bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modification of parallel activity elicited by propagating bursts in developing networks of rat cortical neurones
Authors: Maeda Eisaku , Kuroda Yoichiro , Robinson Hugh P. C. , Kawana Akio 
Published: March 2003

AbstractNetworks of cultured cortical neurones exhibit regular, synchronized, propagating bursts which are synaptically mediated, and which are hypothesized to play a part in activity‐dependent formation of connections during development in vivo. The relationship between the strength of synaptic connections and the characteristics of synchronized propagating bursting, however, is unclear. Modification of synchronized activity in cortical cultures in response to electrical stimulation was examined using multisite electrode array recording. By measuring the response of the network to weak, localized, test stimulation (TS), we observed a potentiation of activity following a relatively stronger inducing stimulation (IS). This potentiation was evident as an increased probability of eliciting bursts by TS, an increased frequency of spontaneous bursts and number of spikes per burst, and increased speed of burst propagation, and it lasted for at least 20 min. Changing the parameters of IS revealed that high frequency tetanic stimulation is not necessary to induce potentiation, while it is essential for IS to produce a regeneratively propagating burst. The results provide a direct demonstration of modification of both the spatial and temporal characteristics of synchronized network activity, and suggest an important physiological role for propagating synchronized bursting, as a mechanism for inducing plastic modifications in the developing cortex.
Selective scarcity of NMDA receptor channel subunits in the stratum lucidum (mossy fibre‐recipient layer) of the mouse hippocampal CA3 subfield
Authors: Watanabe Masahiko , Fukaya Masahiro , Sakimura Kenji , Manabe Toshiya , Mishina Masayoshi , Inoue Yoshiro 
Published: March 2003

AbstractHippocampal synapses express two distinct forms of the long‐term potentiation (LTP), i.e. NMDA receptor‐dependent and ‐independent LTPs. To understand its molecular‐anatomical basis, we produced affinity‐purified antibodies against the GluRε1 (NR2A), GluRε2 (NR2B), and GluRζ1 (NR1) subunits of the N‐methyl‐d‐aspartate (NMDA) receptor channel, and determined their distributions in the mouse hippocampus. Using NMDA receptor subunit‐deficient mice as the specificity controls, section pretreatment with proteases (pepsin and proteinase K) was found to be very effective to detect authentic NMDA receptor subunits. As the result of modified immunohistochemistry, all three subunits were detected at the highest level in the strata oriens and radiatum of the CA1 subfield, and high levels were also seen in most other neuropil layers of the CA1 and CA3 subfields and of the dentate gyrus. However, the stratum lucidum, a mossy fibre‐recipient layer of the CA3 subfield, contained low levels of the GluRε1 and GluRζ1 subunits and almost excluded the GluRε2 subunit. Double immunofluorescence with the AMPA receptor GluRα1 (GluR1 or GluR‐A) subunit further demonstrated that the GluRε1 subunit was colocalized in a subset, not all, of GluRα1‐immunopositive structures in the stratum lucidum. Therefore, the selective scarcity of these NMDA receptor subunits in the stratum lucidum suggests that a different synaptic targeting mechanism exerts within a single CA3 pyramidal neurone in vivo, which would explain contrasting significance of the NMDA receptor channel in LTP induction mechanisms between the mossy fibre‐CA3 synapse and other hippocampal synapses.
Evidence for the involvement of corticotrophin‐releasing hormone in the pathogenesis of traumatic brain injury
Authors: Roe Susan Y. , McGowan Eileen M. , Rothwell Nancy J. 
Published: March 2003

