bluuebunny/crossref_metadata_2025_split huggingface dataset:
Integrins at the neuromuscular junction are important for motoneuron survival
Authors: Wong K. C. K. , Meyer T. , Harding D. I. , Dick J. R. T. , Vrbová G. , Greensmith L. 
Published: March 2003

AbstractDuring development motoneurons depend on target contact for their survival. Following injury to the sciatic nerve in neonatal rats, a large proportion of motoneurons die. However, the same injury inflicted at 5 days of age results in no loss of motoneurons. This critical period of postnatal development coincides with the time during which there is a significant increase in the release of transmitter from the nerve terminals at the neuromuscular junction. We have proposed that the role of the target muscle cell during this period is to induce this up‐regulation of transmitter release from motor nerve terminals. It has been shown that stretch‐induced increase in transmitter release from frog motor nerve terminals is accomplished via an integrin‐dependent mechanism. In this study we examined the role of integrins at the rat neuromuscular junction in motoneuron survival. We found that blocking integrin binding at the developing neuromuscular junction delayed the increase in choline acetyltransferase activity that normally takes place during the early postnatal period, and resulted in motoneuron death. Furthermore, the maturation of those motoneurons that survived was delayed so they remained susceptible to subsequent nerve injury. These results support the possibility that integrins, by their involvement in modulating transmitter release, can influence motoneuron survival.
Action of C‐type natriuretic peptide (CNP) on passive avoidance learning in rats: involvement of transmitters
Authors: Telegdy G. , Kokavszky K. , Nyerges A. 
Published: March 2003

AbstractThe action of C‐type of natriuretic peptide (CNP) was tested on one‐way passive avoidance learning in rats. The involvement of transmitters was investigated by pretreating the animals with different receptor blockers. CNP administered into the lateral brain ventricle caused a dose‐dependent facilitation of learning and consolidation of passive avoidance learning, but was ineffective on retrieval. Pretreatment of the animals with atropine, haloperidol or the nitric oxide synthase inhibitor nitro‐l‐arginine abolished the action of CNP. Phenoxybenzamine, naloxone, bicuculline, propranolol and methysergide were ineffective in modifying the action of CNP on consolidation. The results suggest that CNP is able to improve the learning and consolidation of learning in a passive avoidance paradigm, but is ineffective on retrieval processes. In the action of CNP, dopamine, acetylcholine and nitric oxide could be the mediating transmitters.
The effects of early prenatal monocular enucleation on the routing of uncrossed retinofugal axons and the cellular environment at the chiasm of mouse embryos
Authors: Chan S. ‐O. , Chung K. Y. , Taylor J. S. H. 
Published: March 2003

AbstractWhereas it has been shown that early monocular enucleations produce a reduction in the uncrossed pathway from the surviving eye in rats and ferrets, similar evidence for binocular interactions in the development of the uncrossed component in mice is currently open to question. Using retrograde tracing, we have investigated the time course of changes in the uncrossed retinofugal pathway immediately after the early prenatal monocular enucleation in mouse embryos. Removal of one eye from C57 pigmented mice at embryonic day (E) 13 does not cause a reduction of the earliest uncrossed component from the central retina examined 1 day later at E14. However, a substantial reduction of the uncrossed pathway is seen at E15, the time when the major uncrossed projection first arises from the ventral temporal retina. This reduction is greater in E16 one‐eyed embryos, indicating that most retinal axons from the ventral temporal retina rely on a binocular interaction for their turning at the chiasm. Further, early removal of one eye at E13 does not produce any obvious changes in the cytoarchitecture of RC‐2‐immunopositive radial glia at the chiasm, nor of the stage‐specific antigen‐1 (SSEA‐1) ‐expressing neurons. This lack of changes in the cellular organization at the chiasm indicates that the reduction of the uncrossed pathway is probably produced by an elimination of binocular fibre interactions at the chiasm, rather than through a degenerative change of cellular elements at the chiasm as a consequence of the eye removal procedure.
Long‐term changes in connexin32 gap junction protein and mRNA expression following cocaine self‐administration in rats
Authors: Bennett Steffany A. L. , Arnold Jennifer M. , Chen Jiahua , Stenger Janet , Paul David L. , Roberts David C. S. 
Published: March 2003

