bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pineal arylalkylamine N‐acetyltransferase gene expression is highly stimulated at night in the diurnal rodent, Arvicanthis ansorgei
Authors: Garidou Marie‐Laure , Gauer François , Vivien‐Roels Berthe , Sicard Bruno , Pévet Paul , Simonneaux Valérie 
Published: March 2003

AbstractThe different mechanisms underlying the control of diurnal vs. nocturnal activity are still unknown. Regarding the nocturnal synthesis of the pineal hormone, melatonin, experiments performed on diurnal sheep or bovine and on nocturnal rat or hamster revealed important differences in the regulation of the melatonin rate‐limiting enzyme, arylalkylamine N‐acetyltransferase (AA‐NAT). These observations raised the hypothesis that melatonin synthesis may be different in nocturnal vs. diurnal animals. In this study, we cloned the cDNA coding for Aa‐nat and analysed the mechanisms of AA‐NAT enzyme activation in the pineal gland of the diurnal grass rat, Arvicanthis ansorgei, and compared them to those of the nocturnal Wistar rat, Rattus norvegicus. Aa‐nat gene sequences of both species are 86.6% identical. In Arvicanthis, Aa‐nat gene expression is markedly increased at the beginning of the night and is followed by a large increase in AA‐NAT activity and melatonin content. In contrast, at the end of the night, the decrease in AA‐NAT activity and melatonin content precedes that of Aa‐nat mRNA. A β‐adrenergic agonist given at daytime reproduces the nocturnal activation of melatonin synthesis, whereas, a β‐adrenergic antagonist given at night‐time inhibits AA‐NAT activity and melatonin synthesis independently of Aa‐nat mRNA. The day–night regulation of melatonin synthesis in the pineal of the diurnal Arvicanthis, involving a transcriptional activation in early night and a post‐translational inhibition at late night, is very similar to that of the nocturnal Wistar rat. In conclusion, the fundamental differences underlying melatonin synthesis among species rely upon phylogenetic rather than behavioural differences.
Rapid regrowth of hippocampal mossy fibres and preceding maturation of NMDA receptor‐mediated neurotransmission
Authors: Ikegaya Yuji , Koyama Ryuta , Yamada Maki K. , Nishiyama Nobuyoshi , Matsuki Norio 
Published: March 2003

AbstractEarly in postnatal development, glutamatergic synapses contain primarily NMDA receptors and progressively acquire AMPA receptor function. To determine whether this transformation occurs in a process of regenerative synaptogenesis following axotomy, we investigated the recovery of AMPA and NMDA receptor‐mediated neurotransmission after the transection of mossy fibres (MF) in organotypic hippocampal cultures. An NMDA component could already be elicited 1 day after the lesion and reached a saturated level after 3 days. Thereafter, an AMPA component appeared and slowly matured after 10 days. The preceding establishment of NMDA receptor function implies that immature MF synapses are functionally silent at least for the first several days of recovery. The appearance of AMPA receptor‐mediated neurotransmission was unchanged in the presence of an NMDA‐receptor antagonist or tetrodotoxin, which suggests that the AMPA receptor maturation is virtually independent of neuronal activity. Thus, the conversion of silent to functional synapses is not unique to synaptic plasticity or developmental processes but also occurs in recovery after brain damage, but its mechanism is likely to differ from NMDA receptor‐dependent recruitment of AMPA receptors in synaptic plasticity.
Amphetamine and cocaine do not increase Narp expression in rat ventral tegmental area, nucleus accumbens or prefrontal cortex, but Narp may contribute to individual differences in responding to a novel environment
Authors: Lu W. , Marinelli M. , Xu D. , Worley P. F. , Wolf M. E. 
Published: March 2003