AbstractThe aim of this study was to investigate the role of the neuropeptide corticotrophin‐releasing hormone (CRH) in neurodegeneration induced by traumatic brain injury, using a well characterized model of lateral fluid percussion injury in male, Sprague‐Dawley rats. In the first series of experiments, CRH gene expression was assessed by in situ hybridization after traumatic brain injury. A bilateral increase in CRH mRNA in the paraventricular nucleus was observed in rats subjected to traumatic brain injury compared with sham‐operated controls. A maximal (40%) increase in hybridization signal was detected 2 h after trauma compared with control rat brains. In addition, marked induction of CRH transcripts was found in the ipsilateral amygdala after trauma, but no increase was detected in the ipsilateral cortex around the area of damage. In a separate experiment, the effects of the CRH antagonist, D‐Phe CRH(12–41) (25 μg total dose), or appropriate vehicle injected intracerebroventricularly, was tested on infarct volume caused by brain injury. Repeated intracerebroventricular injection of D‐Phe CRH(12–41) significantly reduced, by 45%, the volume of cortical damage in injured rats compared with vehicle‐treated, trauma animals. The rapid upregulation of CRH gene expression in the paraventricular nucleus and amygdala following lateral fluid percussion injury and the marked neuroprotection achieved by inhibiting CRH action suggest that CRH is involved directly in the pathogenesis of traumatic brain injury. This observation may have important implications for the development of novel therapeutic strategies for treating the neurological consequences of brain trauma and related conditions.
Influence of acetylcholinesterase on embryonic spinal rat motoneurones growth in culture: a quantitative morphometric study
Authors: Bataillé Stephan , Portalier Paule , Coulon Patrice , Ternaux Jean‐Pierre 
Published: March 2003

AbstractRat spinal motoneurones sampled at day embryonic 15 were purified using a Nycodenz gradient and cultured in defined medium, during 7 days, on glass coverslips coated with poly‐l‐lysine and laminine. Purified acetylcholinesterase (AChE), ecothiopate, BW 284C51 and fasciculin II, inhibitors of either the catalytic or peripheral site of AChE, were added to the defined medium. Morphological changes of spinal motoneurones were measured using a statistical quantitative morphometric method, allowing the determination of various parameters such as the number of neurites and bifurcations, the length of neurites, the surface and spreading index. Presence of AChE in the medium (4 units/mL) increases the surface and the total length of neurites and axons without any change in the spreading index. When spinal motoneurones were cultured on AChE coated substrate, neurones rapidly migrate and form clusters. Addition of ecothiopate (10–6m) in the medium, which selectively blocks the catalytic site of AChE, leads to a slight increase in the number of primary neurite and a decrease of the spreading index during the three first days in culture. BW 284C51 (10–5m) which blocks the catalytic site but also affect the peripheral one, significantly reduces the number of primary neurites and increases the number of bifurcations. Fasciculin II, a potent blocker (10–9m) of the AChE peripheral site induces a decrease of both primary neurites and bifurcations with a significant increase of the length and growth velocity of the axon, giving a drastic enhancement of the spreading index. These phenomena are discussed in terms of catalytic and non‐catalytic function of AChE, including the involvement of the enzyme in adhesive processes, occurring during growth and differentiation of spinal motoneurones.
Peptidergic innervation and the nicotinic acetylcholine receptor in the primate basal nucleus
Authors: Csillik Bertalan , Rakic Pasko , Knyihár‐Csillik Elizabeth 
Published: March 2003

