bluuebunny/crossref_metadata_2025_split huggingface dataset:
Arm movement and gap as factors influencing the reaction time of the second saccade in a double‐step task
Authors: Lünenburger Lars , Hoffmann Klaus‐Peter 
Published: June 2003

AbstractTo guide our hand for reaching, we explore our visual environment by sequences of saccades. In the present paper, we studied the eye and hand movements of human subjects looking or looking and pointing at a target that is instantaneously displaced two times (double‐step task). It was previously shown that the second saccade has a much longer reaction time than the first one [Feinstein & Williams (1972) Vision Res., 12, 33–44]. The second reaction time is even longer if the subject also has to point to the target with the hand [Lünenburger et al. (2000) Eur. J. Neurosci., 12, 4107–4116]. The conditions and objective for these effects are further examined in the present paper. It is shown that vision of the hand reduces the first and second saccadic reaction times in parallel. The second reaction time is prolonged for shorter delays between both target steps as well as for larger amplitudes of the second saccade. However, the long second reaction time does not reflect an absolute saccadic refractory period, because a gap before the second target step reduces the second reaction time to a value similar to the first. Hand response time and average hand velocity were increased when the second target step was larger. The response time for the eyes was about 30% of the response time of the hand. We argue that the observed effects reflect the coordination of eye and hand movement to allow a precise and efficient reaching behaviour.
Piriform cortex functional heterogeneity revealed by cellular responses to odours
Authors: Litaudon P. , Amat C. , Bertrand B. , Vigouroux M. , Buonviso N. 
Published: June 2003

AbstractThe role of the piriform cortex (PC) in olfactory information processing remains mainly unknown. Indeed, until recently, only a few studies have investigated the response of PC neurons to odours and these studies did not take into account the functional heterogeneity of the PC previously described using an electrical stimulation paradigm. In this experiment, extracellular activity in response to odour was recorded in urethane anaesthetized rats in the different parts of the cortex ranging from anterior to posterior. A large percentage of cortical cells were silent at rest, and this percentage increased from anterior to posterior. Analysis of odour evoked activity revealed a large percentage of nonresponsive cells that increased from anterior to posterior. Cell activity was largely synchronized with breathing and different temporal patterns were observed. The anterior PC was characterized by odour‐evoked responses phase‐locked with the inhalation‐exhalation transition period. By contrast, activity in the posterior PC was mainly phase‐locked with inhalation or exhalation. These data confirm the spatial functional heterogeneity previously reported in the PC. Functional anatomy of the PC suggests that activity in the anterior PC can be mainly driven by afferent activity coming from the OB whereas posterior cells were certainly entrained by more complex mechanisms.
Purinergic receptors on microglial cells: functional expression in acute brain slices and modulation of microglial activation in vitro
Authors: Boucsein Clemens , Zacharias Robert , Färber Katrin , Pavlovic Sanja , Hanisch Uwe‐Karsten , Kettenmann Helmut 
Published: June 2003

AbstractMicroglial cells are the pathologic sensors in the brain. ATP released from damaged cells is a candidate for signalling neural injury to microglia. Moreover, ATP is an extracellular messenger for propagating astrocyte activity in the form of Ca2+ waves. To test for the functional expression of purinoreceptors in microglial cells we employed the patch‐clamp technique in acute slices of adult mouse brain. ATP triggered a nonselective cationic and a K+ current. Pharmacological screening with purinergic ligands indicated the presence of P2Y1 and P2Y2/4 receptors linked to the activation of a K+ current and P2X receptors, including P2X7, linked to the activation of a nonselective cationic current. These findings suggest that microglial cells in situ express different purinergic receptors with distinct sensitivity and functional coupling. To test for the involvement of purinoreceptors in microglial activation, we stimulated cultured microglial cells with lipopolysaccharide and measured the release of tumour necrosis factor α, interleukin‐6, interleukin‐12 and macrophage inflammatory protein 1α, induction of K+ outward currents and nitric oxide release. All these parameters were reduced in the presence of purinergic ligands, indicating that purinergic receptor activation attenuated indicators of microglial activation.
Axonal morphogenesis controlled by antagonistic roles of two CRMP subtypes in microtubule organization
Authors: Yuasa‐Kawada Junichi , Suzuki Ryoko , Kano Fumi , Ohkawara Takeshi , Murata Masayuki , Noda Masaharu 
Published: June 2003

