bluuebunny/crossref_metadata_2025_split huggingface dataset:
Early coding of reaching: frontal and parietal association connections of parieto‐occipital cortex
Authors: Caminiti Roberto , Genovesio Aldo , Marconi Barbara , Mayer Alexandra Battaglia , Onorati Paolo , Ferraina Stefano , Mitsuda Takashi , Giannetti Stefano , Squatrito Salvatore , Maioli Maria Grazia , Molinari Marco 
Published: March 2003

AbstractThe ipsilateral association connections of the cortex of the dorsal part of the rostral bank of the parieto‐occipital sulcus and of the adjoining posterior part of the superior parietal lobule were studied by using different retrograde flourescent tracers. Fluoro‐Ruby, Fast blue and Diamidino yellow were injected into visual area V6A, and dorso‐caudal (PMdc, F2) and dorso‐rostral (PMdr, F7) premotor cortex, respectively. The parietal area of injection had been previously characterized physiologically in behaving monkeys, through a variety of oculomotor and visuomanual tasks. Area V6A is mainly linked by reciprocal projections to parietal areas 7m, MIP (medial intraparietal) and PEa, and, to a lesser extent, to frontal areas PMdr (rostral dorsal premotor cortex, F7) and PMdc (F2). All these areas project to that part of the dorsocaudal premotor cortex that has a direct access to primary motor cortex. V6A is also connected to area F5 and, to a lesser extent, to 7a, ventral (VIP) and lateral (LIP) intraparietal areas. This pattern of association connections may explain the presence of visually‐related and eye‐position signals in premotor cortex, as well as the influence of information concerning arm position and movement direction on V6A neural activity. Area V6A emerges as a potential ‘early’ node of the distributed network underlying visually‐guided reaching. In this network, reciprocal association connections probably impose, through re‐entrant signalling, a recursive property to the operations leading to the composition of eye and hand motor commands.
The mouse Ptprr gene encodes two protein tyrosine phosphatases, PTP‐SL and PTPBR7, that display distinct patterns of expression during neural development
Authors: Van Den Maagdenberg A. M. J. M. , Bächner D. , Schepens J. T. G. , Peters W. , Fransen J. A. M. , Wieringa B. , Hendriks W. J. A. J. 
Published: March 2003

AbstractThe protein tyrosine phosphatases PTP‐SL and PTPBR7 differ only in the length of their N‐terminal domain. We show here that PTP‐SL and PTPBR7 are isoforms derived from a single gene (Ptprr) through developmentally regulated use of alternative promoters. Isoform‐specific reverse transcriptase‐polymer chain reaction (RT‐PCR) and RNA in situ hybridization experiments reveal that PTPBR7 is expressed during early embryogenesis in spinal ganglia cells as well as in developing Purkinje cells. Post‐natally, PTPBR7 is expressed in various regions of the adult mouse brain, but expression in Purkinje cells has ceased and is replaced by the PTP‐SL‐specific transcript. In transient transfection experiments it is confirmed that PTPBR7 is a type I transmembrane protein tyrosine phosphatase (PTPase). PTP‐SL, however, appears to be a cytosolic membrane‐associated PTPase that is located at perinuclear vesicular structures that partly belong to the endosomal compartment. Thus, during maturation of Purkinje cells, a gene‐promoter switch results in the replacement of a receptor‐type PTPase by a cytosolic vesicle‐associated isoform.
Astroglia inhibit the proliferation of neocortical cells and prevent the generation of small GABAergic neurons in vitro
Authors: De Lima Ana D. , Voigt Thomas 
Published: March 2003

