bluuebunny/crossref_metadata_2025_split huggingface dataset:
Morphine Selectively Depresses the Slowest, NMDA‐independent Component of C‐fibre‐evoked Synaptic Activity in the Rat Spinal Cord In Vitro
Authors: Sivilotti L G. , Gerber G. , Rawat B. , Woolf C. J. 
Published: April 2006

AbstractThe effects of morphine on the depolarizing synaptic responses produced in motoneurons by electrical stimulation of primary sensory neurones have been recorded in hemisected spinal cord preparations (8‐ to 12‐day‐old rat pups). Morphine at concentrations of 0.1‐20 μM reduced a slow, long‐lasting (latency greater than 1 s, duration up to 10 s) component of the ventral root potential (VRP) evoked by C‐fibre strength stimulation of the dorsal root. At 2μM the reduction in area of this slow synaptic potential was 71.7 ± 0.9% of control values (n= 15). The earliest components of the C‐fibre strength VRP (the first 100 ms) and the responses to Aβ strength stimuli were unaffected by the opioid even at 10‐20μM. The intermediate, NMDA receptor antagonist (D‐AP5, 40μM)‐sensitive component (which lasts 100‐1000 ms) was reduced by 34 ± 2.2% of control (n= 15), which was significantly less than the reduction of the later NMDA‐independent component (P < 0.001). Morphine (0.1‐20 μM) also depressed the cumulative depolarization generated by the temporal summation of synaptic responses evoked by brief trains of C‐fibre strength stimuli (1 or 10 Hz). A significantly greater reduction at the lower frequency of stimulation (56.3 ± 2.0%) than at the higher (20.3 ± 1.69%, n = 10, measured at 2 μM morphine) was found (P < 0.005). The effects of morphine were reversible upon wash‐out or superfusion with the opioid receptor antagonist naloxone (2 μM). The depression in the C‐fibre‐evoked VRPs produced by the NMDA receptor antagonist D‐AP5 (10‐40 μM) was different from that produced by morphine, as D‐AP5 only reduced a shorter latency component of the VRP (100 ms‐1 s) and was equally effective in decreasing the cumulative depolarizations evoked by 1 and 10 Hz trains. The preferential effect of morphine on the longest latency and longest lasting components of the high‐threshold VRP are discussed in relation to its possible site and mechanism of analgesic action.
Corticothalamic Projections from the Cortical Barrel Field to the Somatosensory Thalamus in Rats: A Single‐fibre Study Using Biocytin as an Anterograde Tracer
Authors: Bourassa Jacques , Pinault Didier , Deschênes Martin 
Published: April 2006

AbstractThis study investigated the pattern of axonal projections of single corticothalamic neurons from the cortical barrel field representing the vibrissae in the rat. Microiontophoretic injections of biocytin were performed in cortical layers V and VI to label small pools of corticothalamic cells and their intrathalamic axonal projections. After a survival period of 48 h, the animals were perfused and the tissue was processed for biocytin histochemistry. On the basis of the intrathalamic distribution of axonal fields and of the types of terminations found in the thalamus, four types of corticothalamic projections were identified, (i) Cells of the upper part of layer VI projected exclusively to the ventral posteromedial (VPm) nucleus, where they arborized in long rostrocaudally oriented bands or‘rods’, (ii) All cells of the lower part of layer VI projected to the medial part of the thalamic posterior group (Pom) but the vast majority of them also collateralized in VPm where they participated in the formation of rods, (iii) A minority of corticothalamic cells in the lower portion of layer VI, possibly located under the interbarrel spaces (septae), arborized exclusively in Pom. (iv) The corticothalamic projection of layer V cells originated from collaterals of corticofugal cells whose main axons ran caudally towards the brainstem. These collaterals arborized exclusively in Pom or in the central lateral nucleus. All corticothalamic cells from layer VI displayed the same type of axonal network, made of long branches decorated by terminal buttons emitted en passant at the tip of fine stalks. Corticothalamic fibres arising from layer V pyramids, however, remained smooth as they ran across the lateral thalamus and they generated in Pom one or two clusters of large boutons. All corticothalamic axons derived from layer VI cells, but not those derived from layer V cells, gave off collaterals as they traversed the thalamic reticular complex. These observations are discussed in the light of previous studies bearing on the topological organization and function of corticothalamic projections to VPm and Pom in rats. The possibility that a similar cellular specificity and a similar organizational plan may characterize corticothalamic relationships in other sensory systems is also considered.
Effect of SR33557 on Intramembrane Charge Movement in Normal and‘Muscular Dysgenesis’Mouse Skeletal Muscle Cells
Authors: Strube Caroline , Shimahara Takeshi , Bournaud Roland 
Published: April 2006

