bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Fates of Cells in the Developing Cerebral Cortex of Normal and Methylazoxymethanol Acetate‐lesioned Mice
Authors: Gillies Katy , Price David J. 
Published: April 2006

AbstractWe are interested in the mechanisms that generate the mature cerebral cortex. We used bromodeoxyuridine (BrdU) to label cortical cells as they were being born. We followed the fates of specific sets of cortical precursors in normal mice and in mice in which other groups of cortical progenitors had been destroyed with the antimitotic agent methylazoxymethanol acetate (MAM Ac). In normal mice, most cells destined for the cerebral cortex were produced from embryonic day 12 (E12) to E16 in the expected inside‐to‐outside sequence (deep layers first, superficial layers last). Injection of MAM Ac at E13 killed cells that would normally have contributed to the deep cortical layers. As a consequence, the cortex was thinned by ∼25% at postnatal day 21 (P21). However, all laminae were present and had normal connections with subcortical structures, although all were proportionately thinner. BrdU injected on E16 labelled a normally sized complement of cells that spanned a larger proportion of the depth of the thinned cortex. Thus, the deep cortical layers comprised many cells that were born several days later than normal. At embryonic ages prior to E12, a transient set of cells is produced in the early telencephalon. After injection with MAM Ac at E10, the cortex appeared histologically and histochemically normal at P21. However, many cells that would normally have contributed to superficial cortex (born on E15) were significantly deeper than normal. These results suggest that, during the early stages of cortical development, the nervous system is sufficiently plastic to compensate to some extent for the destruction of specific precursor cells by altering the fates of neurons born later. They indicate that the embryonic date on which a cortical cell is born does not necessarily determine its eventual phenotype.
Organization of Auditory Callosal Connections in Hypothyroid Adult Rats
Authors: Berbel Pere , Guadaño‐Ferraz Ana , Martínez Mercedes , Quiles Juan A. , Balboa Rosario , Innocenti Giorgio M. 
Published: April 2006

AbstractCallosal connections were studied with tracers (horseradish peroxidase (HRP) and wheat germ agglutinin‐horseradish peroxidase (WGA‐HRP)) in normal rats and rats deprived of thyroid hormones with methimazole (Sigma) since embryonic day 14 and thyroidectomized at postnatal day 6. In hypothyroid rats, the auditory areas, in particular the primary auditory area, showed cytoarchitectonic changes including blurred lamination and decrease in the size of layer V pyramidal neurons. In control rats, callosally‐projecting neurons were found between layers II and VI with a peak in layer III and upper layer IV. In hypothyroid rats, labelled neurons were found between layers IV and VI with two peaks corresponding to layer IV and upper layer V, and in upper layer VI. Quantitative analysis of radial distribution of callosally‐projecting neurons confirmed their shift to infragranular layers in hypothyroid rats. Three‐dimensional reconstructions showed a more continuous tangential distribution of callosally‐projecting neurons in hypothyroid rats which may be due to the maintenance of a juvenile ‘exuberant’ pattern of projections. These changes in cortical connectivity may be relevant for understanding epilepsy and mental retardation associated with early hypothyroidism in humans and to clarify basic mechanisms of cortical development.
Noradrenaline Decreases Transmission of NMDA‐ and Non‐NMDA‐receptor Mediated Monosynaptic EPSPs in Rat Prefrontal Neurons In Vitro
Authors: Law‐Tho D. , Crepel F. , Hirsch J. C. 
Published: April 2006

AbstractThe effects of noradrenaline on pyramidal cells of layer V of the prefrontal cortex were examined in rat brain slices in vitro. Bath administration of noradrenaline (10 μM) reduced synaptic transmission of afferent inputs from layer 1. The decrease affected all the components of the evoked response and particularly the monosynaptic excitatory postsynaptic potential (EPSP) as evidenced by a reduction of its initial rising slope (mean slope: 71 ± 11% of its control). Pharmacological dissociation of the NMDA‐ and non‐NMDA‐receptor components of the EPSP showed that noradrenaline reduced both (mean EPSP slopes were 71 ± 8% and 73 ± 10% of their control, respectively). Alpha1‐, but not α‐2‐ or β‐adrenoceptor antagonists prevented the noradrenaline‐induced decrease in synaptic efficacy. However, the effect of noradrenaline was not reproduced by α1‐adrenoceptor agonists. Lastly, noradrenaline acting through β‐adrenoceptors reduced the slow hyperpolarization that follows a train of action potentials.
Galanin Antagonists Block Galanin‐induced Feeding in the Hypothalamus and Amygdala of the Rat
Authors: Corwin R. L. , Robinson J. K. , Crawley J. N. 
Published: April 2006