AbstractWe quantitatively studied the dynamics of rat neocortical precursor proliferation in vitro, and additionally examined the effects of neuron–glia interactions on the proliferation and differentiation of neurons, and particularly of γ‐aminobutyric acid (GABA)‐containing cells. In cultures grown on glia‐free substrate, cellular proliferation was detected at least until the end of the second week in vitro, but most neurons which expressed detectable amounts of microtubule‐associated protein at 12 days in vitro were generated early during the first week. Further double‐labelling experiments, combining 5′‐bromo‐2′‐deoxyuridine with GABA or β‐tubulin III immunohistochemistry, provided direct evidence that neuronal proliferation continued through the second week in vitro, and that a population of small GABAergic neurons was generated between 3 and 12 days in vitro. Culturing cells on a glial substrate significantly reduced the generation of small GABAergic cells and strongly inhibited the total cell proliferation. Inhibition also occurred if astrocytes were added to the culture after 6 days in vitro, but was significantly decreased if cells were grown on a fixed glial substrate, suggesting that the effect might be at least partially mediated by active interactions between neurons and glia. In conclusion, our results show that the sustained proliferation of precursor cells in neocortical cultures is necessary for the differentiation of small GABAergic neurons, and that mature astroglia effectively inhibit the proliferation of neocortical precursors thereby affecting the appearance of a population of GABAergic cells.
Neuronal correlates of real and illusory contour perception: functional anatomy with PET
Authors: Larsson Jonas , Amunts Katrin , Gulyás Balázs , Malikovic Aleksandar , Zilles Karl , Roland Per E. 
Published: March 2003

AbstractIllusory contours provide a striking example of the visual system's ability to extract a meaningful representation of the surroundings from fragmented visual stimuli. Psychophysical and neurophysiological data suggest that illusory contours are processed in early visual cortical areas, and neuroimaging studies in humans have shown that Kanizsa‐type illusory contours activate early retinotopic visual areas that are also activated by real contours. It is not known whether other types of illusory contours are processed by the same mechanisms, nor is it clear to what extent attentional effects may have influenced these results, as no attempt was made to match the salience of real and illusory stimuli in previous imaging studies. It therefore remains an open question whether there are any brain regions specifically involved in the perception of illusory contours. To address these questions, we have used 15O‐butanol positron emission tomography (PET) and a novel kind of illusory contour stimulus that is induced only by aligned line ends. By employing a form discrimination task that was matched for attention and stimulus salience across conditions we were able to directly contrast perception of real and illusory contours. We found that the regions activated by illusory contour perception were the same as those activated by real contours. Only one region, located in the right fusiform gyrus, was significantly more strongly activated by perception of illusory contours than by real contours. In addition, a principal component analysis suggested that illusory contour perception is associated with a change in the correlation between V1 and V2. We conclude that different kinds of illusory contours are processed by the same cortical regions and that these regions overlap extensively with those involved in processing of real contours. At the regional level, perception of illusory contours thus appears to differ from perception of real contours by the degree of involvement of higher visual areas as well as by the nature of interaction between early visual areas.
3‐Hydroxykynurenine potentiates quinolinate but not NMDA toxicity in the rat striatum
Authors: Guidetti Paolo , Schwarcz Robert 
Published: March 2003

Abstractl‐3‐Hydroxykynurenine (L‐3‐HK) and quinolinate (QUIN) are two metabolites of the kynurenine pathway, the major route of tryptophan degradation in mammals. L‐3‐HK is a known generator of highly reactive free radicals, whereas QUIN is an endogenous excitotoxin acting specifically at N‐methyl‐d‐aspartate (NMDA) receptors. This study was designed to examine possible synergistic interactions between L‐3‐HK and QUIN in the rat brain in vivo. Intrastriatal coinjection of 5 nmol L‐3‐HK and 15 nmol QUIN, i.e. doses which caused no or minimal neurodegeneration on their own, resulted in substantial neuronal loss, determined both behaviourally (apomorphine‐induced rotations) and histologically (quantitative assessment of lesion size). The excitotoxic nature of the lesion was verified by tyrosine hydroxylase immunohistochemistry, showing the survival of dopaminergic striatal afferents. There was also a relative sparing of large striatal neurons, and neurodegeneration was prevented both by NMDA receptor blockade (using CGP 40116) and free radical scavenging [using N‐tert‐butyl‐α‐(2‐sulphophenyl)‐nitrone, S‐PBN]. The pro‐excitotoxic features of L‐3‐HK were especially pronounced at low QUIN doses and were not observed when QUIN was substituted by NMDA. Notably, the effect of L‐3‐HK was not due to its intracerebral conversion to QUIN and was duplicated by equimolar D,L‐3‐HK. These data indicate that an elevation of L‐3‐HK levels constitutes a significant hazard in situations of excitotoxic injury. Pharmacological interventions aimed at decreasing L‐3‐HK formation may therefore be particularly useful for the treatment of neurological diseases which are associated with an abnormally enhanced flux through the kynurenine pathway.
Time‐dependent induction of depotentiation in the dentate gyrus of freely moving rats: involvement of group 2 metabotropic glutamate receptors
Authors: Kulla Alexander , Reymann Klaus G. , Manahan‐Vaughan Denise 
Published: March 2003

