bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased lesion‐induced sprouting of corticospinal fibres in the myelin‐free rat spinal cord
Authors: Vanek Patrik , Thallmair Michaela , Schwab Martin E. , Kapfhammer Josef P. 
Published: March 2003

AbstractMyelin contains potent inhibitors of neurite growth which have been implicated in the failure of long‐distance regeneration of nerve fibres within the CNS. These myelin‐associated neurite growth inhibitors may also be involved in the stabilization of neural connections by suppressing sprouting and fibre growth. After lesions of the CNS in neonatal animals, extensive rearrangements of the remaining fibre systems have been observed. In the rat, this plasticity of neuronal connections is severely restricted following the first few weeks of postnatal life, coincident with the progression of myelination of the nervous system. A well‐studied example of postnatal plasticity is the sprouting of one corticospinal tract (CST) into the denervated half of the spinal cord after unilateral motor cortex or pyramidal lesions. In the hamster and rat, significant CST sprouting is restricted to the first 10 postnatal days. Here we show that very extensive sprouting of corticospinal fibres occurs after deafferentations as late as P21 if myelination is prevented by neonatal X‐irradiation in the rat lumbar spinal cord. Sprouted fibres from the intact CST cross the midline and develop large terminal arbors in the denervated spinal cord, suggesting the establishment of synaptic connections. Our results suggest that myelin and its associated neurite growth inhibitors play an important role in the termination of neurite growth permissive periods during postnatal CNS development. Corticospinal sprouting subsequent to lesions early in life, i.e. in the absence of myelin‐associated neurite growth inhibitors may explain the frequent occurrence of mirror movements in patients with hemiplegic cerebral palsy.
Attenuation of the seizure‐induced expression of BDNF mRNA in adult rat brain by an inhibitor of calcium/calmodulin‐dependent protein kinases
Authors: Murray Karl D. , Hayes Valerie Y. , Gall Christine M. , Isackson Paul J. 
Published: March 2003

AbstractWe have examined the potential involvement of calcium/calmodulin‐dependent protein kinases in the regulation of brain‐derived neurotrophic factor mRNA in vivo following kainic acid (kainate)‐induced seizure activity by in situ hybridization. KN‐62, a specific inhibitor of calcium/calmodulin‐dependent protein kinase type II and IV, blocked the characteristic induction of brain‐derived neurotrophic factor mRNA seen following seizure activity. This blockade was specific to calcium/calmodulin‐dependent protein kinase type II and IV as inhibitors of both protein kinase C and cAMP‐dependent protein kinase had no effect. Inhibition of brain‐derived neurotrophic factor mRNA increases varied between brain regions; an almost complete inhibition was seen throughout cortical regions, whereas only partial inhibitory effects were noted within hippocampus. A similar inhibition of increased c‐fos mRNA was observed throughout cortical, hippocampal and diencephalic regions. The two predominant brain‐derived neurotrophic factor transcripts induced by kainate, containing exons I or III, were differentially affected by KN‐62. The cortical induction of exon I was blocked by KN‐62, whereas exon III was not, providing additional evidence for the differential regulation of individual brain‐derived neurotrophic factor transcripts and demonstrating that inhibition of brain‐derived neurotrophic factor induction was not due to general blockade of seizure activity throughout the neocortex. These data implicate calcium/calmodulin‐dependent protein kinase type II or IV in the regulation of brain‐derived neurotrophic factor mRNA in vivo and suggest regionally specific mechanisms occur throughout the brain.
Origin and terminal distribution of the trigeminal projections to the inferior and superior colliculi in the lesser hedgehog tenrec
Authors: Künzle Heinz 
Published: March 2003