AbstractDuring development, cells undergo dynamic morphological changes by rearrangements of the cytoskeleton including microtubules. However, molecular mechanisms underlying the microtubule remodeling between orientated and disoriented formations are almost unknown. Here we found that novel subtypes of collapsin response mediator proteins (CRMP‐As) and the originals (CRMP‐Bs), which occur from the alternative usage of different first coding exons, are involved in this conversion of microtubule patterns. Overexpression of CRMP2A and CRMP2B in chick embryonic fibroblasts induced orientated and disoriented patterns of microtubules, respectively. Moreover, sequential overexpression of another subtype overcame the effect of the former expression of the countersubtype. Overexpression experiments in cultured chick retinae showed that CRMP2B promoted axon branching and suppressed axon elongation of ganglion cells, while CRMP2A blocked these effects when co‐overexpressed. Our findings suggest that the opposing activities of CRMP2A and CRMP2B contribute to the cellular morphogenesis including neuronal axonogenesis through remodeling of microtubule organization.
Expression patterns and subcellular localization of the Down syndrome candidate protein MNB/DYRK1A suggest a role in late neuronal differentiation
Authors: Hämmerle B. , Carnicero A. , Elizalde C. , Ceron J. , Martínez S. , Tejedor F. J. 
Published: June 2003

AbstractThe Minibrain (Mnb) gene belongs to a new protein kinase family, which is evolutionarily conserved, and probably plays several roles during brain development and in adulthood. In Drosophila, mnb is involved in postembryonic neurogenesis and in learning/memory. In humans, MNB has been mapped within the Down syndrome critical region of chromosome 21 and is overexpressed in the Down syndrome embryonic brain. It has been widely proposed that MNB is involved in the neurobiological alterations associated with Down syndrome. Nevertheless, little is known about the functional role that MNB plays in vertebrate brain development. We have recently shown [Hämmerle et al. (2002) Dev. Biol., 246, 259–273] that in early vertebrate embryos, Mnb is transiently expressed in neural progenitor cells during the transition from proliferating to neurogenic divisions. Here we have studied in detail a second wave of Mnb expression, which takes place in the brain of intermediate and late vertebrate embryos. In these stages, MNB seems to be restricted to certain populations of neurons, as no consistent expression was detected in astroglial or oligodendroglial cells. Interestingly, MNB expression takes place at the time of dendritic tree differentiation and is initiated by a transient translocation from the cytoplasm to the nucleus. Afterwards, MNB protein is transported to the growing dendritic tree, where it colocalizes with Dynamin 1, a putative substrate of MNB kinases. We propose that MNB kinase is involved in the signalling mechanisms that regulate dendrite differentiation. This functional role helps to build a new hypothesis for the implication of MNB/DYRK1A in the developmental aetiology of Down syndrome neuropathologies.
Decreased ethanol preference and wheel running in Nurr1‐deficient mice
Authors: Werme Martin , Hermanson Elisabet , Carmine Andrea , Buervenich Silvia , Zetterström Rolf H. , Thorén Peter , Ögren Sven Ove , Olson Lars , Perlmann Thomas , Brené Stefan 
Published: June 2003

