bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of the mRNA for the β2 subunit of the voltage‐dependent sodium channel in rat CNS
Authors: Levy‐Mozziconacci Annie , Alcaraz Gisèle , Giraud Pierre , Boudier Jeanne‐Andrée , Caillol Ghislaine , Couraud François , Autillo‐Touati Amapola 
Published: March 2003

AbstractExpression of the voltage‐dependent sodium channel has been analysed in adult rat central nervous system by Northern blotting and in situ hybridization. Northern blots showed that all the territories studied express β2 transcripts, albeit with widely varying levels (with cerebellum >> hippocampus > brain > brainstem > spinal cord). In situ hybridization confirmed that in these structures, all the neuronal cell bodies contain β2 mRNA; expression was particularly high in the granule cells of the cerebellum, in both pyramidal cell layer and dentate gyrus in the hippocampus, and in spinal cord motor neurons. Northern blots also showed that RNA extracted from optic nerve and cultured cortical astrocytes contained β2 mRNA, while it was totally absent from sciatic nerve.In situ hybridization evidenced the presence of a numerous population of β2‐positive cells in cerebellum white matter, spinal cord white matter, and in corpus callosum, where frontal sections showed labelled cells arranged in the chain‐like or row pattern typical of interfascicular oligodendrocytes. Combination of antiglial fibrillary acid protein (GFAP) immunofluorescent histochemistry with detection of β2 mRNA evidenced that expression of the transcripts was indeed restricted to GFAP‐negative cells in white matter.
Potentiometric study of resting potential, contributing K+ channels and the onset of Na+ channel excitability in embryonic rat cortical cells
Authors: Maric Dragan , Maric Irina , Smith Susan V. , Serafini Ruggero , Hu Qian , Barker Jeffery L. 
Published: March 2003

AbstractResting membrane potential (RMP), K+ channel contribution to RMP and the development of excitability were investigated in the entire population of acutely dissociated embryonic (E) rat cortical cells over E11–22 using a voltage‐sensitive fluorescent indicator dye and flow cytometry. During the period of intense proliferation (E11–13), two cell subpopulations with distinct estimated RMPs were recorded: one polarized at ∼–70 mV and the other relatively less‐polarized at ∼–40 mV. Ca2+o was critical in sustaining the RMP of the majority of less‐polarized cells, while the well‐polarized cells were characterized by membrane potentials exhibiting a ∼Nernstian relationship between RMP and [K+]o. Analysis of these two subpopulations revealed that > 80% of less‐polarized cells were proliferative, while > 90% of well‐polarized cells were postmitotic. Throughout embryonic development, the disappearance of Ca2+o‐sensitive, less‐polarized cells correlated with the disappearance of the proliferating population, while the appearance of the K+o‐sensitive, well‐polarized population correlated with the appearance of terminally postmitotic neurons, immuno‐identified as BrdU–, tetanus toxin+ cells. Differentiating neurons were estimated to contain increased K+i relative to less‐polarized cells, coinciding with the developmental expression of Cs+/Ba2+‐sensitive and Ca2+‐dependent K+ channels. Both K+ channels contributed to the RMP of well‐polarized cells, which became more negative toward the end of neurogenesis. Depolarizing effects of veratridine, first observed at E11, progressively changed from Ca2+o‐dependent and tetrodotoxin‐insensitive to Na+o‐dependent and tetrodotoxin‐sensitive response by E18. The results reveal a dynamic development of RMP, contributing K+ channels and voltage‐dependent Na+ channels in the developing cortex as it transforms from proliferative to primarily differentiating tissue.
L‐DOPA‐induced dyskinesia in the rat is associated with striatal overexpression of prodynorphin‐ and glutamic acid decarboxylase mRNA
Authors: Cenci M. A. , Lee C. S. , Björklund A. 
Published: March 2003