AbstractThe trigemino‐tectal projections were investigated with anterograde and retrograde tracing techniques in the Madagascan lesser hedgehog tenrec, Echinops telfairi. There were prominent contralateral projections to the inferior colliculus (CoI) and the superior colliculus (CoS), each showing its own characteristic pattern of terminations. While the projections to the CoI were confined consistently to a circumscribed region in its ventrolateral, external portion, the projections from particularly the rostral trigeminal subdivision to the CoS were distributed inhomogenously across almost the entire rostro‐caudal and mediolateral extents. Comparing these data with the spino‐tectal projections published previously, it demonstrates that the somatotopic organization of ascending tectal afferents is more distinct in the CoI than in the CoS.There were roughly twice as many trigeminal neurones projecting to the CoS than to the CoI. This difference might be due to the fact that the cells projecting to CoS were distributed extensively across the trigeminal nuclear complex (peak densities in the principal and interpolar subdivisions), while the neurones projecting to the CoI were largely confined to the interpolar and caudal trigeminal subdivisions. The latter cells were located adjacent to the spinal trigeminal tract; the neurones projecting to the CoS occupied preferentially the ventral trigeminal regions at rostral levels, while from the interpolar subdivision caudalward the labelled cells shifted dorsolaterally.In comparison to other mammals the trigeminal projection to the tenrec’s CoI is unique. There is evidence for such a projection in other species too, but it is poorly documented, presumably due to technical reasons.
Preprodynorphin mRNA‐expressing neurones in the rat parabrachial nucleus: subnuclear localization, hypothalamic projections and colocalization with noxious‐evoked fos‐like immunoreactivity
Authors: Hermanson Ola , Telkov Miroslav , Geijer Thomas , Hallbeck Martin , Blomqvist Anders 
Published: March 2003

AbstractThe dorsal lateral subnucleus of the rat pontine parabrachial nucleus is a major target for ascending nociceptive information from the spinal cord. With in situ hybridization histochemistry, using a radiolabelled cRNA probe, we demonstrate that neurones in and near the dorsal lateral subnucleus express preprodynorphin mRNA. The cRNA probe was constructed from a PCR product amplified from rat genomic DNA. Sequencing of the PCR product revealed that it corresponded to the sequence 466–1101 of the rat preprodynorphin gene exon 4.Tract tracing experiments, using injection of cholera toxin subunit B into the hypothalamic median preoptic nucleus, showed a retrograde labelling pattern of neurones in the parabrachial nucleus that was almost identical to that of the preprodynorphin mRNA expressing neurones. Double‐labelling, combining immunohistochemical detection of tracer and in situ hybridization, revealed that the retrogradely labelled neurones expressed preprodynorphin mRNA. A similar double‐labelling, combining in situ hybridization with immunohistochemical detection of noxious‐evoked fos following formalin injection into one hindpaw of awake animals, showed that almost all fos‐immunoreactive neurones in the dorsal lateral parabrachial subnucleus also expressed preprodynorphin mRNA. Quantitative analysis suggested that the evoked fos immunoreactivity was accompanied by an increased preprodynorphin mRNA expression.The findings provide evidence that neurones in the dorsal lateral subnucleus produce dynorphin and project to the median preoptic nucleus, and that noxious stimulation in awake animals synaptically activates the dynorphinergic neurones in this subnucleus. These observations are consistent with the idea of a functional and chemical heterogeneity among different parabrachial subnuclei that serves to produce specific homeostatic responses to stimuli that changes the physiological status of the organism, including tissue damage.
Dominant GABAA receptor/Cl– channel kinetics correlate with the relative expressions of α2, α3, α5 and β3 subunits in embryonic rat neurones
Authors: Serafini  , Maric  , Maric  , Ma  , Fritschy  , Zhang  , Barker  
Published: March 2003

AbstractThe embryonic appearance of GABAergic cells and signals in the rat nervous system coincides with the appearance of transcripts encoding some but not all of the subunits forming GABAA receptor/Cl– channels. Quantitative in situ hybridization studies reveal higher variabilities in α2 and α3 subunit transcripts relative to others examined (α5, β2, β3 and γ2) in six spinal and supraspinal regions. Immunocytochemistry of cells dissociated from the embryonic CNS shows that α2 and α3 subunits are detectable in differentiating neurones. FACS analyses of dissociated cells immunostained with α2‐ or α3‐ antibodies reveal immunopositive subpopulations of variable size in each region. Whole‐cell recordings of acutely adherent neurones show that GABA activates Cl– currents whose fluctuations characteristically vary depending on a neurone’s region of origin. Spectral analyses indicate a predominance of the low frequency (< 5 Hz) components, which vary regionally. Regression analyses reveal that (i) channel properties correlate with subunit transcript levels and (ii) dominant channel kinetics correlate with α2 and α3 subunit transcripts indexed as a ratio and with coexpressions of α5 and β3. The correlations strongly suggest that α3 subunits in embryonic neurones are expressed in native receptor/channel complexes with slower kinetics than those containing α2 without α3 subunits. Thus, GABAA receptor/Cl– channels in these embryonic neurones may be encoded by the six transcripts (α2, α3, α5, and β2, β3, and γ2) with proportions of α2, α3, α5, and β3 subunits critical in determining their dominant kinetics.
Distribution of GABA receptor ρ subunit transcripts in the rat brain
Authors: Wegelius Katri , Pasternack Michael , Hiltunen Jukka O. , Rivera Claudio , Kaila Kai , Saarma Mart , Reeben Mati 
Published: March 2003