AbstractNarp is an immediate early gene product that acts extracellularly to cluster AMPA receptors at excitatory synapses. The present study tested the hypothesis that drugs of abuse alter Narp expression and thereby influence AMPA receptor transmission in addiction‐related circuits. Immunohistochemical studies demonstrated the existence of Narp‐positive cells in hippocampus, prefrontal cortex (PFC) and nucleus accumbens (NAc), with lower levels of staining in the ventral tegmental area (VTA). To study the effects of psychomotor stimulants, Narp levels were quantified by Western blotting and normalized to actin. There were no differences in Narp levels in any brain region between rats treated with repeated saline injections, a single amphetamine injection (5 mg/kg), repeated amphetamine injections (5 mg/kg × 5 days), or repeated cocaine injections (20 mg/kg twice daily × 7 days). We also examined the possible role of Narp in individual differences in responding to a novel environment, a predictor of behavioural responses to psychomotor stimulant drugs including the propensity to acquire drug self‐administration. Narp levels in the PFC, but not other regions, were significantly correlated with locomotor activity in a novel environment. These findings suggest that differential Narp expression in the PFC may be involved in determining individual vulnerability to drugs of abuse, perhaps by influencing the activity of its excitatory projections.
5,7‐DHT‐induced hippocampal 5‐HT depletion attenuates behavioural deficits produced by 192 IgG‐saporin lesions of septal cholinergic neurons in the rat
Authors: Lehmann Olivia , Bertrand Fabrice , Jeltsch Hélène , Morer Martine , Lazarus Christine , Will Bruno , Cassel Jean‐Christophe 
Published: March 2003

AbstractAdult Long–Evans male rats sustained injections of 5,7‐dihydroxytryptamine into the fimbria–fornix (2.5 µg/side) and the cingular bundle (1.5 µg/side) and/or to intraseptal injections of 192 IgG‐saporin (0.4 µg/side) in order to deprive the hippocampus of its serotonergic and cholinergic innervations, respectively. Sham‐operated rats were used as controls. The rats were tested for locomotor activity (postoperative days 18, 42 and 65), spontaneous T‐maze alternation (days 20–29), beam‐walking sensorimotor (days 34–38), water maze (days 53–64) and radial maze (days 80–133) performances. The cholinergic lesions, which decreased the hippocampal concentration of ACh by about 65%, induced nocturnal hyperlocomotion, reduced T‐maze alternation, impaired reference‐memory in the water maze and working‐memory in the radial maze, but had no effect on beam‐walking scores and working‐memory in the water maze. The serotonergic lesions, which decreased the serotonergic innervation of the hippocampus by about 55%, failed to induce any behavioural deficit. In the group of rats given combined lesions, all deficits produced by the cholinergic lesions were observed, but the nocturnal hyperlocomotion and the working‐memory deficits in the radial maze were attenuated significantly. These results suggest that attenuation of the serotonergic tone in the hippocampus may compensate for some dysfunctions subsequent to the loss of cholinergic hippocampal inputs. This observation is in close concordance with data showing that a reduction of the serotonergic tone, by pharmacological activation of somatodendritic 5‐HT1A receptors on raphe neurons, attenuates the cognitive disturbances produced by the intrahippocampal infusion of the antimuscarinic drug, scopolamine. This work has been presented previously [Serotonin Club/Brain Research Bulletin conference, Serotonin: From Molecule to the Clinic (satellite to the Society for Neuroscience Meeting, New Orleans, USA, November 2–3, 2000)].
Direction‐specific motion blindness induced by focal stimulation of human extrastriate cortex
Authors: Blanke O. , Landis T. , Safran A. B. , Seeck M. 
Published: March 2003

AbstractMotion blindness (MB) or akinetopsia is the selective disturbance of visual motion perception while other features of the visual scene such as colour and shape are normally perceived. Chronic and transient forms of MB are characterized by a global deficit of direction discrimination (pandirectional), which is generally assumed to result from damage to, or interference with, the motion complex MT+/V5. However, the most characteristic feature of primate MT‐neurons is not their motion specificity, but their preference for one direction of motion (direction specificity). Here, we report that focal electrical stimulation in the human posterior temporal lobe selectively impaired the perception of motion in one direction while the perception of motion in other directions was completely normal (unidirectional MB). In addition, the direction of MB was found to depend on the brain area stimulated. It is argued that direction specificity for visual motion is not only represented at the single neuron level, but also in much larger cortical units.
Effects of intralaminar thalamic nuclei lesion on glutamic acid decarboxylase (GAD65 and GAD67) and cytochrome oxidase subunit I mRNA expression in the basal ganglia of the rat
Authors: Bacci Jean‐Jacques , Kerkerian‐Le Goff Lydia , Salin Pascal 
Published: March 2003

