bluuebunny/crossref_metadata_2025_split huggingface dataset:
Complementary Distribution of Calbindin D‐28k and Parvalbumin in the Basal Forebrain and Midbrain of the Squirrel Monkey
Authors: Côté Pierre‐Yves , Sadikot Abbas F. , Parent André 
Published: April 2006

AbstractThe distribution of cell bodies expressing either calbindin D‐28k or parvalbumin immunoreactivity in the basal forebrain and midbrain of squirrel monkeys (Saimiri sciureus) was studied on contiguous sections incubated with monoclonal antibodies raised against calbindin or parvalbumin. In the nucleus accumbens, medium‐sized calbindin‐positive neurons formed two cell bridges joining the ventral part of the striatum to the olfactory tubercle, whereas medium‐sized parvalbumin‐positive cells in the same area were much less numerous and more uniformly distributed. The medial and dorsal septal nuclei contained a small number of elongated calbindin‐positive neurons and only a few parvalbumin‐immunoreactive cells. In the nucleus of the diagonal band of Broca, calbindin and parvalbumin were found to label two distinct but closely intermingled neuronal populations. In the striatum, medium‐sized calbindin‐immunoreactive cells occurred in very large numbers and appeared to be confined to the extrastriosomal matrix. Medium‐sized, parvalbumin‐immunoreactive neurons were also present in the striatum but they were less numerous than the calbindin‐positive cells. The calbindin‐positive neurons in the dorsal portion of the striatum were less intensely stained than those in the ventral portion, whereas this pattern did not occur for neurons expressing parvalbumin immunoreactivity. At the pallidal level, neurons in both segments were devoid of calbindin but displayed a very strong parvalbumin immunoreactivity. Most of the large neurons of the nucleus basalis of Meynert were strongly calbindin‐immunoreactive and many of them invaded dorsally the medullary laminae of the pallidal complex. The neurons of the subthalamic nucleus were markedly enriched with parvalbumin but displayed only light calbindin staining. In the substantia nigra/ventral tegmental area complex, calbindin‐immunoreactive cells abounded in the ventral tegmental area and in the dorsal tier of the pars compacta of the substantia nigra, but were absent in the ventral tier of the pars compacta and in the entire pars reticulata of the substantia nigra. In contrast, numerous parvalbumin‐immunoreactive neurons occurred in the pars reticulata and pars lateralis, but none were found in the pars compacta and ventral tegmental area. These findings reveal that the patterns of calbindin and parvalbumin distribution in primate basal forebrain and midbrain are strikingly complementary, suggesting a synergistic role for these calcium‐binding proteins in basal forebrain and midbrain function.
Serotonin Reinnervation of the Suprachiasmatic Nucleus by Intrahypothalamic Fetal Raphe Transplants, with Special Reference to Possible Influences of the Target
Authors: Daszuta Annie , Marocco Céile , Bosler Olivier 
Published: April 2006

AbstractSurvival and development of fetal serotonin (5‐HT) neurons grafted to various brain areas in adult mammals have been suggested to be under host influences. The aim of this study was to determine whether the suprachiasmatic nucleus of the hypothalamus (SCN), a region receiving a 5‐HT input which is one of the densest and the most heavily synaptic in the brain, can actually support the development of transplanted 5‐HT neurons. The time course and extent of 5‐HT reinnervation were therefore investigated with 5‐HT immunocytochemistry in adult rats subjected to intraventricular injection of 5,7‐dihydroxytryptamine and subsequent grafting of fetal cell suspension of mesencephalic raphe neurons. The ultrastructural features of the newly formed 5‐HT terminal plexa were also examined. Serotonin reinnervation of the SCN remained partial up to 4 months post‐transplantation, with no apparent predilection of the reinnervating fibres for any particular portion of the nucleus, thus differing from the normal 5‐HT innervation of the SCN both quantitatively and qualitatively. This was in sharp contrast to the 5‐HT hyperinnervation observed in neighbouring areas such as the supraoptic nucleus, a structure normally provided with only few 5‐HT fibres, and the ventral wall of the third ventricle. The graft‐derived 5‐HT‐axons, however, displayed ultrastructural features that did not appear different from those of their normal counterparts; in particular they re‐established defined synaptic contacts with the host population. These results may indicate that the mature SCN specifically lacks a trophic factor necessary for the ingrowth of graft‐derived 5‐HT fibres, or that it represents an inhibitory environment for such an ingrowth. The limited ability of regrowing 5‐HT axons to restore a normal density of 5‐HT innervation could also be related to the fact that these neurons normally establish a relatively high number of synaptic contacts in the target region.
The Distribution of μ and δ Opioid Binding Sites Belonging to a Single Cervical Dorsal Root in the Superficial Dorsal Horn of the Rat Spinal Cord: A Quantitative Autoradiographic Study
Authors: Besse D. , Lombard M. C. , Besson J. M. 
Published: April 2006