AbstractThe γ‐aminobutyric acid (GABA) receptor ρ subunits recently cloned from rat and human retina are thought to form GABA receptor channels belonging to a pharmacologically distinct receptor class, termed GABAC. In this work we have examined the distribution of ρ1, ρ2 and ρ3 subunits, and found expression of all three transcripts in several regions of the rat nervous system. In situ hybridization revealed expression of ρ2 in the adult rat retina and some other parts of the visual pathways. A high local ρ2 expression was seen in the superficial grey layer of the superior colliculus, and in the dorsal lateral geniculate nucleus. Expression was also detected in the 6th layer of visual cortex and in the CA1 pyramidal cell layer of hippocampus. With reverse transcriptase–polymerase chain reaction, expression of ρ1 was mainly seen in the adult rat retina and dorsal root ganglia, as well as, at a significantly lower level, in the superior colliculus, hippocampus, brain stem, thalamus, postnatal day 8 (P8) superior colliculus and P8 hippocampus. Expression pattern of ρ3 mRNA was clearly different from that of ρ1 and ρ2, being strongest in the hippocampus, and significantly lower in the retina, dorsal root ganglia and cortex. No ρ3 expression was observed in adult or P8 superior colliculus or in P8 hippocampus.The present results clearly demonstrate that expression of GABA receptor ρ subunits is not restricted to the retina, but significant expression can also be detected in many other brain regions, especially in those belonging to the visual pathways. The expression pattern of the ρ subunits may be helpful in solving the functional significance of the receptors formed from these subunits.
The rhythmicity of cells of the medial septum/diagonal band of Broca in the awake freely moving rat: relationships with behaviour and hippocampal theta
Authors: King C. , Recce M. , O’Keefe J. 
Published: March 2003

AbstractChronic extracellular recordings were obtained from cells of the medial septum and diagonal band of Broca in rats performing a simple behavioural task. The cells were found to display a variety of bursting patterns phase‐locked to hippocampal theta rhythm to a greater or lesser degree. Among phase‐locked cells, no systematic distribution in preferential phase could be found, and these cells were shown to maintain their preferential phase for extended periods. Cells were classified into those which showed signs of a broadening of the repolarization phase of their action potential (‘inflected’: putative cholinergic) and those without (‘non‐inflected’: putative GABAergic). Non‐inflected cells tended to fire rhythmic bursts while inflected cells mostly fired in an irregular fashion, although still significantly phase‐locked to hippocampal theta. In neither population did the phase‐locked cells show any coherent distribution of their preferential phase. Sixty‐five per cent of the rhythmically bursting cells showed a significant correlation between the interburst frequency and the animal’s running speed. Five cells displayed rhythmic activity only when the rat ran in a specific direction. These results have implications for models of septohippocampal function and the effects of variable septal rhythmicity on the production of hippocampal theta rhythm.
Footshock stress but not contextual fear conditioning induces long‐term enhancement of auditory‐evoked potentials in the basolateral amygdala of the freely behaving rat
Authors: Garcia René , Paquereau Joël , Vouimba Rose Marie , Jaffard Robert 
Published: March 2003