AbstractConsiderable evidence indicates a critical role for dopamine in the reinforcing effects of cocaine. Because dopamine has been shown to be a critical modulator of gap junction communication in both eye and brain, we sought to examine whether extended intravenous cocaine self‐administration would affect the expression of gap junction channel‐forming proteins (connexins). Using ELISA, Western analysis, immunohistochemistry, semi‐quantitative reverse transcriptase polymerase chain reaction (RT‐PCR), and non‐radioactive in situ hybridization, we demonstrate that withdrawal from chronic cocaine self‐administration causes lasting changes in connexin32 (Cx32) expression in the nucleus accumbens and hippocampus at 2, 7 and 21 days after the last cocaine injection. A sustained decrease in Cx32 protein and mRNA levels is noted in areas that have been implicated in cocaine craving (i.e. nucleus accumbens and subfields of the hippocampal formation). A progressive increase in gap junction protein and mRNA expression is noted in areas that become hyperexcitable after chronic cocaine exposure (i.e. CA1 hippocampal neurons). We speculate that gap junction communication may be critically involved in reinforcement processes and neuroadaptive changes produced by drugs of abuse.
A fronto‐parietal circuit for object manipulation in man: evidence from an fMRI‐study
Authors: Binkofski F. , Buccino G. , Posse S. , Seitz R. J. , Rizzolatti G. , Freund H. ‐J. 
Published: March 2003

AbstractFunctional magnetic resonance imaging (fMRI) was used to localize brain areas active during manipulation of complex objects. In one experiment subjects were required to manipulate complex objects for exploring their macrogeometric features as compared to manipulation of a simple smooth object (a sphere). In a second experiment subjects were asked to manipulate complex objects and to silently name them upon recognition as compared to manipulation of complex not recognizable objects without covert naming. Manipulation of complex objects resulted in an activation of ventral premotor cortex [Brodmann's area (BA) 44], of a region in the intraparietal sulcus (most probably corresponding to the anterior intraparietal area in the monkey), of area SII and of a sector of the superior parietal lobule. When the objects were covertly named additional activations were found in the opercular part of BA 44 and in the pars triangularis of the inferior frontal gyrus (BA 45). We suggest that a fronto‐parietal circuit for manipulation of objects exists in humans and involves basically the same areas as in the monkey. It is proposed that area SII analyses the intrinsic object characteristics whilst the superior parietal lobule is related to kinaesthesia.
Axonal transport of synucleins is mediated by all rate components
Authors: Jensen Poul Henning , Li Jia‐Yi , Dahlström Annica , Dotti Carlos G. 
Published: March 2003

AbstractSynucleins are abundant nerve terminal proteins of hitherto unknown function. In diseases with Lewy bodies, human α‐synuclein concentrates in these lesions in the cell body and mutations in α‐synuclein lead to heritable Parkinson's disease with Lewy bodies. This indicates that changes in the normal metabolism and axonal transport of α‐synuclein is perturbed in these diseases. To investigate the normal axonal transport of synucleins we studied the rat visual system by nerve crush operations and metabolic labelling of the retinal ganglion cells followed by immunoprecipitation of nerve segments. We found by immunofluorescence microscopy of the crush‐operated nerves that synucleins are transported by fast antero‐ and retrograde transport and colocalize with synaptophysin and SNAP‐25 around the lesion. The metabolic labelling studies demonstrated that synucleins were moved through the nerve with all the rate components, the fast component and the slow components a and b, with component b predominating. Two‐dimensional gel electrophoresis revealed that both α‐ and β‐synuclein migrate through the nerve by slow component b in a ratio of 2 : 1.
Neural activities of IL‐6‐type cytokines often depend on soluble cytokine receptors
Authors: März Pia , Otten Uwe , Rose‐John Stefan 
Published: March 2003

