bluuebunny/crossref_metadata_2025_split huggingface dataset:
Further Studies on Motor and Sensory Nerve Regeneration in Mice With Delayed Wallerian Degeneration
Authors: Brown M. C. , Perry V. H. , Hunt S. P. , Lapper S. R. 
Published: April 2006

AbstractThe axons of both peripheral and central neurons in C57BL/Wlds (C57BL/Ola) mice are unique among mammals in degenerating extremely slowly after axotomy. Motor and sensory axons attempting to regenerate are thus confronted with an intact distal nerve stump rather than axon‐and myelin‐free Schwann cell‐filled endoneurial tubes. Surprisingly, however, motor axons in the sciatic nerve innervating the soleus muscle regenerate rapidly, and there is evidence that they may use Schwann cells associated with unmyelinated fibres as a pathway. If this is so, motor axon regeneration might be impaired in C57BL/Wlds mice in the phrenic nerve, which has very few unmyelinated fibres. We found that as long as the myelinated axons in the distal stump of the phrenic nerve remained intact (up to 10 days), regeneration of motor axons did not occur, in spite of vigorous production of sprouts at the crush site. In contrast to motor axons, myelinated sensory axons regenerate very poorly in C57BL/Wlds mice, even in the presence of unmyelinated axons. We showed that this was also due to adverse local conditions confronting nerve sprouts, for the dorsal root ganglion cell bodies responded normally to injury with a rapid induction of Jun protein‐like immunoreactivity and when the saphenous nerve was forced to degenerate more rapidly by multiple crush lesions sensory axons regrew much more successfully. The findings show that motor and sensory axons in C57BL/Wlds mice, although very atypical in the way that they degenerate, are able to regenerate normally but only in an appropriate environment. The results also give support to the view that intact peripheral nerves either fail to encourage or actively inhibit axon growth, and that an unsuitable local environment can prevent regeneration even if the cell body is reacting normally to injury.
Differential Foci and Synaptic Organization of the Principal and Spinal Trigeminal Projections to the Thalamus in the Rat
Authors: Williams Matthew N. , Zahm Daniel S. , Jacquin Mark F. 
Published: April 2006

AbstractThe thalamus is known to receive single‐whisker ‘lemniscal’ inputs from the trigeminal nucleus principalis (Prv) and multiwhisker ‘paralemniscal’ inputs from the spinal trigeminal nucleus (Spv), yet the responses of cells in the thalamic ventroposteromedial nucleus (VPM) are most similar to and contingent upon inputs from PrV. This may reflect a differential termination pattern, density and/or synaptic organization of PrV and SpV projections. This hypothesis was tested in adult rats using anterograde double‐labelling with fluorescent dextrans, horseradish peroxidase (HRP) and choleragenoid, referenced against parvalbumin and calbindin immunoreactivity. The results indicated that Prv's most robust thalamic projection is to the whisker‐related barreloids of VPM. The SpV had robust projections to non‐barreloid thalamic regions, including the VPM ‘shell’ encapsulating the barreloid area, a caudal and ventral region of VPM that lacks barreloids and PrV inputs, the posterior thalamic nucleus, nucleus submedius and zona incerta. Within the barreloid portion of VPM, SpV projections were sparse relative to those from PrV, and most terminal labelling occurred in the peripheral fringes of whisker‐related patches and in inter‐barreloid septae. Thus, PrV and SpV have largely complementary projection foci in the thalamus. Intra‐axonal staining of a small sample of trigeminothalamic axons with whisker or guard hair receptive fields revealed highly localized and somatotopic terminal aggregates in VPM that spanned areas no larger than that of a single barreloid. In the electron microscopic component of this study, HRP transport to the barreloid region of VPM from left SpV and right PrV in the same cases revealed PrV terminals contacting dendrites with a broad range of minor axis diameters (mean ± SD: 1. 51 ± 0. 10 μm). SpV terminals were indistinguishable from those of PrV, but they had a disproportionate number of contacts on narrow dendrites (1. 27 ± 0. 07 μm, P 0. 01). PrV endings were also more likely to contact VPM somata (11. 0 ± 4. 2% of all labelled terminals) than those from SpV (3. 0 ± 1. O%, P 0. 01). Insofar as primary dendrites are thicker than distal dendrites in VPM, these data suggest a differential distribution of PrV and SpV inputs onto VPM cells that may account for their relative efficacies in dictating the responses of VPM cells to whisker stimulation. Multiwhisker receptive fields in VPM may also reflect direct transmission of convergent inputs from PrV.
LGN‐projecting Neurons of the Cat's Pretectum Express Glutamic Acid Decarboxylase mRNA
Authors: Wahle Petra , Stuphorn V. , Schmidt M. , Hoffmann K.‐P. 
Published: April 2006

