bluuebunny/crossref_metadata_2025_split huggingface dataset:
A rat G protein‐coupled receptor selectively expressed in myelin‐forming cells
Authors: Allard J. , Barrón S. , Diaz J. , Lubetzki C. , Zalc B. , Schwartz J. ‐C. , Sokoloff P. 
Published: March 2003

AbstractBy screening an olfactory bulb cDNA library using dopamine receptor probes, we isolated the cDNA coding for the rat counterpart of an orphan receptor known as Edg‐2, homologous to G protein‐coupled receptors. In situ hybridization analysis showed that Edg‐2 mRNA expression is restricted to myelinated structures, e.g. corpus callosum or peripheral nerves. A weaker expression in various peripheral organs was also detected in newborns. A 3.8‐kb transcript was found at high levels in highly myelinated brain structures and sciatic nerve, and, at lower levels, in poorly myelinated peripheral organs, consistent with its occurrence in Schwann cells in the peripheral nervous system. One hundred percent of Edg‐2 mRNA‐containing cells in the brain also expressed mRNA encoding myelin‐basic‐protein, a marker of oligodendrocytes. This restricted olygodendrocytes localization was confirmed by the absence of cellular colocalization of Edg‐2 and glial fibrillary acidic protein, an astrocytic marker. During prenatal development, Edg‐2 mRNA expression was high in the cortical neuroepithelium and meningeal layer at E16, extended later to other neuroepithelia, and disappeared shortly after birth. During brain postnatal development, Edg‐2 mRNA expression in myelinated structures followed a caudo‐rostral gradient, similar to that of myelination. Thus, Edg‐2 is the first G protein‐coupled receptor found to be selectively expressed in myelin‐forming cells in the nervous system and its temporal expression pattern is consistent with a dual role (i) in neurogenesis, during embryonic development, and (ii) in myelination and myelin maintenance, during postnatal life.
Growth of pyramidal, but not non‐pyramidal, dendrites in long‐term organotypic explants of neonatal rat neocortex chronically exposed to neurotrophin‐3
Authors: Baker R.E. , Dijkhuizen P.A. , Van Pelt J. , Verhaagen J. 
Published: March 2003

AbstractThe present study was undertaken to determine the effects of neurotrophin‐3 (NT3) and spontaneous bioelectric activity (SBA) on dendritic elongation and branching in long‐term isolated organotypic explants of rat neocortex. Viral vector‐directed expression of NT3 was used as an effective means to ensure a continuous, local production of the neurotrophic factor. Quantitative light microscopic measurement of dendritic branching patterns was carried out on Golgi‐stained materials. Explants were exposed to an adenoviral vector encoding the genetic sequence for neurotrophin‐3 (Ad‐NT3), or to exogenous additions of the neuropeptide NT3. In order to test for activity‐dependent growth effects under control and experimental conditions, explants were exposed to glutamatergic blockade using a cocktail of APV and DNQX. Both Ad‐NT3 and NT3 peptide potently promoted apical and basal dendritic growth (elongation and branching) in pyramidal neurons. This growth was observed to be significant in layers II–IV and V. These growth effects were also not activity dependent, inasmuch as they were elicited from explants in which spontaneous bioelectric activity had been suppressed. Non‐pyramidal neurons, throughout the neocortical slice, showed no significant dendritic responses to the prolonged presence of NT3. These findings show that pyramidal dendritic growth in long‐term neocortical explants responds to at least one neurotrophic growth factor, NT3, and is independent of intrinsic bioelectric activity. The use of viral vectors in delivering a continuous high level of neurotrophic factor within developing neural tissues demonstrates its potential application to in vivo tissues during development, or in the stimulation of neuritogenesis and neuroregeneration following injuries.
Dissociations in dopamine release in medial prefrontal cortex and ventral striatum during the acquisition and extinction of classical aversive conditioning in the rat
Authors: Wilkinson L.S. , Humby T. , Killcross A.S. , Torres E.M. , Everitt B.J. , Robbins T.W. 
Published: March 2003