AbstractNumerous studies have demonstrated a dense concentration of opioid receptors in the superficial layers (laminae I‐II) of the spinal cord. These receptors are located both pre‐ and postsynaptically at this level. The purpose of this study was to assess the distribution of opioid receptors belonging to a single (C7) dorsal root. Thus, quantitative autoradiography of γ ([3H]Tyr‐d‐Ala‐Gly‐NMe‐Phe‐Gly‐ol; [3H]DAMGO) and δ ([3H]Tyr‐d‐Thr‐Gly‐Phe‐Leu‐Thr; [3H]DTLET) opioid binding sites was performed for several experimental groups: control rats with intact dorsal roots and lesioned rats with a unilateral dorsal rhizotomy of (a) the C7 root alone, (b) the three successive roots rostral and caudal to the spared C7 root, and (c) the seven roots C4‐Th2. By subtracting results of the ‘C7 cut’ group from the ‘intact’ group or by subtracting results of the C4‐Th2 cut group from the C7 spaced group, it was possible to measure the distribution of γ. and δ opioid binding sites belonging to the C7 root. The combination of these two methods of calculation allowed us to demonstrate a significant distribution over two segments rostral and one segment caudal to the segment of entry. For [3H]DAMGO, the distribution was 10% (P < 0.05) in the C5, 27%, (P < 0.001) in the C6, 38% (P < 0.001) in the C7 and 14% (P < 0.05) in the C8 segment. For [3H]DTLET, the distribution was 11% (P= 0.05) in the C5, 27%, (P < 0.01) in the C6, 37% (P < 0.001) in the C7 and 18% (P < 0.05) in the C8 segment. It is also noted that rostral distributions spread more densely and further than the caudal ones.
Activation of N‐methyl‐D‐aspartate Receptors Induces Endogenous Rhythmic Bursting Activities in Nucleus Tractus Solitarii Neurons: An Intracellular Study on Adult Rat Brainstem Slices
Authors: Tell Fabien , Jean André 
Published: April 2006

AbstractA brainstem slice preparation and intracellular recording techniques were used to examine the effects of N‐methyl‐D‐aspartate (NMDA) application on neurons within the swallowing area of the nucleus tractus solitarii (NTS). According to their cellular properties, NTS neurons were classified into type I and type II neurons. The most striking difference was the occurrence of delayed excitation in type I but not in type II neurons, when they were depolarized from membrane potentials more negative than ‐60 mV. Bath application of NMDA (30–60 μM) elicited depolarization and triggered stable repetitive firing in all the NTS neurons but one. During the NMDA‐induced depolarization, hyperpolarization below ‐60 mV elicited, in some type I neurons, a rhythmic bursting pattern. The duration of the bursts (300–1000 ms) and their frequency (0.5–2 Hz) depended on the membrane potential. With hyperpolarizations below ‐75 mV, rhythmic bursting was converted into rhythmic single discharges, a pattern elicited directly in the other type I neurons. In all cases, rhythmic patterns were superimposed on cyclic depolarizations of the membrane potential characterized by an initial ramp‐shaped phase. In type II neurons, rhythmic bursting discharges, superimposed on rhythmic oscillations of the membrane potential, were also obtained upon hyperpolarization during the NMDA‐induced depolarization. In all type I neurons tested, NMDA‐induced cyclic ramp‐shaped depolarizations continued after addition of tetrodotoxin to the medium. Rhythmic bursting was not elicited by bath application of kainate (10–20 μM). Application of D‐2‐amino‐5‐phosphonovalerate (50 μM) blocked NMDA‐induced depolarizations without modifying those elicited by kainate, which were selectively depressed by 6‐cyano‐7‐nitroquinoxaline‐2, 3‐dione (10 μM). Moreover, removal of Mg2+ from the medium suppressed NMDA‐induced cyclic depolarizations. Results demonstrate that both NMDA and non‐NMDA receptors are present in NTS neurons and that selective activation of NMDA receptors induced rhythmic bursting and/or rhythmic single discharges. Rhythmic patterns were not driven by synaptic mechanisms but originated from endogenous properties of NTS neurons activated by NMDA. Thus, NTS neurons can be considered as conditional pacemakers. According to the location of the neurons, the conditional properties shown in these in vitro experiments might be involved in vivo in the generation of rhythmic motor activities set up at the NTS level, such as swallowing.
Poor Growth of Mammalian Motor and Sensory Axons Into Intact Proximal Nerve Stumps
Authors: Brown M. C. , Lunn E. R. , Perry V. H. 
Published: April 2006