AbstractCytokines of the interleukin‐6 (IL‐6) family participate in regulatory and inflammatory processes within the nervous system. IL‐6, ciliary neurotrophic factor (CNTF) and IL‐11 act via specific membrane receptors which, together with their ligands, associate with signal‐transducing receptor subunits thereby initiating cytoplasmic signalling. Cells which only express signal‐transducing receptor subunits but no ligand binding subunits for IL‐6, CNTF and IL‐11 are refractory to these cytokines. An unusual feature of the IL‐6 cytokine family is that the soluble forms of the ligand binding receptor subunits generated by one cell type in complex with their ligands can directly stimulate the signal‐transducing receptor subunits on different cell types which lack ligand binding receptor subunits. This process has been named transsignalling. This article focuses on the importance of transsignalling events in neuronal differentiation and survival responses.
Growth responses of different subpopulations of adult sensory neurons to neurotrophic factors in vitro
Authors: Gavazzi Isabella , Kumar Robin D. C. , McMahon Stephen B. , Cohen James 
Published: March 2003

AbstractDifferent subpopulations of adult primary sensory neurons in the dorsal root ganglia express receptors for different trophic factors, and are therefore potentially responsive to distinct trophic signals. We have compared the effect of the neurotrophins nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF) and NT‐3, and of glial cell line‐derived neurotrophic factor (GDNF) on neurite outgrowth in dissociated cultures of sensory neurons from the lumbar ganglia of young adult rats, and attempted to establish subset‐specific effects of these trophic factors. We analysed three parameters of neurite growth (percentage of process‐bearing neurons, length of longest neurite and total neurite length), which may correlate with particular types of axon growth in vivo, and may therefore respond differently to trophic factor presence. Our results showed that percentage of process‐bearing neurons and total neurite length were influenced by trophic factors, whilst the length of the longest neurite was trophic factor independent. Only NGF and GDNF were found to enhance significantly the proportion of process‐bearing neurons in vitro. GDNF was more effective than NGF on small, IB4– neurons, which are known to develop GDNF responsiveness early in postnatal development. NGF, and to a much lesser extent GDNF, enhanced the total length of the neurites produced by neurons in culture. BDNF exerted an inhibitory effect on growth, and both BDNF and NT‐3 could partially block some of the growth‐promoting effects of NGF on specific neuronal subpopulations.
Peripheral but not central axotomy promotes axonal outgrowth and induces alterations in neuropeptide synthesis in the nodose ganglion of the rat
Authors: Reimer Martina , Kanje Martin 
Published: March 2003

AbstractWe investigated the effects of central and peripheral axotomy of the sensory neurons in the nodose ganglion on neurite outgrowth and neuropeptide expression. Axonal outgrowth was studied in ganglia subjected to a conditioning lesion of the vagus nerve 6 days prior to in vitro explantation. In such cultures, a conditioning effect, i.e. a shorter initial delay and faster axonal outgrowth, was observed after peripheral axotomy, while central axotomy had no effect. Neuropeptide expression was measured by immunocytochemistry 3 days after axotomy. Peripheral axotomy induced an increase in the number of neurons expressing the C‐terminal flanking peptide of neuropeptide Y (C‐PON), galanin (GAL) and vasoactive intestinal peptide (VIP). In contrast, central axotomy did not affect neuropeptide expression. These results suggest that both axonal outgrowth and expression of neuropeptides in the sensory neurons of the nodose ganglion could be regulated by the contact of the cells with their peripheral, but not their central targets.
Potentiation of glutamatergic agonist‐induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation
Authors: Blanc Emmanuelle M. , Jallageas Monique , Recasens Max , Guiramand Janique 
Published: March 2003

