bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Adhesion Molecule on Glia (AMOG) Is Widely Expressed by Astrocytes in Developing and Adult Mouse Brain
Authors: Pagliusi S. R. , Schachner M. , Seeburg P. H. , Shivers B. D. 
Published: April 2006

AbstractAdhesion molecule on glia (AMOG) is a 45–50 kD cell surface glycoprotein structurally similar to the Na, K‐ATPase β‐subunit and associated with the catalytic subunit of this enzyme. Previous immunofluorescence results had suggested that AMOG is transiently expressed on Bergmann glia during mouse cerebellar development, and antibody‐inhibition results have implicated it in the migration of granule neurons. We report that, while AMOG mRNA is detected in Bergmann glia during the migratory period, this astrocyte derivative continues to express AMOG mRNA at similar levels in adult mice suggesting a functional role for AMOG in adulthood. Evidence from RNA and protein blot analyses that AMOG is present before birth, increasing about ten fold in adult mouse brain and cerebellum is also provided. RNA blot analysis of astrocyte‐enriched cell populations and in situ hybridization results show that astrocytes synthesize AMOG mRNA in all regions of the developing and adult brain. In the adult, AMOG mRNA is more abundant in grey than white matter and, among grey matter regions, highest in cerebellar cortex. These results indicate a relationship between density of neuronal elements and AMOG expression. It is further speculated that AMOG is part of a Na,K‐ATPase complex expressed preferentially by astrocytes in mouse brain.
B‐50/GAP43 Expression Correlates with Process Outgrowth in the Embryonic Mouse Nervous System
Authors: Biffo S. , Verhaagen J. , Schrama L. H. , Schotman P. , Danho W. , Margolis F. L. 
Published: April 2006

AbstractThe hypothesis that B‐50/GAP43, a membrane‐associated phosphoprotein, is involved in process outgrowth has been tested by studying the developmental pattern of expression of B‐50/GAP43 mRNA and protein during mouse neuroembryogenesis. B‐50/GAP43 mRNA is first detectable at embryonic day 8.5 (E8.5) in the presumptive acoustico‐facialis ganglion. Subsequently, both B‐50/GAP43 mRNA and protein were co‐expressed in a series of neural structures: in the ventral neural tube (from E9.5) and dorsal root ganglia (from E10.5), in the marginal layer of the neuroepithelium surrounding the brain vesicles and in the cranial ganglia (from E9.5), in the autonomic nervous system (from E10.5), in the olfactory neuroepithelium and in the mesenteric nervous system (from E11.5), in a continuum of brain regions (from E12.5) and in the retina (from E13.5). Immunoreactive fibers were always seen arising from these regions when they expressed B‐50/GAP43 mRNA. The spatial and temporal pattern of B‐50/GAP43 expression demonstrates that this protein is absent from neuroblasts and consistently appears in neurons committed to fiber outgrowth. The expression of the protein in immature neurons is independent of their embryological origin. Our detailed study of B‐50/GAP43 expression during mouse neuroembryogenesis supports the view that this protein is involved in a process common to all neurons elaborating fibers.
Hippocampal Complex Spike Cells do not Change Their Place Fields if the Goal is Moved Within a Cue Controlled Environment
Authors: Speakman A. , O'Keefe J. 
Published: April 2006

AbstractIt has been shown that most hippocampal complex‐spike cells fire at specific locations in relation to a set of controlled spatial cues and that they continue to fire in the appropriate places when the cues are removed (O'Keefe and Conway, 1978; O'Keefe and Speakman, 1987). However, the goal remained in a constant position relative to the controlled cues throughout these experiments. It is therefore possible that the unit firing was related to the goal location and not to the controlled cues as was suggested. For example, firing in a particular location might signal the rat's intention to make a particular turn towards the goal from that location and not the location itself. There are many reasons for believing that this is an unlikely class of explanations; nevertheless a test of this hypothesis was undertaken in the present experiment. Nineteen place units were recorded from three rats as they performed the task of finding the goal location. After obtaining an accurate picture of the place fields in relation to the controlled cues and the goal, the location of the goal relative to the cues was moved and the animal retrained to the new goal. After the new goal was being consistently chosen, a second picture of the place fields of the same units was obtained. If the fields were related to the environment created by the cues then they would remain the same during the two stages of the experiment. If they were related to the goal, or to the intended movements towards the goal, then they would rotate relative to the cues. As expected, the majority of place fields remained in the same place in relation to the cues during the two stages of the experiment and were not influenced by the goal relocation. In only two cases was there any suggestion that the place fields changed their location after the goal was moved. It was concluded that the activity of place cells is related to an animal's location in an environment and that the results accord with cognitive map theory of hippocampal function (O'Keefe and Nadel, 1978).
Neural Transplantation in Animal Models of Dementia
Authors: Dunnett S. B. 
Published: April 2006