AbstractWallerian degeneration is very slow in the mouse strain now known as C57BL/Ola. Sensory axon regrowth following peripheral nerve lesions is very poor in these animals but motor axons succeed in reinnervating the distal nerve stump even while the majority of severed axons are still intact (Lunn et al Eur. J. Neurosci., 1, 27–33, 1989). To see if motor axons could grow into a completely undegenerated portion of nerve, the proximal stumps of the peroneal and tibial nerves were sutured together in six BALB/c mice and the ability of large motor and sensory fibres from the tibial nerve to grow into the peroneal nerve was examined electrophysiologically in four of them. For the acute experiment the peroneal nerve was cut ‐ 7 mm central to the point of suture to the tibial nerve. Both at 2 weeks and 7 weeks after surgery the size of the potential recorded in the ventral roots on stimulating the portion of peroneal nerve into which tibial axons were directed to grow was only ‐8% of the potential recorded when the tibial nerve was itself stimulated. The potential recorded in the dorsal roots was only ‐2%. Counts of axon numbers in electron micrographs showed a small but non‐significant increase over normal in the number of unmyelinated axons in the peroneal nerves which’ had been connected to the tibial nerve in this way. It is concluded, in agreement with Langley and Anderson (J. Physiol., 31, 365–391, 1904), that axon growth into intact nerves is extremely limited in mammals and that the distal nerve stump of C57BL/Ola mice, although it degenerates very slowly, is not therefore equivalent to an intact peripheral nerve.
Presynaptic GABAA and GABAB Receptor‐mediated Phasic Modulation in Axons of Spinal Motor Interneurons
Authors: Alford Simon , Christenson Johan , Grillner Sten 
Published: April 2006

AbstractThe lamprey spinal cord has been utilized to investigate the role of presynaptic inhibition in the control of the spinal motor system. Axons of the lamprey spinal cord are comparatively large because of their lack of myelination. Axons impaled with microelectrodes demonstrate depolarizing responses to the application of GABAA and GABAB receptor agonists, muscimol and baclofen. These depolarizing effects are counteracted by the specific GABAA and GABAB receptor antagonists, bicuculline and phaclofen. GABAA receptor activation leads to a gating of Cl− channels on the axons. However, the ionic mechanism leading to axonal depolarization following GABAB receptor activation is unknown. After initiation of fictive locomotion, these axons demonstrate oscillations in axonal membrane potential related to the locomotor cycle. During ficitive locomotion they depolarize in phase with the bursting of the ipsilateral ventral root of the same segment. These axonal membrane potential oscillations are due to a phasic GABAA and GABAB receptor‐mediated gating of ion channels on the axonal membrane. Fictive locomotion in the lamprey spinal cord is largely unaffected by antagonism of one or other GABA receptor subtype alone, but is severely disrupted by simultaneous antagonism of both subtypes. In conclusions, we demonstrate, for the first time, an agonist‐gated depolarization of a vertebrate presynaptic element measured by direct impalement of the axon under study. We also demonstrate that GABA‐mediated presynaptic inhibition occurs in axons of spinal interneurons. It is not limited to the primary afferents as has previously been believed.
A Monoclonal Antibody Defining a Carbohydrate Epitope Restricted to Glial Cells
Authors: Cameron‐Curry Patrizia , Dulac Catherine , Le Douarin Nicole M. 
Published: April 2006

AbstractTo follow cell lineage segregation of glial cell precursors in the central and peripheral nervous systems (CNS and PNS), we made monoclonal antibodies against purified avian myelin glycoproteins and made detailed studies of antibodies reacting with cellular antigens expressed early in development. We describe here the cellular and molecular characterization of the 4B3 epitope, which is first expressed at day 2.5 in quail embryos and appears strictly specific to glial cell membranes in the PNS and CNS. We demonstrate that, not only oligodendrocytes and astrocytes but also myelinating and non‐myelinating Schwann cells, satellite cells of sensory and autonomic ganglia and enteric glial cells are 4B3‐positive. This epitope was identified as an N‐linked carbohydrate determinant shared by several unrelated molecules, one of them already described as the SMP glycoprotein.
Chronic Suppression of Bioelectric Activity and Cell Survival in Primary Cultures of Rat Cerebral Cortex: Biochemical Observations
Authors: Ramakers G. J. A. , Boer G. J. 
Published: April 2006