AbstractThere have been conflicting reports on the chemical nature of the projection of the pretectal nuclei [nucleus of the optic tract and dorsal terminal nucleus of the accessory optic tract (NOT DTN complex) and posterior pretectal nucleus] to the lateral geniculate nucleus and inferior olive. There is evidence that the pretecto‐geniculate pathway is inhibitory. However, most attempts to verify the GABAergic nature of the projection neurons have failed. In order to answer this question, we employed a combination of retrograde transport and in situ hybridization. Rhodamine‐labelled latex microspheres were injected into the electrophysiologically identified lateral geniculate nucleus. In addition, fluorescein‐labelled latex microspheres were injected into the inferior olive. Retrograde axonal transport labelled large pretectal neurons. We then applied riboprobes specific for glutamic acid decarboxylase mRNA. We were able to demonstrate glutamic acid decarboxylase mRNA expression in up to 70% of lateral geniculate nucleus‐projecting NOT‐DTN and posterior pretectal nucleus neurons but in none of the pretecto‐olivary projection neurons. The results suggest that the pretecto‐geniculate projection is GABAergic in nature, which would confirm previous electrophysiological and morphological observations. The pretecto‐olivary projection is not GABAergic.
The Effect of Cycloheximide and Ganglioside GM1 on the Viability of Retinotectally Projecting Ganglion Cells Following Ablation of the Superior Colliculus in Neonatal Rats
Authors: Harvey A. R. , Cui Q. , Robertson D. 
Published: April 2006

AbstractThe time‐course and extent of death of retinal ganglion cells (RGCs) following ablation of the superior colliculus (SC) in neonatal Wistar rats has recently been described [Harvey, A. R. and Robertson, D. (1992) J. Comp. Neurol., 325, 83–94]. Normal and pyknotic nuclei of retinotectally projecting ganglion cells were visualized using the fluorescent retrograde tracer diamidino yellow (DY), which had been injected into the SC at P2 (day of birth = P0), 2 days prior to tectal removal. The present report sets out to determine whether cycloheximide, an inhibitor of protein synthesis, or ganglioside GM1 reduced this lesion‐induced RGC death. All surgery was carried out under ether anaesthesia; DY was injected into the left SC at P2 and the injected area was removed at P4. Cycloheximide (20‐500 ng) was injected into the vitreous chamber of the right eye immediately after the lesion and again 11 ‐12 h later. In some rats, cycloheximide administration was delayed until 12 h after the SC ablation. Control rats received SC lesions alone or lesions plus sham eye injections of saline. Different doses of GM1 were applied i.p. or intraocularly. Rats were perfused 24 h after the SC lesion, at the time of peak RGC death. Retinae of lesion only or sham eye injected rats contained ‐11% pyknotic RGCs and the density of normal RGCs was ‐3400/mm2. The rate of pyknosis in cycloheximide treated retinae was reduced to ‐3%. Normal RGC density in these retinae was ∼5500/mm2, similar to that found in retinae of unlesioned animals. Delaying the application of cycloheximide significantly reduced its effectiveness in preventing RGC death. GM1 treatments had no, or only minor, impact on RGC pyknosis 24 h after SC removal. The data are consistent with the proposal that RGC death after neonatal loss of central target sites is an active process that requires protein synthesis. It is therefore possible that, in the developing mammalian visual system, target‐derived neurotrophic factors maintain RGC viability by suppressing some form of endogenous suicide program within the neurons.
Inhibition of Neuronal Activity in the Nucleus of the Optic Tract due to Electrical Stimulation of the Medial Terminal Nucleus in the Rat
Authors: van der Togt Chris , Schmidt Matthias 
Published: April 2006