AbstractNurr1 (Nr4a2) is a transcription factor expressed in dopamine cells from early development and throughout life. Null mutants for Nurr1 lack the ventral midbrain dopamine neurons and die soon after birth. Animals with a heterozygous deletion are viable and display no apparent abnormality. We have investigated the impact of heterozygous deletion of Nurr1 on ethanol consumption in adult mice as a model for drug‐induced reward and on wheel running as a model for natural reward. Interestingly, Nurr1 heterozygous mice never developed high ethanol consumption nor did they develop as much running behaviour as did the wild‐type animals. Thus, Nurr1 appears to have a key role for the reinforcing properties of ethanol and running that underlies the development of excessive reward‐seeking behaviours characteristic for addiction. Quantitative trait loci mapping using C57Bl/6 and DBA/2 mice describe a locus for ethanol preference on chromosome 2, wherein Nurr1 is located. We found two dinucleotide repeats in the Nurr1 promoter that were longer in mice with low preference for ethanol (DBA/2 and 129/Sv) than in mice with high preference for ethanol (C57Bl/6J and C57Bl/6NIH). These sequential data are compatible with Nurr1 as a candidate gene responsible for the quantitative trait loci for ethanol preference on mouse chromosome 2. Together, our data thus imply involvement of Nurr1 in the transition to a state of high ethanol consumption as well as in the development of a high amount of wheel running in mice.
Early life adversity programs changes in central 5‐HT neuronal function in adulthood
Authors: Gartside Sarah E. , Johnson Daniel A. , Leitch Melville M. , Troakes Claire , Ingram Colin D. 
Published: June 2003

AbstractEarly life adversity is associated with an increased incidence of psychiatric illness in adulthood. Although the mechanisms underlying this association are unclear, one possible substrate is brain 5‐hydroxytryptamine neurotransmission, which is reportedly abnormal in several psychiatric disorders. This study examined the effect of a rat model of early life adversity, early maternal separation, on 5‐hydroxytryptamine neurotransmission in adulthood. In vitro electrophysiological experiments revealed that, in early maternal separation rats compared with controls, the sensitivity of α1‐adrenoceptors on 5‐hydroxytryptamine neurons in the dorsal raphe nucleus was significantly reduced, whilst the sensitivity of 5‐hydroxytryptamine1A receptors showed a nonsignificant trend to reduction. In in vivo microdialysis experiments, the 5‐hydroxytryptamine1A receptor agonist‐induced suppression of 5‐hydroxytryptamine release in the frontal cortex was reduced in early maternal separation animals, suggesting desensitization of 5‐hydroxytryptamine1A autoreceptors. There was no increase in basal 5‐hydroxytryptamine in the frontal cortex as measured by microdialysis and a nonsignificant trend towards increased basal firing activity of classical (non‐bursting) 5‐hydroxytryptamine neurons in the dorsal raphe nucleus measured by in vivo electrophysiology. Finally, early maternal separation failed to alter expression of messenger ribonucleic acids coding for 5‐hydroxytryptamine1A or α1B receptors in the dorsal raphe nucleus as measured by in situ hybridization histochemistry, suggesting that functional changes in receptor sensitivity observed are not due to changes in receptor gene transcription. The findings demonstrate that early life adversity programs changes in sensitivity of the two principal regulators of 5‐hydroxytryptamine neuronal activity. Similar effects in humans may contribute to the increased incidence of psychiatric illness in individuals exposed to early life adversity.
What you believe versus what you think they believe: a neuroimaging study of conceptual perspective‐taking
Authors: Ruby Perrine , Decety Jean 
Published: June 2003

AbstractSocial communication requires shared representations as well as a cognitive flexibility for successful interactions between self and other. What neural mechanisms underlie the ability to distinguish between our own perspective vs. the perspective of others at a conceptual level? In this PET study subjects who were medical students were asked according to the experimental conditions to respond to a list of health‐related questions, taking either their own perspective or the perspective of a ‘lay person’. Third‐person perspective as compared to first‐person perspective was associated with activation in the medial part of the superior frontal gyrus, in the left superior temporal sulcus, in the left temporal pole and in the right inferior parietal lobe. The reverse comparison revealed a specific activation in the postcentral gyrus for the first‐person conceptual perspective. This study provides congruent results at the conceptual level with previous studies investigating the neural correlates of self/other distinction at the motor level, and opens a new area of research in which conceptual cognition can be viewed in the continuity of motor cognition.
Rapid reversal of stress induced loss of synapses in CA3 of rat hippocampus following water maze training
Authors: Sandi Carmen , Davies Heather A. , Cordero M. Isabel , Rodriguez Jose J. , Popov Victor I. , Stewart Michael G. 
Published: June 2003