AbstractGalanin significantly increased food intake when microinjected into the region of the central nucleus of the amygdala as well as into the paraventricular nucleus of the hypothalamus. In the amygdala this effect was specific to feeding; no change in grooming, resting, or other behaviour was observed after galanin treatment. These results provide evidence that the amygdala may be an important site in the mediation of galanin‐induced feeding. The galanin receptor antagonists, C7 and M40, antagonized galanin‐induced feeding, while having no effect alone on food consumption in free‐feeding rats. These new galanin receptor antagonists provide useful tools for further investigating the role of endogenous galanin in the regulation of feeding.
Acidic Fibroblast Growth Factor is Expressed Abundantly by Photoreceptors Within the Developing and Mature Rat Retina
Authors: Bugra K. , Oliver L. , Jacquemin E. , Laurent M. , Courtois Y. , Hicks D. 
Published: April 2006

AbstractIn order to further understand the role(s) of fibroblast growth factors (FGFs) in the development, differentiation and function of the central nervous system, we analysed the expression of the mRNA, and the presence and tissue distribution of the translated product, of one member of the FGF family, acidic FGF (aFGF), within the mammalian retina. Firstly, the relative abundance of aFGF mRNA was assayed in embryonic (between 14 and 17 days of gestation), postnatal (between 1 and 17 days after birth) and adult rat retina by quantitative reverse transcription‐coupled polymerase chain reaction amplification using specific aFGF oligonucleotides. The level of expression remained uniformly low throughout the embryonic period and until postnatal day 7. Therefore the quantity of aFGF mRNA increased rapidly, reaching 80% of adult levels by eye opening (postnatal day 13). Adult levels were three‐fold higher than at early developmental times. In situ hybridization of adult rat retina using specific antisense aFGF riboprobes revealed labelling in all cellular layers. Antisera raised against recombinant human aFGF revealed very little labelling of 4‐day postnatal retina, but by postnatal days 8 and 17 immunoreactive aFGF was localized mainly within the photoreceptor cell bodies. Western blots of retinal extracts derived from 17‐day embryonic, 4‐day postnatal and adult retina probed with the same antibody revealed a single immunoreactive band of the expected molecular weight (18 kDa) in all extracts. Thus aFGF is mostly transcribed and translated within the retina subsequent to the major steps of cell birth, migration and differentiation, and seems to be abundantly expressed by maturing photoreceptor cells.
Localization of Nitric Oxide Synthase in the Mouse Olfactory and Vomeronasal System: a Histochemical, Immunological and In Situ Hybridization Study
Authors: Kishimoto J. , Keverne E. B. , Hardwick J. , Emson P. C. 
Published: April 2006

AbstractThe distribution of nitric oxide synthase (NOS) in the mouse olfactory bulb and olfactory epithelium, including the vomeronasal organ, was studied using an anti‐NOS antibody, NADPH diaphorase histochemistry and in situ hybridization with NOS specific antisense oligonucleotide probes. Interneurons containing NOS protein and mRNA, and exhibiting NADPH diaphorase activity were detected in the plexiform layer of the main olfactory bulb and the granule cell layer of main and accessory olfactory bulbs. Periglomerular cells and granule cells in the main olfactory bulb were also NOS positive with diaphorase and immunostaining for NOS. In contrast, no evidence for NOS expression was found either in the main olfactory epithelium or in the vomeronasal organ, in spite of the strong diaphorase staining of the surface of the main olfactory epithelium. Polymerase chain reaction amplification experiments for detection of NOS gene expression further indicated that NOS is expressed in the olfactory bulb but not in either the main olfactory epithelium or vomeronasal organ. Use of an antibody raised against another enzyme, NADPH‐P450 oxidoreductase, showed that this protein was strongly expressed in the olfactory epithelium. Activity of this enzyme may account for the diaphorase histochemical staining of the epithelia. An involvement of neuronal nitric oxide synthase in signalling in olfactory receptor neurons is therefore doubtful, although NOS is clearly expressed in neurons in both main and accessory olfactory bulbs.
Effects of the HIV‐1 Envelope Glycoprotein gp120 in Cerebellar Cultures. [Ca2+]i Increases in a Glial Cell Subpopulation
Authors: Ciardo Alberto , Meldolesi Jacopo 
Published: April 2006