AbstractIt has been reported that the indolizinsulphone SR33557, which binds to a site on the α1 subunit of the dihydropyridine receptor, blocks both L‐type calcium channel activity and contraction in skeletal muscle. Moreover, we know that charge movement plays a key role in the mechanism of excitation‐contraction coupling and in controlling the opening of L‐type calcium channels. We demonstrate here that SR33557 reduces intramembrane charge movement in skeletal muscle from normal mice with an IC50 of ‐10 nM. The drug does not completely inhibit charge movement since ‐20% of total charge movement persists even in the presence of 30 μM SR33557. However, the SR33557‐sensitive charge component is more important than the dihydropyridine‐sensitive one. Surprisingly, SR33557 also reduces intramembrane charge movement in dysgenic myotubes which are characterized by a very strong reduction of the number of dihydropyridine binding sites. In these muscles, 10 μM SR33557 reduces ‐40% of total charge movement. These observations suggest the presence of a new component of charge movement which is sensitive to SR33557 but insensitive to nifedipine. This component is also present in dysgenic myotubes, and it could be produced by the lower molecular weight α1, subunit described by Malouf, N. N., McMahon, D. K., Hainsworth, C. N. and Kay, B. K. (1992) (Neuron, 8, 899–906).
Receptors and Second Messengers Involved in Long‐term Depression in Rat Cerebellar Slices In Vitro: a Reappraisal
Authors: Hémart Nathalie , Daniel Hervé , Jaillard Danielle , Crépel Francis 
Published: April 2006

AbstractIn patch‐clamped Purkinje cells (PCs), bath application of the ionotropic glutamate receptor antagonist, 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX) prevents induction of long‐term depression (LTD) of parallel fibre (PF)‐mediated EPSPs by a pairing protocol between Ca2+ spike firing and PF stimulation whereas bath application of (RS)‐α‐methyl‐4‐carboxyphenylglycine (MCPG), a metabotropic glutamate (mGLU) receptor antagonist, does not. On the other hand, LTD can be also induced by pairing direct depolarization of PCs with activation of mGLU receptors by 1 S,3R‐aminocyclopentyl‐dicarboxylate (1S, 3R‐ACPD), even in the presence of CNQX. In this case, LTD induction is not consistently blocked by bath application of the nitric oxide synthase inhibitor, NG‐methyl‐l‐arginine (l‐NMMA), whereas it is strongly blocked when the protein kinase C inhibitor peptide 19‐36 is dialysed into PCs. These results are at variance with LTD induced by a pairing protocol between Ca2+ spikes and PF‐mediated EPSPs which depends to the same extent on both cascades. Finally, thapsigargin, which depletes most intracellular Ca2+ pools, does not block induction of LTD by a pairing protocol between Ca2+ spikes and PF‐mediated EPSPs whereas it prevents the induction of LTD depending on strong mGLU receptor activation.
Synchronous High‐frequency Oscillations in Cat Area 18
Authors: Brosch Michael , Bauer Roman , Eckhorn Reinhard 
Published: April 2006

AbstractThe present study extends knowledge of the basic properties of correlated oscillatory activity patterns in the visual cortex of anaesthetized cats. Recordings with multiple electrodes were performed in area 18 and the correlations of multi‐unit activity in the frequency range 35‐80 Hz were determined using the coherence function. Statistical analysis revealed that the multi‐unit correlations depended on the cortical distance between the recording sites, the orientation selectivity of the neurons and their cortical layer. On average, correlations dropped to chance level within several millimetres and were higher in lower than in upper cortical layers. Similar results were found by analysing the correlations of oscillatory patterns in local field potentials recorded from the same electrodes. Correlations of neurons with similar orientation preferences were higher than those of neurons with different orientation preferences. Comparison to a matched sample from area 17 showed that the correlations in areas 18 and 17 depended on similar properties of the neurons. The dependences of correlated oscillations resembled the known pattern and specificity of intra‐areal fibre connections, suggesting that the correlations were intracortically established. Since correlations were specifically and not randomly related to the response properties of cortical neurons and were prominent in a visual area other than area 17, the findings suggest that correlated oscillatory activity provides a potential neural code supporting sensory information processing.
Developmentally Regulated Expression of mRNA for Neurotrophin High‐Affinity (trk) Receptors within Chick Trigeminal Sensory Neurons
Authors: Williams R. , Bäckström A. , Kullander K. , Hallböök F. , Ebendal T. 
Published: April 2006