AbstractIn this study, rats were bilaterally implanted with electrodes in the amygdala for chronic recording. Auditory click stimulation evoked in the basolateral nucleus a field potential characterized by three positive components: P1, P2 and P3 (peak latencies around: 10, 20 and 30 ms, respectively) which were each followed by three negative components: N1, N2 and N3 (peak latencies around: 13, 30 and 50 ms, respectively). Animals were divided into three groups (context‐same, context‐different and control). Following footshock administration, animals were either re‐exposed to the same conditioning chamber (context‐same group) or placed in a different context (context‐different group) for electrophysiological and behavioural (evaluation of freezing response) recordings. The two early positive‐negative complexes (P1‐N1 and P2‐N2) increased in amplitude from 2 min to 24 h following footshock in both context‐same and context‐different groups. No significant difference was observed between these two groups. The demonstration of significantly larger freezing responses in context‐same subjects on exposure to the aversive conditioned environment indicated that this similarity of effects was not due to lack of conditioning of context under the experimental conditions chosen. We conclude that footshock stress produces general long‐lasting changes in amygdala auditory field potentials that are not significantly affected by contextual fear conditioning.
Neuronal expression of inducible nitric oxide synthase after oxygen and glucose deprivation in rat forebrain slices
Authors: Moro M.A. , De Alba J. , Leza J.C. , Lorenzo P. , Fernández A.P. , Bentura M.L. , Boscá L. , Rodrigo J. , Lizasoain I. 
Published: March 2003

AbstractNitric oxide (NO) overproduction has been postulated to contribute significantly to ischaemia‐reperfusion neurotoxicity. Inducible or type II NO synthase (iNOS) synthesizes NO in large quantities for long periods of time. Therefore we investigated the expression and localization of iNOS after oxygen and glucose deprivation in rat forebrain slices. In this experimental model, calcium‐independent NOS activity reached a maximum 180 min after the end of a 20 min oxygen–glucose deprivation period. During the same period of time, the calcium‐independent activity was absent in control forebrain slices. To test whether this calcium‐independent NOS activity was due to the expression of iNOS, the effects of the addition of dexamethasone, cycloheximide and pyrrolidine dithiocarbamate were determined. All of them inhibited the induction of the calcium‐independent NOS activity measured in the rat forebrain slices after oxygen and glucose deprivation. Furthermore, oxygen and glucose deprivation caused the expression of the gene encoding iNOS in rat forebrain slices, as assessed by the detection of iNOS message and protein in these samples. A sixfold increase in the iNOS mRNA levels was observed at 180 min and the time‐course of the expression of iNOS mRNA was in agreement with the temporal profile of iNOS enzymatic activity. Immunohistochemistry analysis revealed that iNOS was highly expressed in neurones, astrocytes and microglial cells. These results demonstrate for the first time that iNOS is expressed in neurones after oxygen and glucose deprivation, and that this expression occurs in short periods of time. These findings suggest that NO can play an important pathogenic role in the tissue damage that occurs after cerebral ischaemia.
Demarcation of prosencephalic regions by CD15‐positive radial glia
Authors: Mai J.K. , Andressen C. , Ashwell K.W.S. 
Published: March 2003

AbstractA subpopulation of radial glial cells has been identified in the mouse prosencephalon during the second half of embryonic development. This subpopulation, specified by the putative cell adhesion molecule CD15 (Lex, FAL), is arranged in a segmented pattern within the telencephalon and diencephalon. Glial processes, spanning the prosencephalic wall, first appear at E10.5 and remain clearly visible until E19, when staining of discrete nuclei begins to appear. Registration of the correspondence between ventricular and pial surfaces, however, is still possible due to the persistence of individual CD15‐positive fibres. These can be traced even when the initial simple linear (radial) orientation between ventricular and pial surfaces becomes complicated and distorted. After birth, CD15 immunoreactivity is distributed in a mosaic pattern in the forebrain. Because radial glial cells provide a scaffolding system for postmitotic neurones, the pattern of CD15‐positive fibres in the embryonic prosencephalon may also demarcate future discrete regions of the postnatal brain.
Modulation of bradykinin‐induced mechanical hyperalgesia in the rat by activity in abdominal vagal afferents
Authors: Khasar Sachia G. , Miao Frederick J. ‐P. , Jänig Wilfrid , Levine Jon D. 
Published: March 2003