AbstractDepotentiation comprises a reversal of tetanization‐induced long‐term potentiation (LTP) which occurs following low‐frequency stimulation (LFS) in the hippocampus in vivo. Although depotentiation has been consistently demonstrated in the CA1 region, no positive reports of the existence of depotentiation in the dentate gyrus in vivo have occurred. This study therefore investigated whether depotentiation is possible in the dentate gyrus in vivo. We found that depotentiation can be induced, but it is very tightly dependent on the interval between tetanization and LFS. Thus, LFS given 2 or 5 min following tetanization produced significant depotentiation, whereas LFS given 10–30 min following tetanization had no significant effect on the expression of LTP. Depotentiation occurred in two phases: a transient depression of evoked responses to below pre‐tetanization values, which occurred in the first 60 min following LFS, and a recovery of this response to a stable level of synaptic transmission which comprised a significant reduction in the magnitude of LTP. Group 2 metabotropic glutamate receptors (mGluRs) play an important role in the expression of long‐term depression in vivo. We therefore investigated whether group 2 mGluRs contribute to depotentiation. The group 2 antagonist (2S)‐α‐ethylglutamic acid (EGLU) inhibited the early transient depression at a concentration which inhibits LTD in vivo, but did not block the expression of depotentiation. EGLU also inhibited the transient depression induced by 5 Hz given alone. Increasing the concentration of EGLU prevented depotentiation, however. The group 2 agonist (S)‐4‐carboxy‐3‐hydroxyphenyl‐ glycine (4C3HPG) inhibited LTP and enhanced depotentiation. These data suggest a role for group 2 mGluRs in depotentiation.
Proliferation of microglia and astrocytes in the dentate gyrus following entorhinal cortex lesion: a quantitative bromodeoxyuridine‐labelling study
Authors: Hailer Nils P. , Grampp Anne , Nitsch Robert 
Published: March 2003

AbstractEntorhinal cortex lesion of adult rats induces glial activation and proliferation in the deafferented dentate molecular layer. Double‐labelling immunocytochemistry for the astrocyte‐specific antigen glial fibrillary acidic protein or the microglial cell marker Griffonia simplicifolia isolectin B4 with bromodeoxyuridine detection revealed that microglia counts and the proliferation rate in the ipsilateral dentate gyrus reached a maximum in the molecular layer at 3 days post‐lesion (dpl) and returned to control levels by 30 dpl. Astrocyte counts in the ipsilateral dentate gyrus peaked at 30 dpl, with maximum proliferation at 7 dpl. At 100 dpl the astrocyte count had reverted to control levels. Glial proliferation was not restricted to the ipsilateral molecular layer but also occurred to some degree in the granule cell layer and the contralateral dentate gyrus. Thus entorhinal cortex lesion induces a rapid microglia reaction and long‐lasting astrocyte activation in the deafferented termination zone of the perforant path. We conclude that glial proliferation after entorhinal cortex lesion follows a complex temporal and spatial pattern that coincides with processes of neuronal and axonal reorganization.
NT‐3 promotes growth of lesioned adult rat sensory axons ascending in the dorsal columns of the spinal cord
Authors: Bradbury Elizabeth J. , Khemani Sameer , Von R . , King . , Priestley John V. , McMahon Stephen B. 
Published: March 2003