AbstractTo investigate the distribution of neurons within the developing trigeminal sensory system which express mRNA for each of the three known high‐affinity neurotrophin receptors (trk, trkB and trkC), we have performed in situ hybridization histochemistry on serial sections through the trigeminal ganglion and trigeminal mesencephalic nucleus at various ages of development using specific antisense oligonucleotide probes. We show that trkC mRNA is first expressed in the chicken embryo at stage 13, in presumptive neurons prior to the formation of the ganglion, that trkB mRNA labelling is initially observed within peripheral neurons slightly later, at stage 19, and that trk mRNA expression is not detectable until around embryonic day 3.5 (stage 21/22). The neurons which exhibit mRNA labelling for each of the high‐affinity receptors occupy discrete regions within the ganglion, indicating that the ganglion comprises distinct neuronal subpopulations, each of which has a different capacity to respond to the different neurotrophins. Neurons which express trk mRNA are confined to the proximal region of the ganglion, whereas those which express trkB mRNA and trkC mRNA are located in two distinct regions within the distal aspect and also within the trigeminal mesencephalic nucleus. From the estimation of the number of neurons which exhibit labelling between embryonic days 9 and 18, we determined that the expression of mRNA for the high‐affinity receptors changes during embryonic development of the ganglion. This is consistent with the observed differences in the response to neurotrophins in vitro.
Evidence for the Existence of a Functional Polysynaptic Pathway From Trigeminal Afferents to Lumbar Motoneurons in the Neonatal Rat
Authors: Vinay Laurent , Cazalets Jean‐René , Clarac François 
Published: April 2006

AbstractStimulation of trigeminal afferents has been reported to have powerful effects on the spinal cord in adult animals of several species. In the present study, the pathway transmitting these influences was investigated in the neonatal rat. Experiments were performed on in vitro brainstem/spinal cord preparations. Stimulation of the trigeminal nerve evoked bilateral polysynaptic discharges in lumbar ventral roots. Intracellular recordings from lumbar motoneurons showed mainly excitatory responses, although a few inhibitory responses were also observed. Experiments with perfusion of different parts of the preparation with general or selective synaptic blockers revealed a synaptic relay under GABAergic control in the brainstem, and at least one synapse in the cervical and in the thoracic spinal cord. The involvement of lumbar interneurons was established by perfusing the lumbar enlargement with saline containing either a high concentration of divalent ions or mephenesin in order to reduce transmission along polysynaptic pathways. The contribution of excitatory amino acid transmission was evaluated and was found to evoke mixed receptor responses. The course of the pathway was traced by using different lesions to the brainstem and spinal cord. The pathway was found to be ipsilateral in the brainstem and to become bilateral in the spinal cord. The results of the present study demonstrate that polysynaptic sensorimotor pathways are present at birth. The results are discussed in relation to the pontomedullary locomotor strip, which has been thought to share many features with the trigeminal system.
Mitosis of Schwann Cells and Demyelination are Induced by the Amyloid Precursor Protein and Other Protease Inhibitors in the Rat Sciatic Nerve
Authors: Alvarez Jaime , Moreno Ricardo D. , Inestrosa Nibaldo C. 
Published: April 2006