AbstractDual perfusion in vivo brain microdialysis was used to monitor extracellular levels of dopamine in the medial prefrontal cortex and ventral striatum during the acquisition and extinction of a classical aversive conditioning paradigm in rats. The main finding was a dissociation in the pattern of release in the two brain areas. The first stimulus–footshock pairing elicited large increases in cortical dopamine over baseline levels that were much greater than the increases elicited by different stimuli of equivalent salience that were unpaired with footshock. In contrast, dopamine levels in ventral striatum were unchanged under these conditions. Over the next two pairings, there was a decline in the cortical response and an increase in the response in ventral striatum. The first presentation of the aversive conditioned stimulus in a separate context elicited the largest response in ventral striatum. Post‐conditioning, the cortical response to the conditioned stimulus was smaller than that elicited by the initial stimulus–footshock pairing and was equivalent in magnitude to that elicited by stimuli unpaired with footshock. Over the final two conditioned stimuli presentations, in the absence of the footshock reinforcer (extinction), responses declined in both brain areas. Simultaneous monitoring of behaviour indicated that the neurochemical events were accompanied by effective aversive learning, as indexed by conditioned freezing responses. The data are discussed in terms of the hypothesis that medial prefrontal cortex is especially engaged during novel circumstances which may, potentially, require new learning, whilst ventral striatal dopamine more closely follows the expression of conditioned responding during learning and extinction.
The onset of parvalbumin‐expression in interneurons of the rat parietal cortex depends upon extrinsic factor(s)
Authors: Weisenhorn D. M. Vogt , Celio M.R. , Rickmann M. 
Published: March 2003

AbstractParvalbumin (PV) belongs to the large family of EF‐hand calcium‐binding proteins and is an excellent marker for a subpopulation of GABAergic neocortical interneurons. During cortical development, PV first appears on postnatal day (P)8, in the infragranular layers; after P14, it also becomes apparent within the supragranular layers. However, nothing is known about the factors controlling its expression, which could involve functional activity, neuronal connectivity and/or neurotrophic factors. It being difficult to manipulate these parameters in vivo, their role may be more readily assessed in organotypic cultures, which are deprived of their subcortical afferents and efferents, and hence of subcortically derived neurotrophic factors and extrinsic functional activity. We prepared slices of the rat brain on P3, P5, P7 and P9, maintained them in culture for 2–5 weeks, and compared the temporal and spatial distribution pattern of PV‐immunoreactivity within these slices with the in vivo situation. We found, first, that during late postnatal in vivo development and ageing, the number of PV‐immunoreactive neurons in the parietal cortex decreases significantly, and second, that the expression of PV‐immunoreactivity in the parietal cortex was markedly influenced by the phase of postnatal development at which slice cultures were explanted. In those removed on P7 and P9, the number of PV‐immunoreactive cells, as well as the temporal and spatial distribution pattern of PV‐immunoreactivity corresponded to the in vivo situation, but in explants obtained on P3 or P5, PV‐immunoreactivity remained confined to layer V of the cortex, reminiscent of the expression profile manifested at the end of the second postnatal week in vivo. Also, the number of PV‐immunoreactive cells in these cultures was significantly lower than in explants at the later stages. Our results indicate that the onset of PV‐expression in the parietal cortex depends upon extrinsic cortical factors subsisting prior to P7. Once the production of this protein has been initiated, such influences are no longer required.
Synaptic loss reflected by secretoneurin‐like immunoreactivity in the human hippocampus in Alzheimer's disease
Authors: Kaufmann W.A. , Barnas U. , Humpel C. , Nowakowski K. , DeCol C. , Gurka P. , Ransmayr G. , Hinterhuber H. , Winkler H. , Marksteiner J. 
Published: March 2003