AbstractPeptidergic innervation and localization of the neuronal nicotinic acetylcholine receptor (nAChR) was studied in the basal forebrain of Macaca fascicularis in order to provide microstructural proofs for the theory ( Changeux et al. 1992
) that calcitonin gene‐related peptide (CGRP) is responsible for the maintenance of the acetylcholine receptor. Distribution and localization of five neuropeptides, namely substance P (SP), CGRP, neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP) neurotensin (NT), and the neuropeptides parvalbumin (PV) and the α‐bungarotoxin‐ (α‐BTX‐) binding protein was studied by means of light‐ and electron microscopic pre‐embedding immunocytochemistry. Immunohistochemical double staining revealed that large cholinergic principal nerve cells in the basal forebrain, corresponding to cell group Ch4 constituting Meynert’s basal nucleus (BNM), and exerting intense choline acetyltransferase (ChAT) immunoreactivity, are synaptically innervated by axons displaying CGRP immunoreactivity. While SP, NPY, PV and CGRP establish dense networks in BNM, innervation by NT and VIP is sparse. Biotinylated α‐BTX visualizes beaded axons that surround dendrites and perikarya of cholinergic principal cells. Electron microscopic organization of the neuropil in BNM is characterized by a glomerular (or rather cartridge‐like) arrangement of axons surrounding dendrites of non‐cholinergic principal nerve cells. At least one of the axons establishing the glomerulus (cartridge) exerts CGRP immunopositivity while α‐BTX‐immunopositive axons, presynaptic to dendrites of principal cells, are attached to the glomeruli (cartridges) from outside. As α‐BTX‐binding indicates localization of the α7 subunit of the neuronal nAChR, the microtopographical arrangement supports the idea that, in a manner similar to that in the neuromuscular junction, CGRP might contribute to the maintenance of nAChR also in BNM. Our results suggest that presynaptic nAChR‐s are involved in the regulation of acetylcholine release from a feed‐forward amplification mechanism of cholinergic principal cells of BNM.
Distribution of L‐type calcium channels in rat thalamic neurones
Authors: Budde Thomas , Munsch Thomas , Pape Hans‐Christian 
Published: March 2003

AbstractOne major pathway for calcium entry into neurones is through voltage‐activated calcium channels. The distribution of calcium channels over the membrane surface is important for their contribution to neuronal function. Electrophysiological recordings from thalamic cells in situ and after acute isolation demonstrated the presence of high‐voltage activated calcium currents. The use of specific L‐type calcium channel agonists and antagonists of the dihydropyridine type revealed an about 40% contribution of L‐type channels to the totalhigh‐voltage‐activated calcium current. In order to localize L‐type calcium channels in thalamic neurones, fluorescent dihydropyridines were used. They were combined with the fluorescent dye RH414, which allowed the use of a ratio technique and thereby the determination of channel density. The distribution of L‐type channels was analysed in the three main thalamic cell types: thalamocortical relay cells, local interneurones and reticular thalamic neurones. While channel density was highest in the soma and decreased significantly in the dendritic region, channels appeared to be clustered differentially in the three types of cells. In thalamocortical cells, L‐type channels were clustered in high density around the base of dendrites, while they were more evenly distributed on the soma of interneurones. Reticular thalamic neurones exhibited high density of L‐type channels in more central somatic regions. The differential localization of L‐type calcium channels found in this study implies their predominate involvement in the regulation of somatic and proximal dendritic calcium‐dependent processes, which may be of importance for specific thalamic functions, such as those mediating the transition from rhythmic burst activity during sleep to single spike activity during wakefulness or regulating the relay of visual information.
Blockade of neuropsin, a serine protease, ameliorates kindling epilepsy
Authors: Momota Yoshiharu , Yoshida Shigetaka , Ito Jiro , Shibata Masao , Kato Keiko , Sakurai Katsutoshi , Matsumoto Kazumasa , Shiosaka Sadao 
Published: March 2003

AbstractThe behavioural and electrographical abnormalities associated with seizures in epileptic (kindled) mice correspond with those of human epilepsy. In kindled mice, neuropsin was markedly increased in the hippocampus and cerebral cortices. A single intraventricular injection of monoclonal antibodies specific to neuropsin reduced or eliminated the epileptic pattern noted on electroencephalograms and, as a result markedly inhibited the progression of kindling. Therefore, neuropsin appears to be a key protein controlling pathogenic events in the hippocampus, and thus neuropsin inhibitors might be useful for treatment of epilepsy.
The intermediate stage and paradoxical sleep in the rat: influence of three generations of hypnotics
Authors: Gottesmann C. , Gandolfo G. , Arnaud C. , Gauthier P. 
Published: March 2003