AbstractThis study investigated the influence of thalamic inputs on neuronal metabolic activity in the rat basal ganglia. By means of in situ hybridization histochemistry, we examined the consequences of ibotenate‐induced unilateral lesion of intralaminar thalamic nuclei on mRNA expression of cytochrome oxidase subunit‐I (CoI) in the striatum and the subthalamic nucleus (STN) and of the two isoforms of glutamate decarboxylase (GAD65 and GAD67) in the striatum, globus pallidus (GP), entopeduncular nucleus (EP) and substantia nigra pars reticulata (SNr). In the striatum, GAD67 mRNA expression decreased selectively in the rostral part of the structure at 5 and 12 days postlesion (≈−30%), whereas, GAD65 mRNA levels was downregulated only in the caudal striatum at 12 days (−29%). In both the striatum and STN, CoI mRNA expression decreased ipsilaterally at 5 and bilaterally at 12 days. In GP, GAD67 and GAD65 mRNA expression decreased ipsilaterally at 5 (−20% and −26%) and 12 days (−23% and −36%). In EP, selective bilateral decreases in GAD67 mRNA expression were found at 5 and 12 days (−50% and −40%). Conversely, in SNr, only GAD65 mRNA expression was reduced bilaterally at both time points. These data show that the thalamus exerts a widespread excitatory influence on the basal ganglia network that cannot be accounted for solely by its known direct connections. Given the recent data showing that intralaminar thalamic nuclei are a major nondopaminergic site of neurodegeneration in Parkinson's disease, these results may have a critical bearing on understanding the cellular basis of basal ganglia dysfunction in parkinsonism.
Effects of transgenic overproduction of CRH on anxiety‐like behaviour
Authors: Van Gaalen Marcel M. , Stenzel‐Poore Mary P. , Holsboer Florian , Steckler Thomas 
Published: March 2003

AbstractCentral administration of corticotropin‐releasing hormone increases anxiety‐like behaviour and arousal in rodents, and increased anxiety‐like behaviour has been shown in mice overproducing corticotropin‐releasing hormone on an elevated plus maze and in a dark–light emergence task. However, evidence is accumulating that measures obtained from different anxiety tasks may reflect different aspects of anxiety‐like behaviour in animals. We therefore tested mice overproducing corticotropin‐releasing hormone in a battery of paradigms, studying spontaneous behaviour after a mild stressor, tasks of innate anxiety‐like behaviour (light–dark box), lick suppression (Vogel conflict), conditioned fear, and forced swimming. Exploratory behaviour was studied in a 16‐hole board task. Furthermore, pain threshold, water intake, locomotor activity and sensorimotor learning/co‐ordination were tested to control for confounding factors. In line with previous findings, increased anxiety‐like behaviour of transgenic mice was observed in the light–dark box paradigm. However, no differences were seen in the conflict paradigm. Conditioned fear was decreased 1 h but not 24 h after conditioning in transgenic mice, and immobility was increased in forced swimming in corticotropin‐releasing hormone overexpressors. Locomotor activity in a novel open field and on the hole board was reduced in transgenics. Exploratory behaviour (hole pokes) was reduced during initial exploration of an unfamiliar hole board. Moreover, sensorimotor performance on a rotorod was impaired, and water intake was reduced in corticotropin‐releasing hormone overproducing mice, while no changes were seen in nociception. No differences in locomotor activity were seen in a second group of mice, tested in a familiar open field. When these animals were challenged with diazepam, transgenic mice were less susceptible to the sedative effects of the drug on locomotor activity. These data suggest that corticotropin‐releasing hormone overproduction leads to specific effects in a subset of anxiety paradigms, and that these transgenic mice suffer from a motor deficit in addition to altered anxiety‐like behaviour/arousal.
SHORT COMMUNICATION Inhibition of GABAergic neurotransmission in the ventral tegmental area by cannabinoids
Authors: Szabo Bela , Siemes Sabine , Wallmichrath Ilka 
Published: March 2003

