migration occurred rostrally and caudally. Although migrating cells could be observed along the meninges and the blood vessels, migration occurred preferentially along white matter tracts. The extent of migration was influenced by the site of implantation, and grafted cells could be found up to 6 mm from the grafting point. No differences in the timing of differentiation or the pattern or extent of migration could thus be demonstrated when transgenic oligodendrocytes were transplanted in the normal or the shiverer brain. This validates our previous studies using the newborn shiverer mouse as recipient.
The Antennal Motor System of Crickets: Proctolin in Slow and Fast Motoneurons as Revealed by Double Labelling
Authors: Bartos Marlene , Allgäuer C. , Eckert M. , Honegger H. W. 
Published: April 2006

AbstractThis study decribes proctolin‐like immunoreactivity (PLI) of identified antennal motoneurons in the brain of adult crickets (Gryllus bimaculatus). The motoneurons were first backfilled with the fluorescent dye Lucifer Yellow and then immunohistochemically labelled with an antibody against proctolin. Altogether 14 of the 17 excitatory antennal motoneurons, including physiologically fast and slow types, showed PLI. The only common inhibitor consistently demonstrated a weak positive PLI. PLI was also present in the dendritic arborizations and varicosities of motor axons in the intrinsic antennal muscles. Densitometric measurements of motoneuron somata showed significant differences in the intensity of PLI in different types of antennal motoneurons, suggesting that antennal motoneurons produce different amounts of proctolin. Identical motoneuron somata display a large variance of PLI intensities in different brains. This observation may indicate up‐and down‐regulation of proctolin in individual crickets.
Human and Rat Primary C‐Fibre Afferents Store and Release Secretoneurin, a Novel Neuropeptide
Authors: Kirchmair Rudolf , Marksteiner Josef , Troger Josef , Mahata Sushil K. , Mahata Manjula , Donnerer Josef , Amann Rainer , Fischer‐Colbrie Reiner , Winkler Hans , Saria Alois 
Published: April 2006

AbstractSecretoneurin is a recently discovered neuropeptide derived from secretogranin II (SgII). Since this peptide could be detected in the dorsal horn of the spinal cord we studied whether it is localized in and released from primary afferent neurons. Secretoneurin was investigated with immunocytochemistry and radioimmunoassay in spinal cord, dorsal root ganglia and peripheral organs. SgII mRNA was determined in dorsal root ganglia. Normal rats and rats pre‐treated neonatally with capsaicin to destroy selectively polymodal nociceptive (C‐) fibres were used. Slices of dorsal spinal cord were perfused in vitro for release experiments. Immunocytochemistry showed a distinct distribution of secretoneurin‐immunoreactivity (IR) in the spinal cord and lower brainstem. A particularly high density of fibres was found in lamina I and outer lamina II of the caudal trigeminal nucleus and of the spinal cord. This distribution was qualitatively identical in rat and human post‐mortem tissue. Numerous small diameter and some large dorsal root ganglia neurons were found to contain SgII mRNA. Capsaicin treatment led to a marked depletion of secretoneurin‐IR in the substantia gelatinosa, but not in other immunopositive areas of the spinal cord and to a substantial loss of small (<25 μm) SgII‐mRNA‐containing dorsal root ganglia neurons. Radioimmunoassay revealed a significant decrease of secretoneurin‐IR in the dorsal spinal cord, the trachea, heart and urinary bladder of capsaicin‐treated rats. Perfusion of spinal cord slices with capsaicin as well as with 60 mM potassium led to a release of secretoneurin‐IR. In conclusion, secretoneurin is a neuropeptide which is stored in and released from capsaicin‐sensitive, primary afferent (C‐fibre) neurons. It may, therefore, be a novel peptidergic modulator of pain transmission or of C‐fibre mediated non‐nociceptive information.
Physiological Properties of Neuronal Nicotinic Receptors Reconstituted from the Vertebrate β2 Subunit and Drosophilaα Subunits
Authors: Bertrand D. , Ballivet M. , Gomez M. , Bertrand S. , Phannavong B. , Gundelfinger E. D. 
Published: April 2006

AbstractThree cDNAs (ALS, Dα2 and ARD) isolated from the nervous system of Drosophila and encoding putative nicotinic acetylcholine receptor subunits were expressed in Xenopus oocytes in order to study their functional properties. Functional receptors could not be reconstituted from any of these subunits taken singly or in twos and threes. In contrast, large evoked currents (in the μA range) were consistently observed upon agonist application on oocytes co‐injected with ALS or Dα2 in combination with the chick β2 structural subunit. The ALS/β2 and Dα2/β2 receptors are highly sensitive to acetylcholine and nicotine, and their physiological properties resemble those of native or reconstituted receptors from vertebrates. Although the physiological properties of ALS/β2 and Dα2/β2 receptors are quite similar, clear differences appear in their pharmacological profiles. The ALS/β2 receptor is highly sensitive to α‐bungarotoxin while the Dα2/β2 receptor is totally insensitive to this agent. These results demonstrate that the Drosophila ALS and Dα2 cDNAs encode neuronal nicotinic subunits responding to physiological concentrations of the agonists acetylcholine and nicotine.
Inhibition of c‐Fos Protein Expression in Rat Spinal Cord by Antisense Oligodeoxynucleotide Superfusion
Authors: Gillardon F. , Beck H. , Uhlmann E. , Herdegen T. , Sandkühler J. , Peyman A. , Zimmermann M. 
Published: April 2006

AbstractPeripheral noxious stimulation leads to a rapid and transient expression of c‐fos, c‐jun and other immediate‐early genes (IEGs) in the spinal cord. However, the role of IEG encoded transcription factors in plasticity of spinal neurons remains speculative. In the present study we have shown that superfusion of rat spinal cord with antisense oligodeoxynucleotides complementary to c‐fos mRNA suppresses heat‐induced c‐Fos protein expression without affecting other members of the Fos and Jun family, thus providing a technique to determine the function of IEGs in vivo.
Neuroanatomical Characterization of a New Mutant Rat with Dopamine Depletion in the Substantia Nigra
Authors: Clarke D. J. , Payne A. P. 
Published: April 2006

AbstractA new mutant rat strain with movement disorders has arisen spontaneously in a closed colony of Albino–Swiss rats at the Department of Anatomy, Glasgow University. The animals possess a progressive locomotor disorder which is first apparent at around post‐natal day 10. We here report that tyrosine hydroxylase immunocytochemistry demonstrates that these mutants have profound depletions in dopaminergic systems in the substantia nigra and corresponding areas of neostriatum.