AbstractNeural transplantation provides a powerful novel technique for investigating the neurobiological basis and potential strategies for repair of a variety of neurodegenerative conditions. The present review considers applications of this technique to dementia. After a general introduction (section 1), attempts to replace damaged neural systems by transplantation are considered in the context of distinct animal models of dementia. These include grafting into aged animals (section 2), into animals with neurotransmitter‐selective lesions of subcortical nuclei, in particular involving basal forebrain cholinergic systems (section 3), and into animals with non‐specific lesions of neocortical and hippocampal systems (section 4). The next section considers the alternative use of grafts as a source of growth/trophic factors to inhibit degeneration and promote regeneration in the aged brain (section 5). Finally, a number of recent studies have employed transplanted tissues to model and study the neurodegenerative processes associated with ageing and Alzheimer's disease taking place within the transplant itself (section 6). It is concluded (section 7) that although neural transplantation does not offer any immediate prospect of therapeutic repair in clinical dementia, the technique does offer a powerful neurobiological tool for studying the neuropathological processes involved in both spontaneous degeneration and specific diseases of ageing. New understandings derived from neural transplantation may be expected to lead to rational development of novel strategies to inhibit the neurodegenerative process and to promote regeneration in the aged brain.
On the Role of Galanin, Substance P and Other Neuropeptides in Primary Sensory Neurons of the Rat: Studies on Spinal Reflex Excitability and Peripheral Axotomy
Authors: Xu X.‐J. , Wiesenfeld‐Hallin Z. , Villar M. J. , Fahrenkrug J. , Hökfelt T. 
Published: April 2006

AbstractThe interaction of intrathecally (i.t.) applied galanin (GAL) with substance P (SP), calcitonin gene‐related peptide (CGRP), vasoactive intestinal polypeptide (VIP), somatostatin (SOM) and C‐fibre conditioning stimulation (CS) with regard to their effects on the spinal nociceptive flexor reflex was studied in decerebrate, spinalized, unanaesthetized rats with intact or sectioned sciatic nerves. SP, CGRP, VIP and SOM applied onto the surface of lumbar spinal cord or a brief CS train (1 Hz, 20 s) to the sural nerve facilitated the flexor reflex for several minutes in animals with intact or sectioned nerves. Pretreatment with GAL, which by itself had a biphasic effect on the flexor reflex in a dose‐dependent manner, antagonized the reflex facilitation induced by sural CS before and after sciatic nerve section. SP‐induced facilitation of the flexor reflex was antagonized by GAL in rats with intact sciatic nerves, but not after nerve section. In contrast, VIP‐induced reflex facilitation was antagonized by GAL only after sectioning of the sciatic nerve. GAL was effective in antagonizing the facilitatory effect of CGRP under both situations, but had no effect on SOM‐induced facilitation. A parallel immunohistochemical study revealed that after sciatic nerve section GAL‐like immunoreactivity (LI) and VIP‐LI are increased in the dorsal root ganglia and that these two peptides coexist in many cells. The present results indicate that GAL antagonizes the excitatory effect of some neuropeptides which exist in the spinal cord. This antagonism could explain the inhibitory effect of GAL on C‐fibre CS‐induced facilitation of the flexor reflex, which is presumably due to the release of some of these neuropeptides from the terminals of primary afferents. Furthermore, the interaction between GAL and other neuropeptides is altered by sciatic nerve section, paralleling changes in the levels of these neuropeptides in primary afferents and their pattern of coexistence after nerve section. It is proposed that SP and CGRP are important mediators of the spinal flexor reflex in intact rats. However, after axotomy VIP may replace SP in this capacity, paralleling the decrease in SP and marked increase in VIP levels. In general the study provides further support for involvement of peptides in sensory function.
Amoeboid Microglial Cells and not Astrocytes Synthesize TNF‐α in Swiss Mouse Brain Cell Cultures
Authors: Hetier Emmanuelle , Ayala Jésus , Bousseau Anne , Denèfle Patrice , Prochiantz Alain 
Published: April 2006