AbstractMorphologically, a GABAergic connection between the medial terminal nucleus of the accessory optic system and the nucleus of the optic tract, two primary visual nuclei involved in the optokinetic reflex, has been demonstrated. In this study it was investigated if the medial terminal nucleus forms an inhibitory input to movement direction selective units in the nucleus of the optic tract. Neurons in the nucleus of the optic tract were visually stimulated with moving large random square patterns in their preferred and non‐preferred direction, and their activity was recorded extracellularly. Concomitantly, bipolar electrical stimulation was applied to the medial terminal nucleus and its effect was studied on the visual responses of units in the nucleus of the optic tract. Units in the nucleus of the optic tract were strongly inhibited during electrical stimulation of the medial terminal nucleus. The role of GABA in mediating this inhibition was investigated by applying bicuculline, a GABAA receptor antagonist, iontophoretically to the recorded units in the nucleus of the optic tract. However, although average spike rate levels of units in the nucleus of the optic tract increased with bicuculline, bicuculline did not reduce inhibition invoked by electrical stimulation of the medial terminal nucleus. A possible explanation for this observation is that this inhibition is GABAB receptor mediated.
Distribution of Glutamatergic Receptors and GAD mRNA‐Containing Neurons in the Vestibular Nuclei of Normal and Hemilabyrinthectomized Rats
Authors: de Waele C. , Abitbol M. , Chat M. , Menini C. , Mallet J. , Vidal P. P. 
Published: April 2006

AbstractVestibular compensation is an attractive model for investigations of cellular mechanisms underlying post‐lesional plasticity in the adult central nervous system. Immediately after hemilabyrinthectomy, the spontaneous activity in the deafferented second‐order vestibular neurons falls to zero, resulting in a strong asymmetry between the resting discharge of the vestibular complexes on the lesioned and intact sides. This asymmetry most probably causes the static and dynamic vestibular deficits observed in the acute stage. After ∼50 h, the deafferented vestibular neurons recover a quasi‐normal resting activity which is thought to be the key of the compensation of the static vestibular syndromes. However, the molecular mechanisms underlying this recovery are unknown. In this study, we investigate possible changes in the distribution of glutamatergic N‐methyl‐d‐aspartate (NMDA) and glutamate metabotropic receptors and of glutamate decarboxylase 67k (GAD 67k) mRNAs in the deafferented vestibular neurons induced by the labyrinthine lesion. Specific radioactive oligonucleotides were used to probe sections of rat vestibular nuclei according to in situ hybridization methods. Animals were killed at different times (5 h, 3 days and 3 weeks) following the lesion. Signal was detected by means of film or emulsion autoradiography. In the normal animals, several brainstem regions including the medial, lateral, inferior and superior vestibular nuclei were densely labelled by the antisense oligonucleotide NMDAR1 probe. However, the vestibular nuclei were not labelled by the glutamate metabotropic oligonucleotide antisense probe (mGluR 1). The GAD 67k antisense oligonucleotide probe labelled numerous small‐ to medium‐sized central vestibular neurons but not the larger cell bodies in the lateral vestibular nucleus. This agrees with previous studies. In the hemilabyrinthectomized rats, no asymmetry could be detected, at either the autoradiographic or cellular levels, between the two medial vestibular nuclei whatever the probe used and whatever the delay following the lesion. However, for the NMDAR1 probe, the mean density of silver grains in both the deafferented and intact medial vestibular neurons was 20% lower 5 h after the lesion. Three days and 3 weeks later, the intensity of labelling over all cells was the same as in the control group. Further studies are necessary to confirm the relatively weak modification of the NMDAR1 mRNAs expression and to exclude a change of GAD 65 and of other NMDA subunit mRNAs during the vestibular compensation process.
Morphological and Molecular Characterization of the Response of Differentiated PC12 Cells to Calcium Stress
Authors: Michel Patrick P. , Vyas Sheela , Anglade Philippe , Ruberg Merle , Agid Yves 
Published: April 2006