AbstractChronic suppression of spontaneously occurring bioelectric activity (BEA) has been shown to increase neuronal cell death in tissue culture, but may also affect astrocytes. We investigated this process in primary cultures of rat cerebral cortex by measuring the levels of NSE (neuron‐specific enolase) and GFAP (glial fibrillary acidic protein) in relation to general tissue markers, including measurements for cell death and proliferation. In electrically active (control) cultures, the content of DNA, protein, and NSE became maximal between 21 and 28 days in vitro (DIV) and thereafter decreased, whereas the content of GFAP rose continuously up to 43 DIV. Chronic suppression of BEA by tetrodotoxin (TTX; from 6 DIV) decreased the content of DNA, total protein, and especially NSE. The content of GFAP was decreased in all culture series investigated, but with great temporal variations among culture series. Chronic TTX treatment (started at 6 DIV) increased the efflux of lactate dehydrogenase, a marker for cell lysis, between 12 and 21 DIV, but this efflux was mainly derived from the supporting glial cells with which the cerebral cortex cultures were cocultured. Chronic, but not acute (7 h) TTX treatment decreased total [3H]thymidine incorporation into DNA from 14 DIV; this appeared to be due to a reduced number of astrocytes. Chronic suppression of BEA with xylocaine from 6 DIV had similar effects on DNA‐, protein‐, and NSE‐content as TTX, but led to an increased content of GFAP at 21 DIV. Chronic suppression of synaptic transmission with 10 mM Mg2+ and 0.2 mM Ca2+, starting at 6 DIV, increased the content of DNA, protein, and GFAP at 21 DIV, but NSE was still decreased. We conclude that chronic suppression of BEA in cerebral cortex cultures enhances neuronal cell death, whereas astrocytes are differentially affected, depending on the suppressing agent. As astrocytes may have a modulating effect on neuronal survival, their involvement should be regarded when studying the effects of chronic suppression of BEA on neuronal development.
Impaired Learning and Abnormal Open‐field Behaviours of Rats After Early Postnatal Anoxia and the Beneficial Effect of the Calcium Antagonist Nimodipine
Authors: Nyakas C. , Markel Éva , Schuurman T. , Luiten P. G. M. 
Published: April 2006

AbstractPerinatal anoxia/hypoxia is considered a serious risk factor for normal brain development. Anoxia induced by repeated asphyxia at 2 and 4 days after birth resulted in a transient hyperactivity in the small open‐field, and a behavioural depression in adult open‐field activity of male Wistar rats. The same treatment impaired adult learning behaviour in pole‐jumping conditioned avoidance and appetitively motivated hole‐board test situations. The calcium entry blocker nimodipine (in doses of 3 and 10 mg/kg) prevented the anoxia‐induced changes in orientation motility in the open‐field tests and almost fully antagonized the learning deficit in the hole‐board test. The behavioural deficit seen during acquisition of the pole‐jumping conditioned avoidance response was ameliorated to a lesser degree. The results indicate that the maintenance of calcium homeostasis during the early postnatal phase of brain development is crucial to prevent anoxia‐induced behavioural abnormalities.
Comparative Distribution of Neurons Containing FLFQPQRFamide‐like (morphine‐modulating) Peptide and Related Neuropeptides in the Rat Brain
Authors: Kivipelto Leena , Panula Pertti 
Published: April 2006