AbstractThe regeneration capacity of spinal cord axons is severely limited. Recently, much attention has focused on promoting regeneration of descending spinal cord pathways, but little is known about the regenerative capacity of ascending axons. Here we have assessed the ability of neurotrophic factors to promote regeneration of sensory neurons whose central axons ascend in the dorsal columns. The dorsal columns of adult rats were crushed and either brain‐derived neurotrophic factor (BDNF), glial cell line‐derived neurotrophic factor (GDNF), neurotrophin‐3 (NT‐3) or a vehicle solution was delivered continuously to the lesion site for 4 weeks. Transganglionic labelling with cholera toxin β subunit (CTB) was used to selectively label large myelinated Aβ fibres. In lesioned rats treated with vehicle, CTB‐labelled fibres were observed ascending in the gracile fasciculus, but these stopped abruptly at the lesion site, with no evidence of sprouting or growth into lesioned tissue. No CTB‐labelled terminals were observed in the gracile nucleus, indicating that the lesion successfully severed all ascending dorsal column axons. Treatment with BDNF did not promote axonal regeneration. In GDNF‐treated rats fibres grew around cavities in caudal degenerated tissue but did not approach the lesion epicentre. NT‐3, in contrast, had a striking effect on promoting growth of lesioned dorsal column axons with an abundance of fibre sprouting apparent at the lesion site, and many fibres extending into and beyond the lesion epicentre. Quantification of fibre growth confirmed that only in NT‐3‐treated rats did fibres grow into the crush site and beyond. No evidence of terminal staining in the gracile nucleus was apparent following any treatment. Thus, although NT‐3 promotes extensive growth of lesioned axons, other factors may be required for complete regeneration of these long ascending projections back to the dorsal column nuclei. The intrathecal delivery of NT‐3 or other neurotrophic molecules has obvious advantages in clinical applications, as we show for the first time that dorsal column axonal regeneration can be achieved without the use of graft implantation or nerve lesions.
Stimulation of adenosine A1 receptors attenuates dopamine D1 receptor‐mediated increase of NGFI‐A, c‐fos and jun‐B mRNA levels in the dopamine‐denervated striatum and dopamine D1 receptor‐mediated turning behaviour
Authors: Ferré Sergi , Rimondini Roberto , Popoli Patrizia , Reggio Rosaria , Pèzzola Antonella , Hansson Anita C. , Andersson Annica , Fuxe Kjell 
Published: March 2003

AbstractAdenosine A1 receptors antagonistically and specifically modulate the binding and functional characteristics of dopamine D1 receptors. In the striatum this interaction seems to take place in the GABAergic strionigro‐strioentopeduncular neurons, where both receptors are colocalized. D1 receptors in the strionigro‐strioentopeduncular neurons are involved in the increased striatal expression of immediate‐early genes induced by the systemic administration of psychostimulants and D1 receptor agonists. Previous results suggest that a basal expression of the immediate‐early gene c‐fos tonically facilitates the functioning of strionigro‐strioentopeduncular neurons and facilitates D1 receptor‐mediated motor activation. The role of A1 receptors in the modulation of the expression of striatal D1 receptor‐regulated immediate‐early genes and the D1 receptor‐mediated motor activation was investigated in rats with a unilateral lesion of the ascending dopaminergic pathways. The systemic administration of the A1 agonist N6‐cyclopentyladenosine (CPA, 0.1 mg/kg) significantly decreased the number of contralateral turns induced by the D1 agonist SKF 38393 (3 mg/kg). Higher doses of CPA (0.5 mg/kg) were necessary to inhibit the turning behaviour induced by the D2 agonist quinpirole (0.1 mg/kg). By using in situ hybridization it was found that CPA (0.1 mg/kg) significantly inhibited the SKF 38393‐induced increase in the expression of NGFI‐A and c‐fos mRNA levels in the dopamine‐denervated striatum. The increase in jun‐B mRNA expression could only be inhibited with the high dose of CPA (0.5 mg/kg). A stronger effect of the A1 agonist was found in the ventral striatum (nucleus accumbens) compared with the dorsal striatum (dorsolateral caudate‐putamen). The results indicate the existence of antagonistic A1–D1 receptor–receptor interactions in the dopamine‐denervated striatum controlling D1 receptor transduction at supersensitive D1 receptors.
Long‐term enhancement of REM sleep by the pituitary adenylyl cyclase‐activating polypeptide (PACAP) in the pontine reticular formation of the rat
Authors: Ahnaou A. , Basille M. , Gonzalez B. , Vaudry H. , Hamon M. , Adrien J. , Bourgin P. 
Published: March 2003