AbstractThe mechanisms that lead ultimately to neuronal death in pathological ageing of the brain remain mostly unknown as in the case of Parkinson's disease where there is a progressive and selective loss of dopaminergic neurons within the substantia nigra. Dopamine‐expressing PC12 cells that were neuronally differentiated by nerve growth factor treatment were chosen as a culture model in which to study some of the changes that may occur during the course of the degenerative process. They were exposed to the calcium ionophore A23187 in order to produce a sustained rise in cytoplasmic calcium, a phenomenon related to various pathological conditions. The degenerative effects of the ionophore were dose‐ and time‐dependent. They were characterized by early fragmentation of the neurites followed ultimately by a loss in cell viability. Biochemical changes, such as a decrease in [3H]dopamine uptake and modulations of the tyrosine hydroxylase gene, were detected before macroscopic evidence of cell suffering (e.g. neurite fragmentation) could be observed. Although an ongoing degenerative process was occurring in cell somata, PC12 cells were able to recover upon ionophore withdrawal. Characteristics of apoptosis such as chromatin condensation and DNA fragmentation were detectable in a small population of dying cells. DNA fragmentation could be prevented by the endonuclease inhibitor aurintricarboxylic acid. New protein synthesis was not required, as cycloheximide failed to prevent degeneration. Taken together, these results suggest that differentiated PC12 cells react to calcium stress through a sequence of regulatory processes which appears to be independent of the apoptotic pathway.
Properties of Single Calcium‐activated Potassium Channels of Large Conductance in Rat Hippocampal Neurons in Culture
Authors: Wann K. T. , Richards C. D. 
Published: April 2006

AbstractPatch‐clamp recordings were made on rat hippocampal neurons maintained in culture. In cell‐attached and excised inside‐out and outside‐out patches a large single‐channel current was observed. This channel had a conductance of 220 and 100 pS in 140 mM [K+]i/140 mM [K+]o and 140 mM [K+]i/3 mM [K+]o respectively. From the reversal potential the channel was highly selective for K+, the PK+/Pna+ ratio being 50/1. Channel activity was voltage‐dependent, the open probability at 100 mM [Ca2+]i increasing by e‐fold for a 22 mV depolarization. It was also dependent on [Ca2+]i at both resting and depolarized membrane potentials. Channel open states were best described by the sum of two exponentials with time constants that increased as the membrane potential became more positive. Channel activity was sensitive to both external (500 μM) and internal (5 mM) tetraethylammonium chloride. These data are consistent with the properties of maxi‐K+ channels described in other preparations, and further suggest a role for maxi‐channel activity in regulating neuronal excitability at the resting membrane potential. Channel activity was not altered by 8‐chlorophenyl thio cAMP, concanavalin A, pH reduction or neuraminidase. In two of five patches lemakalim (BRL 38227) increased channel activity. Internal ruthenium red (10 μM) blocked the channel by shortening the duration of both open states. This change in channel gating was distinct from the ‘mode switching’ seen in two patches, where a channel switched spontaneously from normal activity typified by two open states to a mode where only short openings were represented.
Hypothalamo‐preoptic Histaminergic Projections in Sleep‐Wake Control in the Cat
Authors: Lin J. S. , Sakai K. , Jouvet M. 
Published: April 2006

AbstractCats were chronically implanted with electrodes for polygraphic recordings and cannulae for intracerebral microinjections in order to study the functional role of histaminergic innervation of the preoptic‐anterior hypothalamus in sleep‐wake control. α‐Fluoromethylhistidine (αFMH, 50 μg in 1 μl), a specific inhibitor of the histamine‐synthesizing enzyme, when injected bilaterally into the preoptic area, where numerous histaminergic fibres and terminal‐like structures are present, caused a significant increase in deep slow wave sleep (S2) and paradoxical sleep (PS) and a decrease in wakefulness. In contrast, microinjections of histamine (5 or 30 μg in 1 μl) in the same area dose‐relatedly increased wakefulness and decreased both slow wave sleep and paradoxical sleep. The effects of histamine were reduced by pretreatment with mepyramine (1 mg/kg i. p.), a well known histamine H1receptor antagonist, and were mimicked by a local injection of impromidine (1 μg in 1 μl), a potent histamine H2receptor agonist. Microinjections of mepyramine alone (120 μg in 1 μl) caused an increase in slow wave sleep. These results suggest that preoptic histaminergic innervation is involved in sleep‐wake control and that the action might be mediated via both H1and H2receptors.
Retrograde Axonal Transport of the α‐Subunit of the GTP‐binding Protein Gz in Mouse Sciatic Nerve: a Potential Pathway for Signal Transduction In Neurons
Authors: Crouch Michael F. , Heydon Katharina , Garnaut Sonja M. , Milburn Peter J. , Hendry Ian A. 
Published: April 2006