AbstractRats sustaining unilateral near‐complete 6‐hydroxydopamine lesions of the mesostriatal dopamine pathway received daily injections of 3,4 dihydroxyphenyl‐l‐alanine (L‐DOPA, 8 mg/kg plus 15 mg/kg benserazide) for 3 weeks. During this period, about 50% of the rats gradually developed abnormal involuntary movements, lasting for 2–3 h following each L‐DOPA dose. Rats were killed 3 days after the last L‐DOPA injection, and sections through the striatum were processed for in situ hybridization histochemistry.  Within the L‐DOPA‐treated group, levels of preproenkephalin (PPE) mRNA, glutamic acid decarboxylase (GAD67) mRNA, and prodynorphin (PDyn) mRNA in the dopamine‐denervated caudate‐putamen, as well as GAD67 mRNA expression in the globus pallidus ipsilateral to the 6‐hydroxydopamine (6‐OHDA) lesion, were higher in dyskinetic than non‐dyskinetic animals, and positively correlated with the rats' dyskinesia scores. By contrast, striatal preprotachykinin mRNA expression and D2 receptor‐radioligand binding were not significantly associated with dyskinesia. Among all these markers, PDyn mRNA levels showed the most pronounced treatment‐dependence (three times higher in the L‐DOPA‐treated group than in saline‐injected lesion‐only controls), and the strongest correlation with the rats' dyskinesia scores (r2 = 0.82). However, a multiple regression equation including the three factors, GAD67 mRNA levels in the GP, GAD67 mRNA in the lateral CPu, and striatal PDyn mRNA, gave a better fit for dyskinesia scores than PDyn mRNA alone (r2 = 0.92).  The results show that L‐DOPA‐induced dyskinesia is associated with overexpression of PDyn and GAD67 mRNA in the striatal projection neurons, and GAD67 mRNA levels in the globus pallidus. Due to its treatment‐dependent expression, and strong correlation with the associated dyskinetic symptoms, striatal PDyn mRNA, in particular, may play a role in the mechanisms of behavioural sensitization brought about by the drug.
Influence of handedness on peripheral auditory asymmetry
Authors: Khalfa S. , Veuillet E. , Collet L. 
Published: March 2003

AbstractIt is well established that in humans many differences between right‐ and left‐handers, anatomical, physiological and functional, exist. Left‐ and mixed‐handedness is associated with greater bihemispheric representation of cognitive functions than in right‐handers. Several studies indicate a left–right asymmetry in the function of hearing pathways between cochlea and auditory cortex, and furthermore, that this asymmetry is associated with handedness. Our investigation focuses on the medial olivo‐cochlear system, which has been demonstrated to be more effective in the right than left ear in right‐handers. The aim of the study was to investigate this auditory efferent system asymmetry according to handedness, gender, eyedness, footedness and the presence of spontaneous otoacoustic emissions. The medial efferent system has been found to be more effective in the right than left ear in right‐handers, while functioning symmetrically in left‐handers. Furthermore, the olivo‐cochlear system, assumed to be involved in basic language processing, shows an asymmetrical pattern of functioning influenced by handedness as well as by hemispheric language representation. Reverse medial efferent system asymmetry was observed in left‐handers compared to that in right‐handers, on condition that only left‐handed males were considered, or that the left‐handers were also left‐eyed, or that spontaneous otoacoustic emissions were present in the left ear of the left‐handers, or when only left‐handers without mixed‐handers were considered.
Evidence for functional native NMDA receptors activated by glycine or d‐serine alone in the absence of glutamatergic coagonist
Authors: Paudice Paolo , Gemignani Anita , Raiteri Maurizio 
Published: March 2003

AbstractIn this study we have examined the effects of N‐methyl‐d‐aspartate (NMDA) receptor activation on the release of cholecystokinin and somatostatin from rat neocortical nerve endings. The release of cholecystokinin‐like immunoreactivity (CCK‐LI) and of somatostatin‐like immunoreactivity (SRIF‐LI) elicited by 12 mm K+ from superfused synaptosomes, but not the spontaneous release, was increased by NMDA in a concentration‐dependent manner. The effects of NMDA could be prevented by antagonists selective for the glutamate recognition site, the receptor channel and the glycine site of the NMDA receptor. In the absence of NMDA, glycine increased on its own and in a concentration‐dependent manner the depolarization‐evoked release of both CCK‐LI and SRIF‐LI. This effect of glycine was strychnine‐insensitive and could be mimicked by d‐serine, a stereoselective agonist at the NMDA receptor glycine site. Antagonists selective for the glycine site or for the NMDA receptor channel prevented the effects of glycine/d‐serine; these effects were, however, insensitive to blockade of the glutamate recognition site of the NMDA receptor, suggesting that glutamate released from synaptosomes or present as contaminant was not involved. The neuropeptide release elicited by d‐serine was strongly inhibited by ifenprodil (0.3 μm) and by Zn2+ ions (50 nm), selective ligands at the NR2B and NR2A subunits of NMDA receptors, respectively. It is concluded that nerve terminals of CCK‐ and SRIF‐releasing neurons possess non‐conventional NMDA receptors whose channels can be operated by glycine or d‐serine without apparent activation of the glutamatergic coagonist site. These receptors may display the triple subunit combination NR1/NR2A/NR2B.
Classical conditioning modifies cytochrome oxidase activity in the auditory system
Authors: Poremba Amy , Jones Dirk , Gonzalez‐Lima F. 
Published: March 2003