AbstractParadoxical sleep in the rat, cat and mouse is preceded and sometimes followed by a short‐lasting intermediate stage characterized by high‐amplitude anterior cortex spindles and low‐frequency hippocampal theta rhythm. Several neurophysiological arguments suggest that the intermediate stage corresponds to a brief functional disconnection of the forebrain from the brainstem. This paper is devoted to the review of quantitative and qualitative influences of three generations of hypnotics on the intermediate stage–paradoxical sleep couple. Barbiturates, first‐generation hypnotics, extend the intermediate stage at the expense of paradoxical sleep. Three benzodiazepines are compared, two with a short half‐life (triazolam and midazolam) and one with a long half‐life (diazepam). They also decrease sleep occurrence latency and increase the intermediate stage at the expense of paradoxical sleep, except for midazolam, which increases both the intermediate stage and paradoxical sleep at low dose. Zolpidem and zopiclone, hypnotics of third generation, decrease paradoxical sleep but the intermediate stage never substitutes for paradoxical sleep. The results are discussed in relationship to the functional aspects of this turning‐point period of sleep.
A role for BDNF in early postnatal rat vestibular epithelia maturation: implication of supporting cells
Authors: Montcouquiol M. , Valat J. , Travo C. , Sans A. 
Published: March 2003

AbstractThe early development of the inner ear is largely determined by two members of the neurotrophic family: brain‐derived neurotrophic factor (BDNF) and neurotrophin 3 (NT‐3). Little information is available on the role of these neurotrophins during the late stages of vestibular development in the rat which take place during the first postnatal weeks. At this period where terminal synaptogenesis and maturation occur, we have investigated the expression and the activity of BDNF, the most important neurotrophin in the vestibular system. Using different experimental approaches, we show that BDNF is released by vestibular epithelia on postnatal day 3 (P3) and continues to have a trophic effect on vestibular neurones in vitro. Immunocytochemistry coupled to confocal microscopy revealed a remarkable evolution in BDNF localization during later stages of development. Whereas BDNF is present in both supporting cells and hair cells at P3, its distribution gradually changed and is highly compartmentalized within the upper part of supporting cells at P8 and P15. In parallel, we observed the presence of a truncated form of the BDNF receptor in sensory hair cells. These results suggest an original role for supporting cells, which could be involved in the release of BDNF during the late stages of synaptogenesis in mammalian vestibular epithelia. In particular, BDNF could participate to the set up of the calyx, a specific nerve structure surrounding type I vestibular hair cells.
Schwann cells genetically modified to secrete human BDNF promote enhanced axonal regrowth across transected adult rat spinal cord
Authors: Menei Philippe , Montero‐Menei Claudia , Whittemore Scott R. , Bunge Richard P. , Bunge Mary Bartlett 
Published: March 2003

AbstractThe infusion of BDNF and NT‐3 into Schwann cell (SC) grafts promotes regeneration of brainstem neurones into the grafts placed in adult rat spinal cord transected at T8 (Xuet al. 1995b). Here, we compared normal SCs with SCs genetically modified to secrete human BDNF, grafted as trails 5 mm long in the cord distal to a transection site and also deposited in the transection site, for their ability to stimulate supraspinal axonal regeneration beyond the injury. SCs were infected with the replication‐deficient retroviral vector pL(hBDNF)RNL encoding the human preproBDNF cDNA. The amounts of BDNF secreted (as detected by ELISA) were 23 and 5 ng/24 h per 106cells for infected and normal SCs, respectively. Biological activity of the secreted BDNF was confirmed by retinal ganglion cell bioassay. The adult rat spinal cord was transected at T8. The use of Hoechst prelabelled SCs demonstrated that trails were maintained for a month. In controls, no SCs were grafted. One month after grafting, axons were present in SC trails. More 5‐HT‐positive and some DβH‐positive fibres were observed in the infected vs. normal SC trails. When Fast Blue was injected 5 mm below the transection site (at the end of the trail), as many as 135 retrogradely labelled neurones could be found in the brainstem, mostly in the reticular and raphe nuclei (normal SCs, up to 22, mostly in vestibular nuclei). Numerous neurones were labelled in the ventral hypothalamus (normal SCs, 0). Also, following Fast Blue injection, a mean of 138 labelled cells was present in dorsal root ganglia (normal SCs, 46) and spinal cord (39 vs. 32) rostral to the transection. No labelled spinal neurones rostral to the transection were seen when SCs were not transplanted. Thus, the transplantation of SCs secreting increased amounts of BDNF improved the regenerative response across a transection site in the thoracic cord. Moreover, the enhanced regeneration observed with infected SCs may be specific as the largest response was from neurones known to expresstrkB.
Responses of human primary sensorimotor and supplementary motor areas to internally triggered unilateral and simultaneous bilateral one‐digit movements. A high‐resolution EEG study
Authors: Urbano A. , Babiloni C. , Onorati P. , Carducci F. , Ambrosini A. , Fattorini L. , Babiloni F. 
Published: March 2003