AbstractSecretoneurin is a recently described peptide derived by endoproteolytic processing from secretogranin II, previously named chromogranin C. In this study, we have investigated the distribution of secretoneurin‐like immunoreactivity in the human hippocampus in controls and in Alzheimer's disease patients, and compared the staining pattern to that of calretinin. Secretoneurin‐like immunoreactivity is present throughout the hippocampal formation. At the border of the dentate molecular layer and the granule cell layer, a band of dense secretoneurin immunostaining appeared. In this part, as in the area of the CA2 sector, the high density of secretoneurin‐immunoreactivity coincided with calretinin‐like immunoreactivity. The mossy fibre system displayed a moderate density of secretoneurin‐immunoreactivity. In the entorhinal cortex, a particularly high density of secretoneurin‐immunoreactivity was observed. The density of secretoneurin‐like immunoreactivity was significantly reduced in the innermost part of the molecular layer and in the outer molecular layer of the dentate gyrus in Alzheimer's disease. For calretinin‐like immunoreactivity, a less pronounced decrease was found in the innermost part of the molecular layer. About 40–60% of neuritic plaques were secretoneurin‐immunopositive.This study shows that secretoneurin is distinctly distributed in the human hippocampus and that significant changes of secretoneurin‐like immunoreactivity occur in Alzheimer's disease, reflecting synaptic loss.
The cortical somatotopic map and phantom phenomena in subjects with congenital limb atrophy and traumatic amputees with phantom limb pain
Authors: Montoya Pedro , Ritter Karin , Huse Ellena , Larbig Wolfgang , Braun Christoph , Töpfner Stephanie , Lutzenberger Werner , Grodd Wolfgang , Flor Herta , Birbaumer Niels 
Published: March 2003

AbstractThe extent of the cortical somatotopic map and its relationship to phantom phenomena was tested in five subjects with congenital absence of an upper limb, four traumatic amputees with phantom limb pain and five healthy controls. Cortical maps of the first and fifth digit of the intact hand, the lower lip and the first toe (bilaterally) were obtained using neuroelectric source imaging. The subjects with congenital upper limb atrophy showed symmetric positions of the left and right side of the lower lip and the first toe, whereas the traumatic amputees with pain showed a significant shift (about 2.4 cm) of the cortical representation of the lower lip towards the hand region contralateral to the amputation side but no shift for the toe representation. In healthy controls, no significant hemispheric differences between the cortical representation of the digits, lower lip or first toe were found. Phantom phenomena were absent in the congenital but extensive in the traumatic amputees. These data confirm the assumption that congenital absence of a limb does not lead to cortical reorganization or phantom limbs whereas traumatic amputations that are accompanied by phantom limb pain show shifts of the cortical areas adjacent to the amputation zone towards the representation of the deafferented body part.
Relations between cortical and thalamic cellular activities during absence seizures in rats
Authors: Seidenbecher Thomas , Staak Rainer , Pape Hans‐Christian 
Published: March 2003

AbstractIn a rat model of generalized absence epilepsies (Genetic Absence Epilepsy Rats from Strasbourg, GAERS), multiunit activity was recorded simultaneously at different sites of the thalamocortical system under neurolept anaesthesia (fentanyl‐droperidol). Under these conditions, bilaterally synchronized spike‐and‐wave‐discharges (SWDs) occurred spontaneously on the electroencephalogram (EEG) that were in principle identical to those reported earlier from unanaesthetized preparations. The generation of SWDs on the EEG was associated with spike‐concurrent, rhythmic burst‐like activity in (mono‐)synaptically connected regions of specific (somatosensory) thalamic regions and layers IV/V of the somatosensory cortex, and the reticular thalamic nucleus. Precursor activity was typically recorded in cortical units, concomitant with ‘embryonic’ SW seizures on the EEG, before the paroxysm was evident on the gross EEG and in the thalamus. On average, SWD‐correlated activity in layers IV/V of the somatosensory cortex started significantly earlier than correlated burst‐like firing in reticular and in ventrobasal thalamic neurons. Cellular peak firing in thalamus and cortex during bilaterally synchronized SWDs was related to the spike component on the gross EEG with the temporal rank order ventroposteromedial > ventrolateral ≥ ventroposterolateral thalamic > > rostral reticular thalamic nuclei ≥ cortex (layers IV/V) = caudal reticular thalamic nucleus. A spike‐related depression and wave‐related increase in firing was recorded in anteroventral ventrolateral thalamic areas, presumably reflecting their peculiar anatomical arrangement within the thalamus. These results from an in vivo preparation with intact synaptic connections that spontaneously produces SWDs indicate that SWDs spread within the thalamocortical network, involving short and long delays. The order of concurrent rhythmic firing observed in thalamocortical circuits during SW seizures are supportive of the hypothesis that the processes of rhythmogenesis recruit local thalamic networks, while cortical mechanisms appear to synchronize rhythmic activities on a larger spatiotemporal scale, thereby providing an important contribution to the generalization of epileptiform activity and expression of SWDs on the EEG.
The relation between dopamine oxidation currents in the nucleus accumbens and conditioned increases in motor activity in rats following repeated administration of d‐amphetamine or cocaine
Authors: Di Ciano Patricia , Blaha Charles D. , Phillips Anthony G. 
Published: March 2003