AbstractThe various types of cells present in cultures prepared from the postnatal rat cerebellum, identified by their gross morphology and immunocytochemistry, were loaded with the specific dye fura‐2 and analysed individually for [Ca2+]i changes induced by the HIV‐1 envelope glycoprotein gp120 and a variety of other treatments. In granule neurons [Ca2+]i increases were induced by high KCl and glutamate (mainly through the NMDA receptor) while in type‐1 astrocytes this effect was observed after serotonin, carbachol and also quisqualate. In contrast, administration of gp120 was always without effect in these cells. Type‐2 astrocytes (an arborized cell type responsive to agonists targeted to the glutamatergic AMPA and cholinergic receptors) were also most often unresponsive to the viral glycoprotein. However, among the cells exhibiting the arborized phenotype, a subpopulation (‐13%) responded to gp120 with conspicuous [Ca2+]i increases sustained by both release from intracellular stores and influx across the plasma membrane. These responses to the viral protein did not involve activation of either voltage‐gated Ca2+ channels or glutamatergic receptors. Although not yet conclusively identified by specific cytochemical markers, the gp120‐responsive cells resemble type‐2 astrocytes and differ from neurons and type‐1 astrocytes both in gross phenotype and in a number of receptor/channel properties: positivity to AMPA and cholinergic agonists; negativity to NMDA, serotonin and high KCl. From these results it is concluded that a subpopulation of glial cells is affected by gp120. The role of these cells in HIV brain infection and damage requires further studies to be precisely established.
Heterogeneity of Synaptic Density in the Adult Pigmented Rabbit's Visual Cortex
Authors: Choudhury B. P. 
Published: April 2006

AbstractIn the adult pigmented rabbit, synaptic density in the lateral and medial part of the visual cortex was estimated along the projection area of the visual streak. A higher synaptic density distribution was observed in the lateral cortex (projection area of the nasal visual field) than in the medial cortex (projection area of the temporal visual field). This shows that there is a higher synaptic density in the region of the visual cortex receiving input from a retinal area with a high ganglion cell concentration than the area of the cortex receiving input from the retina with a low concentration of such cells. The regions of the visual cortex with higher and lower synaptic densities are the areas having a higher and lower magnification factor respectively.
Tonic Activation of NMDA Receptors Causes Spontaneous Burst Discharge of Rat Midbrain Dopamine Neurons In Vivo
Authors: Chergui K. , Charléty P. J. , Akaoka H. , Saunier C. F. , Brunet J.‐L. , Buda M. , Svensson T. H. , Chouvet G. 
Published: April 2006

AbstractMidbrain dopamine neurons in vivo discharge in a single‐spike firing pattern or in a burst‐firing pattern. Such activity in vivo strikingly contrasts with the pacemaker activity of the same dopamine neurons recorded in vitro. We have recently shown that burst activity in vivo of midbrain dopamine neurons is due to the local activation of excitatory amino acid receptors, as microapplication of the broad‐spectrum antagonist of excitatory amino acids, kynurenic acid, strongly regularized the spontaneous firing pattern of these dopamine neurons. In the present study, we investigated which subtypes of excitatory amino acid receptors are involved in the burst‐firing of midbrain dopamine neurons in chloral hydrate‐anaesthetized rats, Iontophoretic or pressure microejections of 6‐cyano,7‐nitroquinoxaline‐2,3‐dione (CNQX), a non‐N‐methyl‐d‐aspartate (NMDA) receptor antagonist, did not alter the spontaneous burst firing of dopamine neurons (n= 36). In contrast, similar ejections of (±)2‐amino,5‐phos‐phonopentanoic acid (AP‐5), a specific antagonist at NMDA receptors, markedly regularized the firing pattern by reducing the occurrence of bursts (n= 52). In addition, iontophoretic ejections of NMDA, but not kainate or quisqualate, elicited a discharge of these dopamine neurons in bursts (n= 20, 12 and 14, respectively). These data suggest that burst‐firing of midbrain dopamine neurons in vivo results from the tonic activation of NMDA receptors by endogenous excitatory amino acids. In view of the critical dependency of catecholamine release on the discharge pattern of source neurons, excitatory amino acid inputs to midbrain dopamine neurons may constitute a major physiological substrate in the control of the dopamine level in target areas.
Single‐channel Activity in Cultured Cortical Neurons of the Rat in the Presence of a Toxic Dose of Glutamate
Authors: Backus Kurt Harald , Trube Gerhard 
Published: April 2006