AbstractThe impact was examined of exposing rats to two life experiences of a very different nature (stress and learning) on synaptic structures in hippocampal area CA3. Rats were subjected to either (i) chronic restraint stress for 21 days, and/or (ii) spatial training in a Morris water maze. At the behavioural level, restraint stress induced an impairment of acquisition of the spatial response. Moreover, restraint stress and water maze training had contrasting impacts on CA3 synaptic morphometry. Chronic stress induced a loss of simple asymmetric synapses [those with an unperforated postsynaptic density (PSD)], whilst water maze learning reversed this effect, promoting a rapid recovery of stress‐induced synaptic loss within 2–3 days following stress. In addition, in unstressed animals a correlation was found between learning efficiency and the density of synapses with an unperforated PSD: the better the performance in the water maze, the lower the synaptic density. Water maze training increased the number of perforated synapses (those with a segmented PSD) in CA3, both in stressed and, more notably, in unstressed rats. The distinct effects of stress and learning on CA3 synapses reported here provide a neuroanatomical basis for the reported divergent effects of these experiences on hippocampal synaptic activity, i.e. stress as a suppressor and learning as a promoter of synaptic plasticity.
Normal sensitivity to acute pain, but increased inflammatory hyperalgesia in mice lacking the nociceptin precursor polypeptide or the nociceptin receptor
Authors: Depner Ulrike B. , Reinscheid Rainer K. , Takeshima Hiroshi , Brune Kay , Zeilhofer Hanns Ulrich 
Published: June 2003

AbstractNociceptin/orphanin FQ (N/OFQ) is the endogenous agonist of the N/OFQ peptide receptor (NOP receptor). It is released from a larger precursor polypeptide, called prepro‐nociceptin (ppN/OFQ) from which, in addition to N/OFQ, other biologically active neuropeptides may be derived. Increasing evidence indicates that exogenous application of N/OFQ to the central nervous system of mice and rats induces pro‐ and antinociceptive effects depending on the dose and site of administration. Much less is known about a potential contribution of endogenous N/OFQ to pain control. Here, we have used a genetic approach to address this topic. Mice deficient in either the NOP receptor (NOP‐R−/− mice) or the N/OFQ precursor polypeptide (ppN/OFQ−/− mice) or both (double knockout mice) were compared with wild‐type littermates in animal models of acute and tonic pain. Nociceptive responses to acute noxious heat of all three types of mutant mice were indistinguishable from those of wild‐type mice. Accordingly, nociceptive behaviour was very similar in the early phase of the formalin test. However, NOP‐R−/−, ppN/OFQ−/− and double knockout mice showed markedly stronger nociceptive responses during prolonged nociceptive stimulation in the second phase of the formalin test and significantly lower thermal pain thresholds in inflamed tissue after zymosan A injection. These results indicate that N/OFQ contributes significantly to endogenous pain control during prolonged nociceptive stimulation but does not affect acute pain sensitivity. Among the three types of mutant mice nociceptive behaviour was nearly identical, indicating that the lack of other potential ppN/OFQ products in the ppN/OFQ−/− mice was apparently without effect on the nociceptive phenotype.
Morphine withdrawal precipitated by specific mu, delta or kappa opioid receptor antagonists: a c‐Fos protein study in the rat central nervous system
Authors: Le Guen Stéphanie , Gestreau Christian , Besson Jean‐Marie 
Published: June 2003