AbstractChronoamperometric recording techniques were used to monitor extracellular dopamine efflux in the nucleus accumbens associated with unconditioned and conditioned increases in motor activity in rats, following the intravenous administration of either d‐amphetamine (0.63 mg/kg) or cocaine (3 mg/kg), or the presentation of a conditioned stimulus paired repeatedly with one of these psychostimulants. Each drug was administered daily for 7 days, either in the home cage or an environment in which a compound stimulus (light offset, odour) was presented. Rats in control groups received saline instead of drug in the distinctive test environment. On day 7 of training, significant increases in unconditioned motor activity were observed in the 30 min session following infusions of either d‐amphetamine or cocaine. Associated dopamine oxidation currents in the nucleus accumbens increased immediately following administration of either drug and remained significantly elevated above baseline during the entire 30 min recording period. On the test day, presentation of the conditioned stimulus with vehicle infusions, in the distinct environment, was accompanied by an increase in dopamine oxidation currents and a conditioned increase in motor activity, only in the groups in which these stimuli had been paired with d‐amphetamine or cocaine. Neither the magnitude or duration of the conditioned motor activity matched the corresponding change in extracellular dopamine efflux in the nucleus accumbens. Accordingly, it is argued that the increase in dopamine concentration serves as a neurochemical correlate of the unconditioned and conditioned stimuli. The change in motor activity constitutes the unconditioned and conditioned responses that are subserved by the neural systems activated by the initial rise in extracellullar dopamine.
Conditioned changes in dopamine oxidation currents in the nucleus accumbens of rats by stimuli paired with self‐administration or yoked‐administration of d‐amphetamine
Authors: Di Ciano Patricia , Blaha Charles D. , Phillips Anthony G. 
Published: March 2003

AbstractIn vivo chronoamperometry was used to monitor changes in dopamine oxidation currents corresponding to dopamine efflux in the nucleus accumbens of rats after presentation of a conditioned light stimulus repeatedly paired with either yoked‐ or self‐administered intravenous injections of the psychostimulant d‐amphetamine. Daily conditioning trials began with a non‐contingent drug injection, paired with a conditioned stimulus consisting of a 5 s flashing light and 30 s lights out, after which a house light was illuminated during the 3 h session, signalling drug availability. Each subsequent injection of d‐amphetamine was paired with the conditioned stimulus. Electrochemical measures were taken on conditioning trials 4–7, and on each trial, intravenousd‐amphetamine (0.25 mg/kg per injection) self‐administration produced a significant maximal increase in mean dopamine oxidation currents of ≈ 8 nA above baseline. Dopamine oxidation currents in rats receiving yokedd‐amphetamine were ≈ 5 nA above baseline by the fourth day of drug administration and reached ≈ 8 nA on the seventh and final day of drug administration. On day 9 the first presentation of the vehicle injection and conditioned stimulus, in combination with illumination of the house lights, induced an immediate increase in nucleus accumbens dopamine oxidation currents in all rats that had previously received d‐amphetamine. Subsequent presentations of the conditioned stimulus at 30 min intervals induced further increases in extracellular dopamine oxidation currents in both drug‐treated groups. By the end of the 3 h session, both groups had similar maximal conditioned increases in dopamine oxidation currents of ≈ 6 nA. These data are discussed with relation to the neurochemistry of drug craving.
Spatiotemporal distribution of a late synchronized activity in olfactory pathways following stimulation of the olfactory bulb in rats
Authors: Mouly Anne‐Marie , Litaudon Philippe , Chabaud Pascal , Ravel Nadine , Gervais Rémi 
Published: March 2003