AbstractThe effects of excitatory classical conditioning on cytochrome oxidase activity in the central auditory system were investigated using quantitative histochemistry. Rats in the conditioned group were trained with consistent pairings of a compound conditional stimulus (a tone and a light) with a mild footshock, to elicit conditioned suppression of drinking. Rats in the pseudorandom group were exposed to pseudorandom presentations of the same tone, light and shock stimuli without consistent pairings. Untrained rats in a naive group did not receive presentations of the experimental stimuli. The findings demonstrated that auditory fear conditioning modifies the metabolic neuronal responses of the auditory system, supporting the hypothesis that sensory neurons are responsive to behavioural stimulus properties acquired by learning. There was a clear distinction between thalamocortical and lower divisions of the auditory system based on the differences in metabolic activity evoked by classical conditioning, which lead to an overt learned behavioural response versus pseudorandom stimulus presentations, which lead to behavioural habituation. Increases in cytochrome oxidase activity indicated that tone processing is enhanced during associative conditioning at upper auditory structures (medial geniculate nucleus and secondary auditory cortices). In contrast, metabolic activation of lower auditory structures (cochlear nuclei and inferior colliculus) in response to the pseudorandom presentation of the experimental stimuli suggest that these areas may be activated during habituation to tone stimuli. Together these findings show that mapping the metabolic activity of cytochrome oxidase with quantitative histochemistry can be successfully used to map regional long‐lasting effects of learning on brain systems.
Interaction of frontal and perirhinal cortices in visual object recognition memory in monkeys
Authors: Parker Amanda , Gaffan David 
Published: March 2003

AbstractMonkeys were trained preoperatively in visual object recognition memory. The task was delayed matching‐to‐sample with lists of trial‐unique randomly generated visual stimuli in an automated apparatus, and the stimuli were 2D visual objects made from randomly generated coloured shapes. We then examined the effect of either: (i) disconnecting the frontal cortex in one hemisphere from the perirhinal cortex in the contralateral hemisphere by crossed unilateral ablations; (ii) disconnecting the magnocellular portion of the mediodorsal (MDmc) thalamic nucleus in one hemisphere from the perirhinal cortex in the contralateral hemisphere; or (iii) bilaterally ablating first the amygdala, then adding fornix transection, then finally perirhinal cortex ablation. We found that both frontal/perirhinal and MDmc/perirhinal disconnection had a large effect on visual object recognition memory, whereas both amygdalectomy and the addition of fornix transection had only a mild effect. We conclude that the frontal lobe needs to interact with the perirhinal cortex within the same hemisphere for visual object recognition memory, but that routes through the amygdala and hippocampus are not of primary importance.
NT‐3, but not BDNF, prevents atrophy and death of axotomized spinal cord projection neurons
Authors: Bradbury Elizabeth J. , King Von R. , Simmons Lucinda J. , Priestley John V. , McMahon Stephen B. 
Published: March 2003

AbstractFollowing spinal cord injury, projection neurons are frequently axotomized and many of the cells subsequently die. One goal in spinal injury research is to preserve damaged neurons so that ultimately they are accessible to regeneration‐promoting strategies. Here we ask if neurotrophin treatment can prevent atrophy and death of axotomized sensory projection neurons. In adult rats, a hemisection was made in the thoracic spinal cord and axotomized neurons were retrogradely labelled with Fluoro‐Gold. Four distinct populations of cells were identified in the lumbar spinal cord, and both numbers and sizes of labelled cells were assessed at different time points postlesion. A progressive and significant degeneration was observed over time with severe atrophy apparent in all cell populations and significant cell loss evident by 4 weeks postlesion. This time point was used to assess neurotrophin effects. Hemisected rats were treated with either neurotrophin 3 (NT‐3) or brain‐derived neurotrophic factor (BDNF, 12 μg/day for each), or a vehicle solution, delivered continuously to the lesion site via an osmotic minipump. Treatment with NT‐3, but not BDNF, completely reversed cell atrophy in three of the four cell populations and also induced a significant increase in the number of surviving cells. In situ hybridization experiments showed trkB and trkC mRNA to be expressed in the majority of ascending spinal projection neurons, suggesting that these cells should be responsive to both BDNF and NT‐3. However, only NT‐3 treatment was neuroprotective, indicating that BDNF may not have reached the cell bodies of injured neurons. These results demonstrate that NT‐3 may be of benefit in preventing the secondary cell loss that occurs following spinal injury.
Excitatory convergence of Y and non‐Y channels onto single neurons in the anterior ectosylvian visual area of the cat
Authors: Wang C. , Dreher B. , Assaad N. , Ptito M. , Burke W. 
Published: March 2003