AbstractThe role of tumour necrosis factor (TNF‐α) in brain physiology and pathology has been the focus of several studies. However, the source of this lymphokine in the central nervous system and the regulation of its synthesis is still poorly understood. We have therefore used purified astrocytes and brain macrophages in culture to compare the abilities of these two cell types to synthesize TNF‐α and its mRNA. We find that, in the Swiss mouse, no significant TNF activity or TNF‐α mRNA are produced by astrocytes, even following activation with lipopolysaccharides (LPS). On the other hand, purified microglial cells express a cytotoxic activity able to kill TNF‐sensitive LM cells. Part of this activity is released into the culture medium and part remains bound to the membrane after mild paraformaldehyde treatment, demonstrating the existence in the culture of the soluble and membrane‐bound forms of TNF activity. The fact that amoeboid microglial cells, and not astrocytes, are the actual source of TNF in brain cultures was further demonstrated by Northern blot analysis and in situ hybridization using a TNF‐α specific oligonucleotide probe. The definition of the cell type which, in the CNS, is responsible for TNF synthesis will allow the regulation of this lymphokine to be analysed and opens the way for a better understanding of the interactions between amoeboid microglial cells and the other cell types which make up the nervous system.
Endothelin Induces a Rise of Inositol 1,4,5‐Trisphosphate, Inositol 1,3,4,5‐Tetrakisphosphate Levels and of Cytosolic Ca2+ Activity in Neural Cell Lines
Authors: Reiser Georg , Donié Frédéric 
Published: April 2006

AbstractThe mechanism of action of the vasoconstricting peptide endothelin was investigated in two neural cell lines. In rat glioma cells endothelin‐1 caused a biphasic rise in cytosolic Ca2+ activity. A large peak of 40 s duration was followed by another, however smaller, transient rise of comparable duration. In the absence of extracellular Ca2+ only the first peak was detected. Pretreatment with Ca2+ ionophores suppressed the Ca2+ response to endothelin. At the concentrations used the Ca2+ ionophores primarily deplete internal Ca2+ stores and prevent their refilling. Measurements of 45Ca2+ fluxes corroborate the conclusion that in the glioma cells endothelin induces firstly a release of Ca2+ from internal stores and subsequently a stimulation of Ca2+ entry. In neuronal cells (mouse neuroblastoma × rat glioma hybrid cells), endothelin caused a monophasic rise in cytosolic Ca2+ activity, most likely due to release from internal stores. In the glioma cells the concentrations of both inositol 1,4,5‐trisphosphate and inositol 1,3,4,5‐tetrakisphosphate were raised about 2.5‐fold for ca. 90 s after addition of endothelin. In the neuronal cells a shorter, smaller rise in inositololigophosphate concentrations was induced. Thus, endothelin seems to act as a neuropeptide activating phospholipase C and intracellular Ca2+.
Glucocorticoid Hormones Negatively Regulate Nerve Growth Factor Expression In Vivo and in Cultured Rat Fibroblasts
Authors: Lindholm Dan , Hengerer Bastian , Heumann Rolf , Carroll Patrick , Thoenen Hans 
Published: April 2006

AbstractSciatic nerve transection leads to an up‐regulation of nerve growth factor (NGF) production in non‐neuronal cells surrounding the axons. The lesion‐mediated increase in NGF‐mRNA levels in the nerve can be blocked by pretreating the animals with the synthetic glucocorticoid dexamethasone. Dexamethasone also reduces NGF‐mRNA levels in cultured sciatic fibroblasts stimulated with fetal calf serum or interleukin‐1. In order to study at which level glucocorticoids down‐regulate NGF expression, sciatic fibroblasts where transfected with a construct in which a reporter gene (chloramphenicol acetyltransferase) is expressed under the control of the NGF promotor. The results demonstrated that dexamethasone effectively represses NGF gene transcription. Deletion experiments showed that a 162 nucleotide promotor region mediates the glucocorticoid hormone suppression of NGF expression. The negative regulation of NGF synthesis by glucocorticoids is a factor to be considered in the treatment of patients with peripheral nerve lesions.
Feedback Inhibition of Ca2+ Currents by Dopamine in Glomus Cells of the Carotid Body
Authors: Benot A. R. , López‐Barneo J. 
Published: April 2006