AbstractThe evoked potential recorded in the rat piriform cortex in response to electrical stimulation of the olfactory bulb is composed of an early component occasionally followed by a late component (60–70 ms). We previously showed that the late component occurrence was enhanced following an olfactory learning. In the present study carried out in naive rats, we investigated the precise conditions of induction of this late component, and its spatiotemporal distribution along the olfactory pathways. In the anaesthetized rat, a stimulating electrode was implanted in the olfactory bulb. Four recording electrodes were positioned, respectively, in the olfactory bulb, the anterior and posterior parts of the piriform cortex, and the entorhinal cortex. Simultaneous recording of signals evoked in the four sampled structures in response to stimulation of the olfactory bulb revealed that the late component was detected in anterior and posterior piriform cortex as well as in entorhinal cortex, but not in the olfactory bulb. The late component occurred reliably for a narrow range of low intensities of stimulation delivered at frequencies not exceeding 1 Hz. Comparison of late component amplitude and latency across the different recorded sites showed that this component appeared first and with the greatest amplitude in the posterior piriform cortex. In addition to showing a functional dissociation between anterior and posterior parts of the piriform cortex, these data suggest that the posterior piriform cortex could be the locus of generation of this late high amplitude synchronized activity, which would then propagate to the neighbouring regions.
Optokinetic reflex in squirrel monkeys after long‐term monocular deprivation
Authors: Hoffmann K‐P. , Distler C. , Grüsser O‐J. 
Published: March 2003

AbstractHorizontal optokinetic nystagmus (OKN) as well as neuronal response properties in the nucleus of the optic tract and the dorsal terminal nucleus of the accessory optic system (NOT‐DTN) were investigated in three monocularly deprived squirrel monkeys. In two monkeys occlusion of one eye was performed at birth (early) and in the third after 7 weeks (late). In adulthood, in early deprived monkeys monocular horizontal OKN tested through the non‐deprived eye was symmetrical and in no way different from normal, i.e. stimulation in the temporonasal and nasotemporal direction elicited equal and robust responses. OKN through the early occluded eye, however, was grossly abnormal with low gain and great variability in the consistency of nasotemporal and temporonasal slow phase eye movements. When in the late deprived monkey the non‐deprived eye was occluded a strong spontaneous nystagmus developed despite the deprived eye viewing a stationary pattern. The slow phases were directed from nasal to temporal for the deprived eye. When tested through the non‐deprived eye all neuronal responses of the NOT‐DTN were normal. The deprived eye's influence on NOT‐DTN neurons was extremely weak. No neuron with a moderate or even dominant input from the deprived eye was found after early deprivation. In the late deprived case the deficit was not as severe but still the non‐deprived eye was clearly dominating the responses in all neurons tested. Velocity tuning of neurons tested through the non‐deprived eye was normal and qualitatively corresponded well to slow phase eye velocity in response to equivalent retinal slip during OKN. Through the early deprived eye, however, velocity tuning was extremely poor. It was somewhat better through the late deprived eye. We suggest that the dramatic deterioration in the optokinetic reflex found after long‐term monocular deprivation for the amblyopic eye is probably caused by the almost complete loss of retinal and cortical input driven by that eye to the NOT‐DTN. These results are discussed in relation to our previous results in cats and reports in the literature for humans with occlusion amblyopia.