AbstractIn rats, rapid eye movement (REM) sleep can be elicited by microinjection of vasoactive intestinal polypeptide (VIP) into the oral pontine reticular nucleus (PnO). In the present study, we investigated whether this area could also be a REM‐promoting target for a peptide closely related to VIP: the pituitary adenylyl cyclase‐activating polypeptide (PACAP). When administered into the posterior part of the PnO, but not in nearby areas, of freely moving chronically implanted rats, PACAP‐27 and PACAP‐38 (0.3 and 3 pmol) induced a marked enhancement (60–85% over baseline) of REM sleep for 8 h that could be prevented by prior infusion of the antagonist PACAP‐(6–27) (3 pmol) into the same site. Moreover, injections of PACAP into the centre of the posterior PnO resulted in REM sleep enhancement which could last for up to 11 consecutive days. Quantitative autoradiography using [125I]PACAP‐27 revealed the presence in the PnO of specific binding sites with high affinity for PACAP‐27 and PACAP‐38 (IC50 = 2.4 and 3.2 nm, respectively), but very low affinity for VIP (IC50 > 1 μm). These data suggest that PACAP within the PnO may play a key role in REM sleep regulation, and provide evidence for long‐term (several days) mechanisms involved in such a control. PAC1 receptors which have a much higher affinity for PACAP than for VIP might mediate this long‐term action of PACAP on REM sleep.
Granule cell dispersion is restricted across transverse boundaries in mouse chimeras
Authors: Hawkes Richard , Beierbach Elaine , Tan Seong‐Seng 
Published: March 2003

AbstractThe granular layer of the developing and adult cerebellum is marked by the presence of several transverse boundaries, revealed in gene expression patterns or as a consequence of genetic mutations. It is unclear whether these boundaries represent fundamental differences between granule cell populations or if they are a secondary response to regional differences in the underlying Purkinje cells. One possibility is that boundaries mark different spatial domains of granule cells in a lineage‐dependent fashion. To test this hypothesis, we have analysed a series of murine embryonic stem cell chimeras marked by the constitutive expression of β‐galactosidase in donor granule cells. The chimeras show a consistent spatial restriction boundary, located in the granular layer of lobule VI in the vermis and extending laterally into crus I of the hemispheres. A second boundary was found separating lobules IX and X in the vermis. No correlation was found between the genotypes of molecular layer interneurons and the underlying granule cells, suggesting that they arise independently. No transverse boundaries were observed for the molecular layer interneurons, consistent with the hypothesis that they are not generated from precursors in the external granular layer. These results indicate that the granular layer of the cerebellum comprises cellular domains with different histories separated by consistent spatial restriction boundaries.
Brain activity underlying stereotyped and non‐stereotyped retrieval of learned stimulus–response associations
Authors: Vandenberghe R. , Dupont P. , Bormans G. , Mortelmans L. , Orban G. A. 
Published: March 2003

AbstractWhen humans retrieve learned stimulus–response associations in a stereotyped manner the necessary brain structures may differ from those required when the same associations must be retrieved and adapted to new circumstances. We tested this hypothesis by means of tasks that resembled those employed in monkeys, using positron emission tomography (PET). Stimuli consisted of abstract two‐dimensional shapes. Stereotyped retrieval of learned stimulus–response associations was studied by the use of a concurrent discrimination task with fixed pairing. This was contrasted with conditions requiring retrieval and adaptation of learned associations: forced‐choice recognition, response reversal and concurrent discrimination with random pairing. Visuomotor control, passive viewing and fixation conditions were also included. During concurrent discrimination with fixed pairing, the left lower precentral gyrus and rostral anterior cingulate demonstrated higher blood flow levels in comparison with recognition, concurrent discrimination with random pairing, and to a lesser degree, response reversal. In the left lower precentral gyrus these blood flow levels were also higher in comparison with control conditions. Conversely, during recognition, concurrent discrimination with random pairing and reversal, a single region within the right inferior frontal gyrus demonstrated higher blood flow levels in comparison with concurrent discrimination with fixed pairing and control conditions. This right inferior frontal gyrus activation did not depend on the need for active familiarity judgements or response inhibition. To conclude, the left lower precentral gyrus is more active during stereotyped retrieval of learned stimulus–response associations and the right inferior prefrontal cortex is more active when a learned stimulus–response association must be retrieved and adapted to new circumstances.