AbstractWe modelled the responses of human primary sensorimotor areas and supplementary motor area to simple, self‐initiated unilateral and simultaneous bilateral middle finger movements using a novel high‐resolution electroencephalography technology. The results support the view that these cortical motor areas are involved in parallel and present similar activity in the preparation, initiation, and execution of the contralateral and bilateral movements. Furthermore, the left primary sensorimotor area (dominant hemisphere) appears to be activated more than the right primary sensorimotor area during the preparation and performance of the ipsilateral movements.
A caspase inhibitor blocks ischaemia‐induced delayed neuronal death in the gerbil
Authors: Himi Toshiyuki , Ishizaki Yasuki , Murota Sei‐itsu 
Published: March 2003

AbstractCaspases play a critical role in the cell death machinery in various cell types. Here we investigated the involvement of caspases in the delayed neuronal death after transient global forebrain ischaemia in the gerbil. Intrahippocampal injection of benzyloxycarbonyl‐Asp‐CH2‐dichlorobenzene (zD), an irreversible inhibitor of caspases, saved hippocampal CA1 neurones from chromatin condensation and DNA fragmentation at post‐ischaemia day 4, and these neurones maintained normal morphology at day 8 post‐insult. Intrahippocampal injection of interleukin‐1β (IL‐1β) after ischaemic insults did not influence the neuroprotective effect of zD, suggesting that the neuroprotective effect does not depend on the inhibition of mature IL‐1β production. Animals that received zD‐injection showed significant improvement in step‐through and step‐down passive avoidance learning at post‐ischaemia days 4 and 5, suggesting that neural functions were preserved in these animals. At post‐ischaemia day 4, the cleavage of poly(ADP‐ribose)polymerase was observed, and this cleavage was almost completely suppressed in zD‐injected hippocampus, suggesting involvement of caspase‐3 and caspase‐3‐like caspase in the delayed neuronal death. Our findings indicate that caspases play important roles in the delayed neuronal death after transient global forebrain ischaemia in the gerbil, and suggest that ischaemia‐induced brain damage can be blocked by caspase inhibitors.
Comparing the effects of selective cingulate cortex lesions and cingulum bundle lesions on water maze performance by rats
Authors: Warburton E.C. , Aggleton J.P. , Muir J.L. 
Published: March 2003

AbstractThe ability of rats to learn the location of a hidden platform in a swim maze was compared in animals with excitotoxic lesions of the anterior or posterior (retrosplenial) cingulate cortex or radiofrequency lesions of the cingulum bundle or fimbria‐fornix. Performance of this allocentric spatial task was unaffected by the posterior cingulate cortex lesions, while anterior cingulate cortex damage produced only a mild acquisition deficit. Transection of the fornix and lesions of the cingulum bundle produced similar patterns of impairment on initial acquisition, but the cingulum bundle lesions had less effect on reversal of the task. The results from the water maze, and from a subsequent T‐maze alternation task, indicate that cingulum bundle lesions can produce a spatial deficit that is similar, but milder, to that observed after fornix transection. The results of the excitotoxic lesions suggest that previous studies examining conventional cingulate lesions may have been influenced by damage to adjacent fibre tracts, such as the cingulum bundle.