AbstractRat cortical neurons grown in cell culture were exposed to 500 μM glutamate for 5 min during continuous current recording from cell‐attached patches. The Ca2+‐dependence and ion selectivity of the membrane channels activated during and after glutamate application were studied in inside‐out patches. Glutamate blocked spontaneous action potential firing. In 77% of the experiments glutamate activated several types of ion channels indirectly, i.e. via a change of cytoplasmic factors. Channel activity did not disappear after removing glutamate from the bath. A K+ channel requiring intracellular calcium ([Ca2+]i) was activated in 44% of the experiments (conductance for inward currents in cell‐attached patches 118 ± 6 pS;‘BK channel'). Another Ca2+‐dependent channel permeable for Cl‐ (conductance for outward currents in cell‐attached patches 72±17 pS), acetate and methanesulphonate appeared in 26% of the patches. Other K+ channels of smaller conductance were infrequently observed. During and after glutamate application the activity of the BK channel showed an initial increase followed by a transient decay and a second rise to a plateau, probably reflecting a similar time course of changes in [Ca2+]i. Both phases of increasing channel activity required the presence of extracellular Ca2+ suggesting that [Ca2+]i was mainly increased by Ca2+ influx. The N‐methyl‐d‐aspartate (NMDA) antagonists dizocilpine (MK‐801, 10 μM) and dl‐2‐amino‐5‐phosphonovaleric acid (AP5; 100 μM), added within 5 min after glutamate application, stopped BK channel activity and restored the spontaneous action potential firing. We conclude that the influx of Ca2+ through NMDA receptor channels causes a strong activation of Ca2+‐dependent K+ channels, which is likely to result in pronounced loss of intracellular K+. NMDA receptor channels seem to remain active for a long time (>10 min) after the end of glutamate application.
Electrophysiological and Pharmacological Characterization of Vestibular Inputs to Identified Frog Abducens Motoneurons and Internuclear Neurons In Vitro
Authors: Straka Hans , Dieringer Norbert 
Published: April 2006

AbstractSynaptic vestibular inputs of antidromically identified motoneurons and internuclear neurons in the abducens nucleus were studied electrophysiologically and pharmacologically in the isolated brain of grass frogs (Rana temporaria). The prevailing response pattern of abducens motoneurons (AbMOT) following stimulation of the VIIIth nerve was crossed disynaptic excitation and uncrossed disynaptic inhibition. A few AbMOT (five of 46), however, exhibited uncrossed excitation instead of inhibition. Abducens internuclear neurons (AbINT), identified by antidromic activation following stimulation of the contralateral medial longitudinal fascicle, exhibited disynaptic response patterns to stimulation of the VIIIth nerve that were very similar in latency and rise time to those of AbMOT except for the absence of uncrossed disynaptic inhibition. Bath application of strychnine (50 μM), a glycine antagonist, blocked the uncrossed inhibitory vestibular input to AbMOT and AbINT completely and reversibly, whereas picrotoxin (100 μM), a GABA (γ‐aminobutyric acid) antagonist, had no detectable effect on these disynaptic potentials. These results suggest glycine as the transmitter of inhibitory vestibular projections onto AbMOT and AbINT. The pharmacology of the excitatory vestibular input of these neurons was studied by electrical stimulation of the vestibular nuclear complex. Crossed monosynaptic excitatory inputs in AbMOT and AbINT were blocked completely by CNQX (6‐cyano‐7‐nitroquinoxaline‐2,3‐dione) (10 μM), an antagonist of AMPA (α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid) receptors, indicating glutamatergic excitation. Comparison of these results with those in the cat suggests the presence of a basic horizontal vestibulo‐ocular reflex that is very similarly organized, and corroborates the hypothesis that major behavioural differences in the performance of compensatory eye movements between species result from the properties of supplementary networks and not from differences in a common‘three‐neuron’vestibulo‐ocular arc.
Decrease in the Reactivity of Locus Coeruleus Neurons to Hypotension after an Increase in their Tyrosine Hydroxylase Content: A Subregional In Vivo Voltammetry Study in the Rat
Authors: Vachette Cédric , Bourde Odile , Gillon Jean‐Yves , Pujol Jean‐François , Renaud Bernard 
Published: April 2006