AbstractNumerous functional and hodological studies of the anterior ectosylvian visual area (AEV) of the cerebral cortex of the cat suggest that this area plays an important role in processing information about visual motion. In the present study, in cats with selective conduction block of Y fibres in one optic nerve, we have examined the extent of the excitatory convergence of Y (presumed ‘motion channel’) and non‐Y information channels on single neurons in AEV, as well as the contribution of the Y channel to the receptive field properties of AEV neurons. While in normal cats all neurons recorded from AEV were binocular, i.e. could be photically activated via either eye, in cats with selective conduction block of Y fibres in one optic nerve, a significant proportion (about 15%) of AEV cells could be photically activated only via the normal eye. In comparison to those in normal cats, the peak discharge rates of AEV neurons in the Y‐blocked cats were drastically reduced not only when photic stimuli were presented via the Y‐blocked eye, but also when they were presented via the normal eye. Selective block of Y input also resulted in a significant shift in velocity preferences towards the lower velocities. However, the direction selectivity indices of AEV neurons were not affected by selective Y block. Thus: (i) the responses of AEV neurons to a high velocity of motion are dependent on the integrity of the Y input; (ii) the ‘spontaneous’ (i.e. not photically evoked) discharges of Y retinal ganglion cells exert a facilitatory influence on the responses of AEV cells to photic stimuli; (iii) although the responses of AEV neurons are dominated by the Y inputs, AEV neurons also receive significant non‐Y excitatory inputs; and (iv) the strong direction selectivity revealed in most AEV neurons does not dependent on the integrity of Y input.
Long‐term depression of C‐fibre‐evoked spinal field potentials by stimulation of primary afferent Aδ‐fibres in the adult rat
Authors: Liu X. ‐G. , Morton C. R. , Azkue J. J. , Zimmermann M. , Sandkühler J. 
Published: March 2003

AbstractLong‐term potentiation (LTP) of spinal C‐fibre‐evoked field potentials can be induced by brief electrical stimulation of afferent C‐fibres, by natural noxious stimulation of skin or by acute nerve injury. Here, we report that in urethane anaesthetized, adult rats prolonged high frequency burst stimulation of the sciatic nerve at Aδ‐fibre strength produced long‐term depression (LTD) of C‐fibre‐evoked field potentials, and also depressed the increased amplitudes of C‐fibre‐evoked field potentials recorded after LTP had been established (depotentiation). Electrical stimulation of Aβ‐fibres failed to induce LTD or depotentiation. In spinalized rats, prolonged Aδ‐fibre conditioning stimulation induced LTP rather than LTD of C‐fibre‐evoked field potentials. Thus, tonic descending inhibition may determine the direction of plastic changes in C‐fibre‐mediated synaptic transmission. Spinal application of the N‐methyl‐d‐aspartic acid receptor antagonist D‐APV blocked induction of LTD in intact rats and LTP in spinalized rats. The presently described LTD and the depotentiation of established LTP of C‐fibre‐evoked field potentials in spinal dorsal horn may underlie some forms of prolonged analgesia induced by peripheral nerve stimulation procedures.
Characterization of neuronal migration disorders in neocortical structures: extracellular in vitro recordings
Authors: Luhmann Heiko J. , Raabe Kristin , Qü Meishu , Zilles Karl 
Published: March 2003