AbstractWe studied the cytological alterations produced in the rat sciatic nerve by the amyloid precursor protein (APP) containing the Kunitz insert (APP K+) and other protease inhibitors. Conditioning of nerve segments with APP K+, aprotinin or leupeptin for 5 days or more resulted in mitosis of Schwann cells, demyelination of fibres, and a <10‐fold increase in Schwann cells, associated with demyelinated fibres. Altered fibres nevertheless involved a small part of the population. Nerve segments proximal and distal to the conditioned region showed almost no alteration. Conditioning with saline, heated APP K+, or APP without the Kunitz insert was not effective. We conclude that APP K+ and other protease inhibitors induce Schwann cells to enter the cell cycle, and once committed to proliferate they resorb their myelin. These functional properties of APP may be relevant to the pathogenesis of Alzheimer's disease.
Functional Neuroanatomy of the Human Visual Fixation System
Authors: Petit Laurent , Tzourio Nathalie , Orssaud Christophe , Pietrzyk Uwe , Berthoz Alain , Mazoyer Bernard 
Published: April 2006

AbstractThe regional cerebral blood flow correlates of the active fixation of an imagined target were studied in five healthy humans using the positron emission tomography activation paradigm. The fixation task was contrasted to a passive control condition, both tasks being performed in total darkness. Blood flow increases were observed in the frontal eye fields and supplementary eye fields and in the median cingulate gyrus. We suggest that the network of these activated regions mediates the interactions between ocular fixation, eye movements and directed visual attention.
Cholecystokinin Excites Neostriatal Neurons in Rats via CCKA or CCKB Receptors
Authors: Davidowa H. , Albrecht D. , Gabriel H.‐J. , Heublein S. , Wetzel K. 
Published: April 2006

AbstractThe effect of iontophoretically applied cholecystokinin (CCK) on neurons of the neostriatum was studied in rats anaesthetized with urethane. The most frequently observed effect of the sulphated octapeptide (CCK‐8S) on striatal neurons was excitation. Spontaneously active neurons responded more often to CCK‐8S than quiescent cells. Silent, primarily non‐responsive neurons could often be stimulated with CCK‐8S using glutamate to induce an ongoing discharge. Thus, 45.8% of the 177 neurons studied changed their discharge rate by more than 30%. Certain CCK receptor antagonists could prevent the effect of CCK‐8S, fully or at least partly, in the majority of CCK‐responsive neurons. The data suggest that cholecystokinin modulates the firing of active neostriatal neurons via the CCKA or the CCKB receptor type. Furthermore, we compared neuronal responses to glutamate with those recorded during concomitant administration of CCK‐8S in order to study the interaction of both transmitters, which may be colocalized in striatal afferents. CCK‐8S mainly enhanced the excitatory effect of glutamate on striatal neurons, but in several neurons the response to glutamate was reduced. The CCKB receptor antagonist could prevent CCK‐8S from increasing the glutamate‐induced activation.
Intraperitoneal Administration of Bacterial Endotoxin Enhances Noradrenergic Neurotransmission in the Rat Preoptic Area: Relationship with Body Temperature and Hypothalamic‐Pituitary‐Adrenocortical Axis Activity
Authors: Linthorst Astrid C. E. , Flachskamm Cornelia , Holsboer Florian , Reul Johannes M. H. M. 
Published: April 2006

AbstractA combined in vivo microdialysis/biotelemetry method in freely moving rats was used to study the effects of an endotoxic challenge on brain neurotransmission, hypothalamic‐pituitary‐adrenocortical (HPA) axis activity, autonomic functions and behaviour. Rats were equipped with a microdialysis probe in the preoptic area and a transmitter for biotelemetry in the peritoneal cavity. Time‐dependent changes in noradrenergic and serotonergic neurotransmission, and HPA axis activity were monitored by measuring noradrenaline, serotonin, their metabolites and free corticosterone concentrations in dialysates. Core body temperature, heart rate and locomotion were measured simultaneously by biotelemetry. In addition, total behavioural activity was scored by measuring the time during which rats were active. Intraperitoneal administration of endotoxin (lipopolysaccharide; 100 μg/kg body weight) caused a pronounced increase in preoptic extracellular concentrations of noradrenaline and its metabolite 3‐methoxy‐4‐hydroxyphenylglycol (MHPG; 500 and 400% of baseline respectively). No effect was found on preoptic concentrations of serotonin, although the levels of its metabolite 5‐hydroxyindoleacetic acid were slightly elevated (120% of baseline). Intraperitoneal lipopolysaccharide caused a marked increase in corticosterone levels, a decline in behavioural activity, and biphasic rises in body temperature and heart rate. Analysis of the time curves revealed that noradrenaline rose in parallel with the first increase in body temperature and the increase in corticosterone levels. Moreover, maximum noradrenaline levels were reached ˜60 min earlier than the peak in body temperature and corticosterone concentrations. Intraperitoneal pretreatment with the cyclo‐oxygenase inhibitor indomethacin prevented the lipopolysaccharide‐induced changes in body temperature, heart rate and behavioural activity, whereas the changes in noradrenaline, MHPG and corticosterone were largely, but not completely, reduced. Taken together, the results show that an endotoxic challenge results in a highly differentiated response in brain neurotransmission. We postulate that the profound increase in preoptic noradrenergic neurotransmission may be related to the lipopolysaccharide‐evoked induction of fever and/or activation of the HPA axis.
Eye Position Influence on the Parieto‐occipital Area PO (V6) of the Macaque Monkey
Authors: Galletti C. , Battaglini P. P. , Fattori P. 
Published: April 2006