AbstractWe investigated the modulation by growth factors of phospholipase C (PLC)‐linked glutamate receptors during in vitro development of hippocampal cultures. In defined medium, glial cells represent between 3 and 14% of total cell number. When we added basic fibroblast growth factor (bFGF) 2 h after plating, we found: (i) a neuroprotection from naturally occurring death for up to 5 days; (ii) a proliferation of glial cells from day 3; and (iii) a potentiation of quisqualate (QA)‐induced inositol phosphate (IP) formation from 1 to 10 days in vitro (DIV) and 1s,3r‐amino‐cyclopentane‐1,3‐dicarboxylate (ACPD) response from 3 to 10 DIV. The antimitotic cytosine‐β,d‐arabinofuranoside (AraC) blocked glial cell proliferation induced by bFGF, but not neuroprotection. Under these conditions, the early potentiation of the QA response (1–3 DIV) was not changed, while the ACPD and late QA response potentiations were prevented (5–10 DIV). Epidermal growth factor was not neuroprotective but it induced both glial cell proliferation and late QA or ACPD potentiation. Surprisingly, the early bFGF‐potentiated QA‐induced IP response was blocked by 6,7‐dinitro‐quinoxaline‐2,3‐dione (DNQX), suggesting the participation of ionotropic (rs)‐α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA)/kainate (KA) receptors. The delayed bFGF‐potentiated ACPD‐induced IP response is inhibited by (s)‐α‐methyl‐4‐carboxyphenylglycine (MCPG), indicating possible activation of glial metabotropic receptors. These results suggest that, in hippocampal cultures, bFGF modulates AMPA and metabotropic glutamate receptors linked to the IP cascade, possibly in relation to the regulation of neuronal survival and glial cell proliferation, respectively.
Effects of microdialysis application of monoamines on the EEG and behavioural states in the cat mesopontine tegmentum
Authors: Crochet Sylvain , Sakai Kazuya 
Published: March 2003

AbstractThe peri‐locus coeruleus alpha (peri‐LCα) of the mediodorsal pontine tegmentum contains cholinergic and non‐cholinergic neurons, and is critically implicated in the regulation of both wakefulness and paradoxical sleep (PS). The peri‐LCα receives dense monoaminergic (adrenergic, noradrenergic, serotonergic, dopaminergic and histaminergic) afferent projections, but little is known about their exact roles in the control of sleep–wake cycles. We have therefore examined the in vivo effects of microdialysis application of monoamines to the peri‐LCα and adjacent cholinergic and non‐cholinergic tegmental structures on behavioural states and the electroencephalogram (EEG) in freely moving cats. Norepinephrine, epinephrine and dopamine selectively inhibited PS and induced PS without atonia when applied to the caudal part of the peri‐LCα, which mainly contains non‐cholinergic descending neurons, whereas histamine and serotonin had no effect at this site. In the rostral part of the peri‐LCα and the adjacent X area (nucleus tegmenti pedunculopontinus, pars compacta), which contain many ascending cholinergic neurons, norepinephrine and epinephrine suppressed PS with a significant increase in waking and a decrease in slow‐wave sleep, as expressed by a marked decrease in the power of the cortical and hippocampal delta (0.5–2.5 Hz) and cortical alpha (8–14 Hz) bands, and an increase in the cortical gamma (30–60 Hz) band. At these sites, histamine had similar waking and EEG‐desynchronizing effects, but never suppressed PS, while dopamine and serotonin had no effect. These findings indicate a special importance of the adrenergic, noradrenergic and dopaminergic systems in the inhibitory or permissive mechanisms of PS, and of the adrenergic, noradrenergic and histaminergic systems in the control of behavioural and EEG arousal.
Role of membrane conductances and protein synthesis in subjective day phase advances of the hamster circadian clock by neuropeptide Y
Authors: Hall Adam C. , Earle‐Cruikshanks Germaine , Harrington Mary E. 
Published: March 2003