AbstractThe majority of patients showing neuronal migration disorders in cortical structures suffer from pharmaco‐resistant epilepsy. In order to study the molecular and cellular mechanisms underlying this pronounced hyperexcitability, we used an animal model of focal cortical dysplasia demonstrating structural malformations which resemble the human pathology of microgyria. Neocortical slices prepared from adult rats, which at the day of birth received a cortical freeze lesion, were analysed in vitro with an array of eight extracellular recording electrodes to investigate the pattern and pharmacology of propagating epileptiform activity in microgyric cortex. In cortical slices exhibiting neuronal migration disorders, orthodromic synaptic stimulation elicited late recurrent activity and early epileptiform responses that spread with 0.06 m/s over ≥ 3.5 mm across the cortex. Application of a N‐methyl‐d‐aspartate (NMDA) antagonist blocked the late recurrent activity, but not the propagation of the early epileptiform responses. The latter were blocked by an (±)‐α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA) antagonist, indicating that the spread of this activity was predominantly mediated by activation of AMPA receptors. A very similar response pattern could be observed in neocortical slices obtained from untreated age‐matched control rats, when the slice was partially disinhibited by bath‐application of 5 μm bicuculline methiodide. Stimulus‐evoked epileptiform signals recorded in disinhibited slices propagated with 0.08 m/s across the cortex and showed the same sensitivity to ionotropic glutamate antagonists as in dysplastic cortex. Our results indicate that widespread structural and/or functional modifications of the AMPA receptor and possibly also of the γ‐amino‐butyric acid type A receptor contribute to the pronounced hyperexcitability in dysplastic cortex.
Hippocampal neuronal activity and imprinting in the behaving domestic chick
Authors: Nicol A. U. , Brown M. W. , Horn G. 
Published: March 2003

AbstractThe hippocampus of the chick projects to the intermediate and medial part of the hyperstriatum ventrale (IMHV) which stores information acquired through the learning process of imprinting. We have investigated whether the response properties of hippocampal neurons are similar to those of IMHV neurons. Chicks were imprinted by exposure, one group (n = 7) to a rotating red box (RB), the other (n = 5) to a rotating blue cylinder (BC). Four chicks were untrained. The following day, when the chicks were ∼ 48 h old, neuronal activity was recorded in the left hippocampus. The proportion of neurons responding to the RB and that to the BC in untrained chicks were compared with the proportions in trained birds. (i) In RB‐trained chicks both the proportion responding to the RB and that to the BC were significantly increased. (ii) In BC‐trained chicks no significant effect on these proportions was found. Of the responsive neurons some were colour (red or blue) sensitive and others were shape (box or cylinder) sensitive; the proportions so responsive were not influenced by training condition. Certain neurons responded significantly differently when a stimulus was 0.5 m or 2 m from the chick (35%;d‐sensitive); very few neurons were equivalently responsive to a stimulus at both distances (3%;d‐invariant). These proportions were not significantly affected by training condition. Hippocampal responses are compared with those in the left IMHV. It is concluded that IMHV responses do not passively reflect those of hippocampal neurons.
The effects of anti‐nerve growth factor monoclonal antibodies on developing basal forebrain neurons are transient and reversible
Authors: Molnar Margherita , Tongiorgi Enrico , Avignone Elena , Gonfloni Stefania , Ruberti Francesca , Domenici Luciano , Cattaneo Antonino 
Published: March 2003

AbstractIn order to reassess the role of nerve growth factor (NGF) on rat basal forebrain cholinergic neurons (BFCNs) survival and/or phenotype maturation during the early postnatal life, we immunoneutralized NGF in vivo. Hybridoma cells producing the neutralizing anti‐NGF monoclonal antibody αD11 were implanted in the lateral ventricle of the rat at different postnatal ages (P2, P8 and P15) and the effects on the number and the soma size of cholinacetyltransferase (ChAT) positive neurons were analysed 1, 2 or 3 weeks after the injection. A marked decrease in the number and in the soma size of BFCNs was observed implanting hybridoma cells at P2 and performing the analysis 1 week later. These effects are reversed 3 weeks after the implant of hybridoma cells at P2. At this time point, the levels of αD11 antibodies in the brain parenchyma are still in a vast molar excess over endogenous NGF. No effects on BFCNs were observed implanting αD11 cells at P15 while LGN neurons showed marked shrinkage. Our results demonstrate that the reduction in the number of ChAT‐positive neurons during the first two postnatal weeks of anti‐NGF treatment is not due to cell death. We conclude that NGF is not a survival factor for BFCNs, and that the influence of NGF on BFCNs cell maturation during the first 2 postnatal weeks is transient and reversible. Our results on tyrosine kinase (Trk) coexpression, suggest that NGF may cooperate with other factors in the cholinergic phenotype differentiation and maintenance after the second postnatal week.