AbstractWe have recently shown concurrent changes in behavioural responses and c‐Fos protein expression in the central nervous system in both naive and morphine‐dependent rats after systemic administration of the opioid antagonist naloxone. However, because naloxone acts on the three major types of opioid receptors, the present study aimed at determining, in the same animals, both changes in behaviour and c‐Fos‐like immunoreactivity after intravenous injection of selective opioid antagonists, such as mu (β‐funaltrexamine, 10 mg/kg), delta (naltrindole, 4 mg/kg) or kappa (nor‐binaltorphimine, 5 mg/kg) opioid receptor antagonists, in naive or morphine‐dependent rats. In a first experimental series, only β‐funaltrexamine increased c‐Fos expression in the eight central nervous system structures examined, whereas no effect was seen after naltrindole or nor‐binaltorphimine administration in naive rats. These results suggest a tonic activity in the endogenous opioid peptides acting on mu opioid receptors in normal rats. A second experimental series in morphine‐dependent rats showed that β‐funaltrexamine had the highest potency in the induction of classical signs of morphine withdrawal syndrome, as well as the increase in c‐Fos expression in the 22 central nervous system structures studied, suggesting a major role of mu opioid receptors in opioid dependence. However, our results also demonstrated that naltrindole and, to a lesser extent, nor‐binaltorphimine were able to induce moderate signs of morphine withdrawal and relatively weak c‐Fos protein expression in restricted central nervous system structures. Therefore, delta and kappa opioid receptors may also contribute slightly to opioid dependence.
Illusory contours and specific regions of human extrastriate cortex: evidence from rTMS
Authors: Brighina F. , Ricci R. , Piazza A. , Scalia S. , Giglia G. , Fierro B. 
Published: June 2003

AbstractFunctional magnetic resonance imaging studies showed that perception of illusory contours is associated with extrastriate cortex activation prevailing on the right side. 1 Hz repetitive transcranial magnetic stimulation (rTMS) is able to induce lasting inhibition of cortical activity. The objective of the study was to investigate the role of extrastriate cortex in illusory contour perception inducing 1 Hz rTMS interference in healthy subjects. Eight healthy subjects underwent 1 Hz rTMS (600 pulses) through a figure‐of‐eight coil over right and left occipital cortex (O1 and O2 of 10/20 EEG system); sham magnetic stimulation on the same sites and right motor cortex rTMS (in three subjects) were given as control. Subjects performed a computerized task requiring perception of illusory and real contours of Kanizsa squares in baseline and after rTMS. After stimulus presentation the subject made a forced‐choice decision about the regularity or irregularity of stimulus contour, by hitting as fast as possible one of two keys on the computer keyboard. Reaction times (RT) were measured. Right occipital stimulation significantly increased RT for illusory contour perception (vs. baseline, P < 0.05). No significant RT changes were observed in the other experimental conditions with respect to the baseline condition. It is concluded that 1Hz rTMS of right extrastriate cortex can disrupt perception of illusory contours and the effect appears to be side‐specific, being evident only after right occipital stimulation. This study supports the critical role of right extrastriate cortex in illusory contour perception.
Cloning and characterization of an ionotropic glutamate receptor subunit expressed in the squid nervous system
Authors: Battaglia A. A. , Nardi G. , Steinhardt A. , Novakovic A. , Gentile S. , Iaccarino Idelson P. , Gilly W. F. , Santis A. De 
Published: June 2003

AbstractIn this paper we describe the cloning of a putative ionotropic glutamate receptor subunit, SqGluR, and its distribution in the nervous system of the squid. A full‐length cDNA was assembled from a cDNA library of the stellate ganglion/giant fibre lobe complex of Loligo opalescens. The deduced amino acid sequence of the mature SqGluR displayed 44–46% amino acid identity with mammalian GluR1–GluR4 and 53% with Lym‐eGluR1 from Lymnaea stagnalis. In situ hybridizations in adult squid confirmed that the SqGluR mRNA is abundant in giant fibre lobe neurons, in large, presumptive motor neurons of the stellate ganglion proper and in the supraoesophageal and optic lobes of the central nervous system. In newborn squid, SqGluR mRNA expression was detected throughout the nervous system but not elsewhere. A synthetic peptide corresponding to the last 15 amino acids of the SqGluR C‐terminus was used to generate polyclonal antibodies, which were used for immunoblot analysis to demonstrate widespread expression in the squid central and peripheral nervous systems. Injection of the synthetic peptide into the postsynaptic side of the giant synapse inhibited synaptic transmission.