AbstractFLFQPQRF‐NH2 (F8Famide; morphine‐modulating peptide), isolated from bovine brain, is an FMRFamide‐like peptide with opioid analgesia modulating effects. In the rat brain, F8Famide is immunohistochemically localized in neurons of the medial hypothalamus and medulla oblongata. Neuropeptide Y (NPY) is structurally related to F8Famide and the mammalian FMRFamide‐like immunoreactivity (LI) was once thought to be due to an NPY‐like peptide. We compared the anatomical distribution of F8Famide‐LI with the localization of enkephalin‐ and NPY‐LI‐containing structures in the rat brain to find out if NPY or enkephalins coexist with F8Famide‐LI. Cryostat sections of colchicine‐treated Wistar rat brains were incubated with specific antisera against F8Famide, NPY, YGGFMRGL (Met‐enkephalin‐Arg‐Gly‐Leu), or YGGFMRF (Met‐enkephalin‐Arg‐Phe) raised in rabbits. The immunoreactivity was visualized by the peroxidase – antiperoxidase or immunofluorescence method. The light microscopic mirror method was applied to study the colocalization of F8Famide and NPY. The F8Famide‐immunoreactivity was concentrated in smaller areas of medial hypothalamus and nucleus of the solitary tract than that of enkephalins and NPY. In all brain areas, the distributions of F8Famide‐, enkephalin‐ and NPY‐immunoreactive neurons were distinct. F8Famide‐, NPY‐and enkephalin‐LI‐containing nerve terminals were seen in the nucleus of the solitary tract and in the lateral parabrachial nucleus. These results show that the neuronal systems containing F8Famide‐, enkephalin‐ or NPY‐LI are anatomically separate in all brain regions. However, there are terminal areas in which more than one type of these immunoreactivities are detected. These results have anatomical correlation with pharmacological reports, suggesting modulatory functions for these peptides on regulation of blood pressure, feeding behaviour and endocrine functions.
Projections from Areas 18 and 19 to Cat Striate Cortex: Divergence and Laminar Specificity
Authors: Henry G. H. , Salin P. A. , Bullier J. 
Published: April 2006

AbstractThe results of electrical stimulation experiments [Bullier et al., (1988) Exp. Brain Res., 70, 90–98] demonstrated that afferents from areas 18 and 19 contact different functional types of neurons in area 17. We were therefore interested in examining whether these results could be explained by differences in the morphology of the terminals of these two groups of afferent connections to area 17. We also wanted to confirm, by a direct method, our earlier results [Salin et al. (1989) J. Comp. Neurol., 283, 486–512] that cortical afferents to area 17 in the cat present extensive divergences. We therefore placed small injections of anterograde tracers in areas 18 and 19 and examined the laminar distributions of terminals thus revealed and the extent of the surface of area 17 contacted by these terminals. Three tracers were used: wheat germ agglutinin – horseradish peroxidase (WGA–HRP), Phaseolus vulgaris leucoagglutinin (Pha‐L) and biocytin. The results show that the divergence of these afferent connections are very extensive: 7–8 mm in the rotrocaudal direction and 3.5–6 mm in the mediolateral direction. In other words, neurons located in a region a few hundreds micron wide in areas 18 or 19 contact a region of area 17 covering several millimeters. Corticocortical connections are therefore not organized in a point‐to‐point fashion but are strongly divergent. The laminar distributions of terminals from areas 18 and 19 displayed a specific pattern. Area 19 projects most heavily to layers 5 and 6, also terminates in layers 1–3 and very little is present in layer 4. In contrast, the afferent terminals from area 18 are heaviest in layers 1, 2, 3, 4A and 5 and are rare in layer 6. Injections placed at different depths in area 18 revealed that upper layer neurons in that area mostly project to layers 1, 2, 3 and 5 in area 17, whereas lower layer neurons send their heaviest projections to layers 4A, 5 and 6 and hardly project to layers 1, 2 and 3.
On the Life Span of Olfactory Receptor Neurons
Authors: Mackay‐Sim A. , Kittel P. W. 
Published: April 2006

AbstractThe life span of olfactory receptor neurons was investigated after injection of a retrograde tracer into the olfactory bulb. Mice were injected unilaterally with colloidal gold conjugated with Concanavalin A and their olfactory epithelia were examined after 7, 14, 30, 60, and 90 days. Gold particles could be seen in the epithelia at all survival periods after silver intensification. There was no gold in the epithelia on the uninjected side. In order to test whether gold could be recycled within the epithelium upon the death of receptor neurons, the olfactory bulbs of some mice were ablated 4 days after colloidal gold injection. None of the receptor neurons in these epithelia contained gold at any survival period. To investigate whether gold was continuously available at the injection site, olfactory bulbs were examined by electron microscopy. By 7 days after injection all gold was sequestered intracellularly and was presumably unavailable for uptake by the olfactory axons. These results indicate that olfactory receptor neurons live for at least three times the commonly accepted life span of 30 days. A long life span challenges the widely held view that olfactory receptor neurons are regularly replaced.