AbstractWe have utilized antibodies against the α subunit of Gz in fluorescence immunohistochemistry to determine whether this GTP‐binding protein can translocate along nerves by intra‐axonal transport. After ligation of the mouse sciatic nerve we found an increase in Gz‐like immunoreactivity on the proximal and distal side with time, suggesting that the α subunit undergoes orthograde axonal transport and also returns to the cell body by retrograde axonal transport in the sciatic nerve. Unlike the retrograde transport of Giα, shown in a previous study to be present in most sciatic axons, Gzα only accumulated in a subpopulation of axons, suggesting that different G‐proteins could convey information specific to neuronal subtypes. These results support our proposal that Gz may play a second messenger role in communicating information from the terminals back to cell bodies. Giαand Gzα may be representative of relatively stable signalling molecules by which the signal from some neurotrophic molecules can be translocated from the neuronal periphery to the cell body without the need for the retrograde transport of the neurotrophic factor itself.
A Neuromagnetic Study of the Functional Organization of the Sensorimotor Cortex
Authors: Kristeva‐Feige R. , Walter H. , Lütkenhöner B. , Hampson S. , Ross B. , Knorr U. , Steinmetz H. , Cheyne D. 
Published: April 2006

AbstractMovement‐related neuromagnetic fields from eight healthy human subjects were investigated in a Bereitschaftspotential paradigm. The three conditions studied were right‐sided mouth, index finger and foot movement. The neuromagnetic field patterns corresponding to the motor field and the movement‐evoked field I were analysed using a moving dipole model. For both components a somatotopic organization was found: the estimated dipole locations for the mouth were more lateral and those for the foot more medial than the estimated dipole positions for the index finger movement. With regard to possible clinical applications, e.g. non‐invasive mapping of the sensorimotor cortex and studies of plasticity of the motor function, the present results suggest that the investigation of movement‐evoked field I for the index finger condition is most likely to yield further results.
Melanin and the Regulation of Mammalian Photoreceptor Topography
Authors: Jeffery Glen , Darling Katherine , Whitmore Alan 
Published: April 2006

AbstractMelanin, or products directly associated with it, regulates the maturation of the neural retina because in hypopigmented mammals the central retina fails to develop fully. To determine whether this deficit is reflected in the distribution of photoreceptors, their topography has been studied in the retinae of normally reared pigmented and albino ferrets and animals reared under reduced light conditions. In both strains, the general distribution of rods and cones was similar to that in the cat, cone density peaking in the central retina and rod density peaking in an annulus around the area centralis. The cone population was organized in the form of an orderly mosaic whose regularity was measured at a wide range of retinal eccentricities. No differences were found in cone numbers or their mosaic distribution between pigmented and albino strains, either at the area centralis or at more peripheral regions. In both cases order within the cone mosaic was independent of cell density or retinal eccentricity. In the albinos there was a significant deficit in the number of rods at all retinal locations when compared with rod numbers in the pigmented animals. There were no differences between normally reared and dark‐reared animals in this respect either within or between the strains. Therefore, the albino gene must have a selective and specific effect on the development of this cell type in the outer retina. Ganglion cells and rods are both affected by the albino gene, while cones are not. Because cones and ganglion cells are generated during the same period and rods are generated later, the albino gene cannot be acting during a particular developmental time window. Because the cone mosaic was normal in the albinos, in spite of a large rod deficit, the factors that regulate the spacing of cones cannot depend in any significant manner upon the later generation and subsequent addition of rods to the outer retina.