AbstractThe effect of dopamine on the voltage‐dependent ionic channels of enzymatically dispersed glomus cells from rabbit carotid bodies was studied. Whole‐cell currents were recorded on isolation with patch electrodes and dopamine applied to the bath solution. Dopamine at nanomolar concentrations produced a reversible attenuation of the calcium current whereas sodium and potassium currents remained unaltered. Dopamine inhibition of Ca2+ current was observed in all cells tested (n= 48) and at a saturating concentration (1μM) the average reduction was of 40 ± 6.5% (n= 8). The effect of dopamine was probably caused by a decrease in the number of channels activatable on depolarization since it did not modify the voltage‐dependent parameters of the current. These results indicate that dopamine, which is the major transmitter secreted by glomus cells, regulates further transmitter release by feedback inhibition of Ca2+ channels.
Opposed Behavioural Outputs of Increased Dopamine Transmission in Prefrontocortical and Subcortical Areas: A Role for the Cortical D‐1 Dopamine Receptor
Authors: Vezina P. , Blanc G. , Glowinski J. , Tassin J.‐P. 
Published: April 2006

AbstractThe possibility that the dopaminergic neurons innervating the medial prefrontal cortex (mPFC) can inhibit locomotor behaviour has been suggested in several studies. The evidence remains indirect, however, because the manipulations tested aimed exclusively at permanently depleting mPFC dopamine. Here we demonstrate in rats that acute increases in dopamine transmission in this site by local injections of amphetamine inhibit the known locomotor‐activating effects of amphetamine in the nucleus accumbens (N.Acc). Further, intra‐mPFC injections of the D‐1 dopamine receptor antagonist SCH‐23390, but not other dopamine antagonists with greater affinities for noradrenergic, serotonergic and D‐2 dopamine receptors, enhanced the locomotion induced by intra‐N.Acc. amphetamine. These findings provide direct evidence for the inhibition of locomotor activity by mPFC dopamine and suggest that it is acting at D‐1 dopamine receptors in this site.
Binocular Interactions in the Lateral Suprasylvian Visual Area of Strabismic Cats Following Section of the Corpus Callosum
Authors: Di Stefano M. , Lepore F. , Ptito M. , Bédard S. , Marzi C. A. , Guillemot J. P. 
Published: April 2006

AbstractVisually responsive neurons have been recorded in the lateral suprasylvian area (LSA) of cats raised with either a convergent or a divergent strabismus. In contrast to areas 17 and 18, where many studies have documented a profound loss of binocularly activated neurons following early strabismus, in the LSA the majority of cells could still be binocularly driven. Acute or chronic section of the splenium of the corpus callosum reduced but did not abolish binocularity in the LSA. We propose that the widespread callosal connections, the large size of the receptive fields and the peculiar internal circuitry of the LSA all concur in permitting the maintenance of binocular coding in spite of early misalignment of the eyes.
Ca2+ Mobilization in Cultured Rat Cerebellar Cells: Astrocytes are Activated by t‐ACPD
Authors: de Barry Jean , Ogura Akihiko , Kudo Yoshihisa 
Published: April 2006

AbstractUsing primary rat cerebellar cell cultures we observed that trans‐1‐amino‐cyclopentyl‐1, 3‐dicarboxylic acid (t‐ACPD) was able to induce an increase in intracellular [Ca2+] in different cell types. This response was not abolished by external Ca2+ withdrawal, indicating that t‐ACPD triggered the release of intracellularly stored Ca2+. In neurons the t‐ACPD response was monophasic and inhibited by L‐2‐amino‐4‐phosphonobutyrate (APB). In astrocytes, characterized by their immunoreactivity to antisera to glial fibrillary acidic protein and S‐100 protein, the response was oscillatory and resistant to APB application. These results suggest the presence of glutamate metabotropic receptor subtypes in the mammalian brain.
Topographical Aspects of Intracortical Excitation and Inhibition Contributing to Orientation Specificity in Area 17 of the Cat Visual Cortex
Authors: Wörgötter Florentin , Eysel U. T. 
Published: April 2006