AbstractThe aim of this work was to study the effect of eye position on the activity of neurons of area PO (V6), a cortical region located in the most posterior part of the superior parietal lobule. Experiments were carried out on three awake macaque monkeys. Animals sat in a primate chair in front of a large screen, and fixated a small spot of light projected in different screen locations while the activity of single neurons was extracellularly recorded. Both visual and non‐visual neurons were found. About 48% of visual and 32% of non‐visual neurons showed eye position‐related activity in total darkness, while in ˜61% of visual neurons the visual response was modulated by eye position in the orbit. Eye position fields and/or gain fields were different from cell to cell, going from large and quite planar fields up to peak‐shaped fields localized in more or less restricted regions of the animal's field of view. The spatial distribution of fixation point locations evoking peak activity in the eye position‐sensitive population did not show any evident laterality effect, or significant top/bottom asymmetry. Moreover, the cortical distribution of eye position‐sensitive neurons was quite uniform all over the cortical region studied, suggesting the absence of segregation for this property within area PO (V6). In the great majority of visual neurons, the receptive field‘moved’with gaze according to eye displacements, remaining at the same retinotopic coordinates, as is usual for visual neurons. In some cases, the receptive field did not move with gaze, remaining anchored to the same spatial location regardless of eye movements (‘real‐position cells'). A model is proposed suggesting how eye position‐sensitive visual neurons might build up real‐position cells in local networks within area PO (V6). The presence in area PO (V6) of real‐position cells together with a high percentage of eye position‐sensitive neurons, most of them visual in nature, suggests that this cortical area is engaged in the spatial encoding of extrapersonal visual space. Since lesions of the superior parietal lobule in humans produce deficits in visual localization of targets as well as in arm‐reaching for them, and taking into account that the monkey's area PO (V6) is reported to be connected with the premotor area 6, we suggest that area PO (V6) supplies the premotor cortex with the visuo‐spatial information required for the visual control of arm‐reaching movements.
The Coat Protein gp120 of HIV‐1 Inhibits Astrocyte Uptake of Excitatory Amino Acids via Macrophage Arachidonic Acid
Authors: Dreyer Evan B. , Lipton Stuart A. 
Published: April 2006

AbstractThe human immunodeficiency virus coat protein gp120 injures central mammalian neurons both in vitro and in vivo, and this observation may contribute, at least in part, to the neurological dysfunction associated with the acquired immunodeficiency syndrome. Recent work suggests that gp 120 mediates neuronal damage predominantly via an indirect route involving activation of brain macrophages. We have previously shown that the stimulation of N‐methyl‐D‐aspartate receptors by excitatory amino acids is essential for the neuronal injury observed with gp 120. Here we show that gp 120 impairs astrocyte uptake of excitatory amino acids and the excess glutamate thus engendered may contribute to the increased neuronal damage. We also studied the mechanism whereby gp 120 inhibits the uptake of excitatory amino acids by astrocytes. We present data suggesting that at least one pathway involves a direct effect of gp120 on macrophages, which in turn release arachidonic acid, a known inhibitor of excitatory amino acid uptake by astrocytes. Our findings suggest that the observed effects on glia and neurons of gp120 may be secondary, at least in part, to its initial activation of macrophages.