AbstractNeurons of the mammalian circadian pacemaker in the hypothalamic suprachiasmatic nuclei exhibit a rhythm in firing rate that can be reset by neuropeptide Y. We recorded the effects of neuropeptide Y on Na+ and K+ conductances of hamster suprachiasmatic nuclei neurons using whole‐cell, perforated‐patch and cell‐attached patch‐clamp recordings, both in dissociated and brain slice preparations. While neuropeptide Y had no effect on voltage‐gated Na+ currents, neuropeptide Y activated a leak K+ current. Neuropeptide Y phase advances in the suprachiasmatic nuclei brain slice preparation were blocked by a number of K+ channel blockers (tetraethylammonium chloride, dendrotoxin‐I, glybenclamide). However, a K+ ionophore, valinomycin, did not shift the rhythm. The inhibition by tetraethylammonium chloride did not persist in the presence of glutamatergic receptor blockers. We have previously shown that glutamate can oppose neuropeptide Y phase‐shifting actions, suggesting that K+ channel inhibition acts by inducing glutamate release. Protein synthesis inhibitors had no effect on clock phase when applied during the subjective day, and had no influence on neuropeptide Y‐induced phase shifts. On the other hand, glutamate's ability to inhibit neuropeptide Y shifts was abolished by protein synthesis inhibition. Thus, while neuropeptide Y phase shifts do not require protein synthesis, glutamate blocks neuropeptide Y shifts via increased gene expression during the subjective day, at a time when it does not reset the clock. These results indicate that neuropeptide Y phase shifts via a mechanism that does not involve changes in membrane conductance or protein synthesis.
Central effects of 5‐HT on respiratory rhythm in newborn rats in vivo
Authors: Khater‐Boidin J. , Rose D. , Glérant J. C. , Duron B. 
Published: March 2003

AbstractThe role of 5‐HT in inducing apnoeas (a major element in sudden infant death syndrome) is controversial because while 5‐HT is a respiratory depressant in vivo, it evokes respiratory analeptic effects when applied to the isolated brainstem of the newborn rat. In decerebrate newborn rats, the electrical activity of the diaphragm and that of a hypoglossally innervated tongue muscle, as well as the cardiac frequency (Fc), were recorded before and after the application of 5‐HT and related agents to the floor of the IVth ventricle. To assess the spontaneous variability in inspiratory frequency (Fi) and Fc, a sham group was studied. A decrease in Fi was observed in response to 5‐HT. This respiratory depressant effect was associated with an activation of the tongue muscle, but there was no change in Fc. Application of agonists elicited a small increase in Fi linked to activation of 5‐HT1A receptors, and decreases in both Fi and the activity of the tongue muscle resulting predominantly from activation of 5‐HT2 receptors. The decrease in Fi was much smaller in newborn rats than that reported in newborn kittens. Indeed, in newborn rats, we did not observe long‐lasting apnoeas. Our results differ from those obtained from the newborn rat in vitro, inasmuch as in vivo 5‐HT essentially depressed the respiratory rhythm generator. The role of the afferent system appears to be crucial in modulating the action of 5‐HT.
Spontaneous and evoked activity of intercalated amygdala neurons
Authors: Collins Dawn R. , Paré Denis 
Published: March 2003

AbstractThe intercalated cell masses are clusters of GABAergic neurons interposed between the basolateral and centromedial nuclear groups of the amygdala. Tract‐tracing studies have revealed that the main projection sites of intercalated neurons are the central amygdaloid nucleus and the basal forebrain. Through these projections, intercalated neurons could influence the activity of widespread regions of the central nervous system. However, no data are available regarding their physiological properties because of the paramount methodological difficulties raised by the small size of intercalated cell masses. Here, we have investigated the spontaneous and evoked activity of intercalated neurons in unanaesthetized, chronically implanted cats. Extracellular recording sites were identified using stringent histological criteria. The intercalated cell masses were found to contain a population of neurons firing at much higher rates than commonly observed in neighbouring amygdaloid nuclei. Individual intercalated neurons displayed state‐dependent changes in firing rates, but these varied from cell to cell. Most tested intercalated neurons displayed short‐latency orthodromic responses to cortical shocks and were responsive to a variety of auditory stimuli. Considering that the vast majority of intercalated neurons use γ‐aminobutyric acid (GABA) as a transmitter, the presence of neurons with high spontaneous firing rates within the intercalated cell masses suggests that these cell clusters may provide a tonic inhibitory input to their projection sites. Moreover, the fact that the firing probability of some intercalated neurons could be altered by the presentation of sensory stimuli suggests that this inhibitory input can be modulated as a function of environmental contingencies.