AbstractIntracortical mechanisms contributing to orientation and direction specificity were investigated with a method of local cortical inactivation. Single‐unit activity was recorded in area 17 of the anaesthetized cat while a small volume of cortical tissue 400–2900 μm lateral to the recorded cell was inactivated by γ‐aminobutyric acid (GABA) microiontophoresis. Cells were stimulated with moving bars of variable orientation and changes of the response were monitored. Recording and inactivation sites were histologically verified. Statistically significant changes in orientation tuning during GABA‐induced remote inactivation were observed in 80 of 145 cells (55%), and consisted in a reduced orientation specificity due to either increased (36%) or decreased (19%) responses. Increases of responses were more pronounced for the non‐optimal orientations. This effect mainly occurred with GABA application at distances around 500 μm and is interpreted as loss of inhibition. Reduced orientation specificity as a result of decreasing response mainly to the optimal orientation was interpreted as loss of excitation. This effect most frequently occurred with inactivation at distances around 1000 μm. Loss of inhibition was also elicited from a distance of 1000μm; such inhibition, however, affected only directionality, without inducing changes in orientation tuning. For several cells at distances <1000 μm from the inactivation site a temporal sequence consisting of a change in direction specificity followed by a reduction of orientation specificity, and finally by direct GABAergic inhibition of the cell under study, could be induced with gradually increasing ejecting currents. The results indicate that excitation and inhibition originating from populations of neurons at different horizontal distances differentially contribute to direction and orientation specificity of a given visual cortical cell.
Long Survival of Retinal Ganglion Cells in the Cat After Selective Crush of the Optic Nerve
Authors: Cottee Lynne J. , FitzGibbon T. , Westland K. , Burke W. 
Published: April 2006

AbstractIn each of four cats gentle pressure was applied to one optic nerve by means of an inflatable cuff in order to disrupt the largest axons (Y fibres) and so produce a conduction block in them. It has previously been shown that this technique, as used by us, causes Wallerian degeneration in the fibres posterior to the site of application of the pressure (the crush site). The optic nerves and retinas in these cats were examined 2–2.8 years later. The optic nerves were prepared for electron microscopy and the retinas were flat‐mounted. Here we report an average 90% loss of large axons (>5 μm diameter) in the nerve posterior to the crush site. However, in the part of the nerve anterior to the crush site there was only a 33% loss and in the retina only a 57.5% reduction in the number of neurons of soma diameter >25 μm (i.e. alpha cells, the cell bodies of the Y neurons). These last two sets of values were significantly different, suggesting that the retinal ganglion cells had shrunk relatively more than the axons. Thus, the crushing technique has effectively axotomized almost all the Y fibres but, in spite of this, about half of the alpha retinal ganglion cells have survived this particular form of axotomy, with their axons intact at least for some distance into the optic nerve. This long survival raises the possibility that these neurons may have regenerated axons which have found targets and thus ensured their survival.
Outward Currents in Rat Entorhinal Cortex Stellate Cells Studied with Conventional and Perforated Patch Recordings
Authors: Eder C. , Ficker E. , Gündel J. , Heinemann U. 
Published: April 2006

AbstractWe have studied outward currents of neurons acutely isolated from superficial layers of the entorhinal cortex with whole‐cell patch‐clamp recordings. If cells were held more negative than ‐50 mV, depolarizing voltage commands activated a transient A‐type current together with a sustained outward current. Both currents were sensitive to 4‐aminopyridine, while only the sustained current was blocked by tetraethylammonium. The sustained outward current showed a considerable rundown in amplitude over prolonged recording periods. At the same time its half‐maximal inactivation shifted from ‐74 to ‐ 114 mV. Nystatin perforated patch recordings were used to minimize these perfusion effects. Under such conditions the amplitude and the steady‐state inactivation properties of the sustained outward current remained stable for more than 1 h. Pharmacological investigations revealed that only a small part of the sustained outward current could be attributed to a calcium‐activated potassium current. Therefore most of the rundown has to be due to changes in the delayed rectifier outward current. These results may suggest that the delayed rectifier current is under considerable metabolic control.