AbstractBradykinin‐induced plasma extravasation and mechanical hyperalgesia are sympathetic‐dependent components of inflammation. Noxious stimulation has been found to inhibit bradykinin‐induced plasma extravasation by activating the hypothalamo‐pituitary‐adrenal axis. The sensitivity of this nociceptive‐neuroendocrine feedback control of inflammation is modulated by activity in subdiaphragmatic vagal afferents. In the present study, we tested the hypothesis that activity in the subdiaphragmatic vagus also modifies bradykinin‐induced mechanical hyperalgesia in the rat, using the Randall–Selitto method.Following subdiaphragmatic vagotomy, the baseline paw‐withdrawal threshold to mechanical stimulation decreased and bradykinin‐induced mechanical hyperalgesia was enhanced. Mechanical hyperalgesia produced by prostaglandin E2, a direct‐acting hyperalgesic agent, was not significantly affected by vagotomy. The effect of subdiaphragmatic vagotomy on bradykinin‐induced hyperalgesia, but not on baseline paw‐withdrawal threshold, was mimicked by coeliac branch vagotomy.Indomethacin blocked the hyperalgesia in normal rats, but not in vagotomized rats, suggesting that bradykinin‐induced hyperalgesia in normal rats is mediated by prostaglandins, whose role was unexpectedly diminished after vagotomy.Bradykinin‐induced hyperalgesia in normal rats was abolished by lumbar sympathectomy but not by sympathetic decentralization (cutting the preganglionic axons). In rats that were both vagotomized and sympathectomized, hyperalgesia induced by low‐dose bradykinin was no longer present.These results demonstrate that vagotomy induces a decrease in baseline mechanical paw‐withdrawal threshold and an enhancement of bradykinin‐induced mechanical hyperalgesia and suggest that these phenomena are generated by actions in peripheral tissues.
Enhanced neurotransmitter release is associated with reduction of neuronal branching in a Drosophila mutant overexpressing frequenin
Authors: Angaut‐Petit D. , Toth P. , Rogero O. , Faille L. , Tejedor F.J. , Ferrús A. 
Published: March 2003

AbstractFrequenin is a Drosophila Ca2+ binding protein whose overexpression causes a chronic facilitation of transmitter release at the larval neuromuscular junction and multiple firing of action potentials. These functional abnormalities are similar to those found in other hyperexcitable mutants (Shaker, ether‐a‐gogo, Hyperkinetic) which, in turn, exhibit increased branching at the motor nerve endings. We report here that mutants which overexpress frequenin have motor nerve terminals with reduced number and length of branches as well as number of synaptic boutons. Similar defects are observed in transgenic flies which have additional copies of the frequenin gene indicating that the phenotype can be adscribed to the overexpression of the protein. The ultrastructure of boutons, however, appears indistinguishable from wild type. In addition, we show here that frequenin overexpression leads also to a down regulation of Shaker proteins expression. The contrast between the observations in frequenin and the other hyperexcitable mutants indicates that nerve terminal morphology and enhanced transmitter release do not have a direct causal relationship.
Suppression of kindling epileptogenesis in rats by intrahippocampal cholinergic grafts
Authors: Ferencz I. , Kokaia M. , Elmér E. , Keep M. , Kokaia Z. , Lindvall O. 
Published: March 2003

AbstractSelective immunolesioning of the basal forebrain cholinergic system by 192 IgG‐saporin, which leads to a dramatic loss of the cholinergic innervation in cortical and hippocampal regions, facilitates the development of hippocampal kindling in rats. The aim of the present study was to explore whether grafted cholinergic neurones are able to reverse the lesion‐induced increase of seizure susceptibility. Intraventricular 192 IgG‐saporin was administered to rats which 3 weeks later were implanted with rat embryonic, acetylcholine‐rich septal‐diagonal band tissue (‘cholinergic grafts’) or cortical tissue/vehicle (‘sham grafts’) bilaterally into the hippocampal formation. After 3 months, the grafted animals as well as non‐lesioned control rats were subjected to daily hippocampal kindling stimulations. In the animals with cholinergic grafts, which had reinnervated the hippocampus and dentate gyrus bilaterally, there was a marked suppression of the development of seizures as compared with the hyperexcitable, sham‐grafted rats. This effect was significantly correlated to the density of the graft‐derived cholinergic innervation of the host hippocampal formation. The kindling rate in the rats with cholinergic grafts was similar to that in non‐lesioned controls. These results provide further evidence that the intrinsic basal forebrain cholinergic system dampens kindling epileptogenesis and demonstrate that this function can be exerted also by grafted cholinergic neurones.