AbstractThe aim of the present work was to determine if noradrenergic neurons of the anterior and the posterior subregions of the locus coeruleus exhibit a difference in reactivity in response to sodium nitroprusside‐induced arterial hypotension, and if the pharmacological induction of tyrosine hydroxylase by RU24722 modifies the reactivity of locus coeruleus neurons to this hypotensive stimulus. Previous findings have demonstrated that administration of RU24722 increases the concentration of tyrosine hydroxylase in the rat locus coeruleus by two different mechanisms in the anterior and in the posterior locus coeruleus subregions. The goal of the present study was to measure in vivo the changes in catecholaminergic metabolism in the locus coeruleus after treatment with RU24722 using differential normal pulse voltammetry (DNPV). In vehicle‐treated rats, arterial hypotension increased catecholaminergic metabolism with the same pattern in the two locus coeruleus subregions. However, the changes in the magnitude of the catechol oxidation current throughout the recording period were significantly smaller in the posterior subregion (P < 0.001). In the RU24722‐pretreated rats, there was a 39% increase in tyrosine hydroxylase and dihydroxyphenylacetic acid in the locus coeruleus. The functional reactivity to hypotension measured by DNPV was significantly decreased (P < 0.001) in both the anterior and posterior locus coeruleus subregions with RU24722 treatment. Therefore, this study suggests that the response of locus coeruleus cells to a hypotensive stimulus depends upon the intracellular tyrosine hydroxylase concentration both in the basal condition and during pharmacological induction of tyrosine hydroxylase gene expression.
Neurons in the Primate Superior Colliculus are Active Before and During Arm Movements to Visual Targets
Authors: Werner Wilfried 
Published: April 2006

AbstractThe activity of single neurons in the superior colliculus was recorded while a rhesus monkey made arm movements to visual targets located on a screen in front of him. It was found that the activity of a subpopulation of cells was clearly related to these arm movements. The neurons began to discharge either with the onset of the movement, during the movement period, or well before the onset of electromyogram (EMG) activity and movement, and could be active for the entire duration of EMG activity. While the discharge pattern of some of these‘reach’neurons was not different for movements to different target positions, other cells showed graded changes in activity depending on the direction of movement. The peak discharge rate could rise to > 100 impulses/s. Some units received somatosensory input; other reach cells exhibited a visual response and/or presaccadic activity. It is likely that the primate superior colliculus is not only involved in the initiation and control of orientating movements of the eyes but also in reaching movements of the arms.
Reversal of Rigidity and Improvement in Motor Performance by Subthalamic High‐frequency Stimulation in MPTP‐treated Monkeys
Authors: Benazzouz Abdelhamid , Gross Christian , Féger Jean , Boraud Thomas , Bioulac Bernard 
Published: April 2006

AbstractIn Parkinson's disease the loss of dopaminergic neurons in the substantia nigra is associated with global disorganization of basal ganglia activity and, in particular, with increased activity of the excitatory glutamatergic neurons of the subthalamic nucleus. Recent experimental studies have shown that parkinsonian symptoms can be alleviated by selective lesioning of the subthalamic nucleus in monkeys treated with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP). We measured the effect of high‐frequency stimulation of the subthalamic nucleus in two unilaterally MPTP‐treated monkeys in order to determine whether it was possible to obtain reversible, gradual and controllable functional impairment of this structure. Clinical, mechanographic and electromyographic results demonstrate that this technique can alleviate parkinsonian rigidity and bradykinesia without causing dyskinesia or hemiballismus. This study supports the hypothesis that the subthalamic nucleus and its excitatory projections have an important role in the mechanisms sustaining the expression of parkinsonian motor changes, and suggests that high‐frequency stimulation of the subthalamic nucleus could be included in treatment for parkinsonism.