AbstractIt was shown recently that Δ9‐tetrahydrocannabinol, like several other drugs eliciting euphoria, stimulates dopaminergic neurons projecting from the ventral tegmental area (VTA) to the nucleus accumbens. The aim of the present work was to clarify the mechanism of this stimulatory effect. Our hypothesis was that cannabinoids depress the GABAergic inhibition of dopaminergic neurons in the VTA. Electrophysiological properties of VTA neurons in rat coronal midbrain slices were studied with the patch‐clamp technique. GABAA receptor‐mediated inhibitory postsynaptic currents (IPSCs) were evoked by electrical stimulation in the vicinity of the recorded neurons. The amplitude of IPSCs was depressed by the synthetic mixed CB1/CB2 cannabinoid receptor agonist WIN55212‐2 (10−6 and 10−5 m). The CB1 cannabinoid receptor antagonist SR141716A (10−6 m) prevented the inhibition produced by WIN55212‐2 (10−5 m). Two observations showed that IPSCs were depressed with a presynaptic mechanism. WIN55212‐2 (10−5 m) did not change the amplitude of miniature IPSCs recorded in the presence of tetrodotoxin. Currents evoked by pressure ejection of muscimol from a pipette were also not changed by WIN55212‐2 (10−5 m). The results indicate that activation of CB1 cannabinoid receptors inhibits GABAergic neurotransmission in the VTA with a presynaptic mechanism. Depression of the GABAergic inhibitory input of dopaminergic neurons would increase their firing rate in vivo. Accordingly, dopamine release in the projection region of VTA neurons, the nucleus accumbens, would also increase.
Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task
Authors: Kempermann G. , Gage F. H. 
Published: March 2003

AbstractA number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD‐2 and BXD‐8, showed a 26‐fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.
SHORT COMMUNICATION Selective enhancement of spatial learning under chronic psychosocial stress
Authors: Bartolomucci Alessandro , De Biurrun Gabriel , Czéh Boldizsár , Van Kampen Marja , Fuchs Eberhard 
Published: March 2003

AbstractThe hippocampus has long been proved to be implicated in several learning and memory processes. Being integrated into the limbic‐hypothalamus‐pituitary‐adrenal axis, the hippocampus also plays an active role in the regulation of the stress response. Long lasting elevated levels of glucocorticoids resulting from a prolonged stress exposure affect hippocampal functions and structure, inducing learning and memory alterations and suppressing cell proliferation in the adult dentate gyrus. Here, adult male tree shrews (Tupaia belangeri) exposed to chronic psychosocial stress were tested repeatedly on a holeboard apparatus using two different learning tasks devised to evaluate hippocampal‐dependent and hippocampal‐independent cognitive function. We show that chronic stress enhanced learning in animals performing the hippocampal‐dependent task, whereas no stress‐induced effect was found in the hippocampal‐independent task. Additionally, after five weeks of stress, cell proliferation was reduced in the hippocampal dentate gyrus. These results indicate that specific memory processes not only may remain intact, but indeed are facilitated by chronic stress, despite elevated cortisol levels and suppressed hippocampal cell proliferation.
Recovery following peripheral destruction of olfactory neurons in young and adult mice
Authors: Ducray Angélique , Bondier Jean‐Robert , Michel Germaine , Bon Karine , Propper Alain , Kastner Anne 
Published: March 2003

AbstractOlfactory neurons (ON) which are located in the olfactory epithelium are responsible of odorous molecule detection. A unique feature of these cells is their continuous replacement throughout life due to the proliferation and differentiation of local neural precursors, the basal cells. Thus, experimental destruction of all ON induces a stimulation of basal cell division followed by tissue regeneration. The fact that ON precursors display such proliferative and neurogenic activity in adults makes these cells particularly attractive as a potential tool for nervous system repair. However, basal cell proliferation and, thus, ON production, decrease in relation to age; mostly during the first months of life. Therefore, we aimed to seek whether the ability of ON precursors to yield new functional ON in regenerative conditions was consequently impaired in adult. ZnSO4 intranasal perfusion administered to young (1 month) and adult (6 months) mice leads in a few days to total ON destruction and to hyposmia. Tissue and function restoration occurred in the following weeks in both mice groups and was preceded by a transient peak of cell division. In adults, although neurogenesis in the impaired olfactory epithelium was less efficient than in young mice, neural precursors retain their ability to provide new functional ON as indicated by the butanol detection recovery. This was achieved more rapidly than total ON regeneration, suggesting that a reduced number of reconnected ON may be sufficient for odor discrimination.
Evaluation of GluR2 subunit involvement in AMPA receptor function of neonatal rat hypoglossal motoneurons
Authors: Essin K. , Nistri A. , Magazanik L. 
Published: March 2003

AbstractAMPA receptors (AMPAr) mediate fast synaptic responses to glutamate and, when they lack the GluR2 subunit, are strongly Ca2+ permeable and may increase intracellular Ca2+ levels. Because hypoglossal motoneurons possess restricted ability to buffer internal Ca2+ and are vulnerable to Ca2+ excitotoxicity, we wondered if, in these cells, any significant Ca2+ influx could be generated via AMPAr activity. Using whole cell patch‐clamp recording from neonatal rat hypoglossal motoneurons, we tested the AMPAr properties conferred by GluR2 subunits, namely Ca2+ permeability, current rectification and sensitivity to pentobarbital or to the subunit‐specific channel blockers, IEM‐1460 and IEM‐1925. We recorded membrane currents generated by the agonist, kainate, and compared them with those obtained from hippocampal pyramidal neurons (expressing GluR2‐containing AMPAr) and from striatal giant aspiny or hippocampal interneurons (with GluR2‐lacking AMPAr). Ca2+ vs. Na+ permeability of motoneuron AMPAr was relatively low (0.25 ± 0.05), although higher than that of pyramidal neurons. With intracellularly applied spermine, significant inward rectification was absent from motoneurons. These data indicated the prevalence of functional GluR2 subunits. However, the sensitivity of motoneuron AMPAr to pentobarbital did not differ from that of GluR2‐lacking AMPAr on interneurons. Motoneurons possessed sensitivity to IEM‐1460 (IC50 = 90 ± 10 µm) approximately 10‐fold lower than striatal interneurons, although 10‐fold higher than hippocampal pyramidal cells. IEM‐1925 also reduced the amplitude of excitatory synaptic currents in brainstem slice motoneurons. We hypothesize that hypoglossal motoneuron AMPAr (moderately Ca2+ permeable because they contain few GluR2 subunits) may contribute to intracellular Ca2+ rises especially if persistent AMPAr activation (or the pathological GluR2 down‐regulation) occurs.
Corticofugal modulation of midbrain sound processing in the house mouse
Authors: Yan Jun , Ehret Günter 
Published: March 2003

AbstractAn understanding of the neural mechanisms responsible for auditory information processing is incomplete without a careful examination of substantial descending pathways. This study focuses on the functional role of corticofugal projections. Our work with the house mouse reveals that the focal electrical stimulation of the primary auditory cortex leads to profound changes in auditory response properties in the central nucleus of the inferior colliculus of the midbrain. Cortical stimulation does not impact on the collicular best frequencies when the best frequencies of stimulated cortical neurons and recorded collicular neurons are similar. Rather, collicular best frequencies are shifted toward the stimulated cortical best frequencies when cortical and collicular frequencies are different. Such a shift is unrelated to the differences in minimum thresholds between cortical and collicular neurons. In addition to frequency‐specific shifts in collicular best frequencies, cortical stimulation elevates collicular minimum thresholds and reduces both dynamic ranges and response magnitudes if cortical and collicular best frequencies are different. If cortical and collicular best frequencies are similar but minimum thresholds are different, collicular minimum thresholds are shifted toward the stimulated cortical thresholds; dynamic ranges and response magnitudes may either increase or decrease in this scenario. Our results suggest that the corticofugal adjustment has a centre–surround organization with regard to both cortical best frequencies and cortical minimum thresholds. The midbrain processing of sound components in the centre of cortical feedback is largely enhanced while processing in the surround is suppressed.