bluuebunny/crossref_metadata_2025_split huggingface dataset:
Developmental expression of the cellular prion protein in elongating axons
Authors: Salès Nicole , Hässig Raymonde , Rodolfo Katia , Di Giamberardino Luigi , Traiffort Elisabeth , Ruat Martial , Frétier Philippe , Moya Kenneth L. 
Published: March 2003

AbstractPrPc, a sialoglycoprotein present in the normal adult hamster brain, is particularly abundant in plastic brain regions but little is known about the level of expression and the localization of the protein during development. Western blot analysis of whole brain homogenates with mab3F4 show very low levels of the three main molecular weight forms of the protein at birth, in contrast to the strong and wide expression of mRNA transcripts. The PrPc levels increase sharply through P14 and are diminished somewhat in the adult. Regional analysis showed that in structures with ongoing growth or plasticity such as the olfactory bulb and hippocampus, PrPc remains high in the adult, while in areas where structural and functional relationships stabilize during development, such as the cortex and the thalamus, PrPc levels decline after the third postnatal week. In the neonate brain PrPc was prominent along fiber tracts similar to markers of axon elongation and in vitro experiments showed that the protein was present on the surface of elongating axons. PrPc is then localized to the synaptic neuropil in close spatio‐temporal association with synapse formation. The localization of PrPc on elongating axons suggests a role for the protein in axon growth. In addition, the relative abundance of the protein in developing axon pathways and during synaptogenesis may provide a basis for the age‐dependent susceptibility to transmissible spongiform encephalopathies.
Whole‐cell recording from honeybee olfactory receptor neurons: ionic currents, membrane excitability and odourant response in developing workerbee and drone
Authors: Laurent Stéphanie , Masson Claudine , Jakob Ingrid 
Published: March 2003

AbstractWhole‐cell recording techniques were used to characterize ionic membrane currents and odourant responses in honeybee olfactory receptor neurons (ORNs) in primary cell culture. ORNs of workerbee (female) and drone (male) were isolated at an early stage of development before sensory axons connect to their target in the antennal lobe. The results collectively indicate that honeybee ORNs have electrical properties similar, but not necessarily identical to, those currently envisaged for ORNs of other species. Under voltage clamp at least four ionic currents could be distinguished. Inward currents were made of a fast transient, tetrodotoxin‐sensitive sodium current. In some ORNs a cadmium‐sensitive calcium current was detected. ORNs showed heterogeneity in their outward currents: either outward currents were made of a delayed rectifier type potassium current, which was partially blocked by tetraethyl ammonium or quinidine, or were composed of a delayed rectifier type and a transient calcium‐dependent potassium current, which was cadmium‐sensitive and abolished by removal of external calcium. The proportion of each of the two outward currents, however, was different within the ORNs of the two sexes suggesting a gender‐specific functional heterogeneity. ORNs showed heterogeneity in action potential firing properties: depolarizing current steps elicited either one action potential or, as in most of the cells, it led to repetitive spiking. Action potentials were tetrodotoxin‐sensitive suggesting they are carried by sodium. Odourant stimulation with different mixtures and pure substances evoked depolarizing receptor potentials with superimposed action potentials when spike threshold was reached. In summary, honeybee ORNs are remarkably mature at early stages in their development.
Gradients in the circadian expression of Per1 and Per2 genes in the rat suprachiasmatic nucleus
Authors: Yan Lily , Okamura Hitoshi 
Published: March 2003

AbstractThe suprachiasmatic nucleus (SCN) is the mammalian circadian pacemaker, which consists of thousands of oscillator cells. It is believed that the circadian oscillation in each cell is generated by the transcription/(post)‐translation feedback loop of a set of clock genes. However, little is known about how these oscillator cells are organized to produce the robust circadian rhythms in the SCN. In the present study, we examined the expression of the clock genes Per1 and Per2 paying particular attention to the topographic compartmentalization of the SCN. In the rat SCN, the dorsomedial (SCNDM) and ventrolateral (SCNVL) compartments are clearly delineated by chemical characteristics of neurons and neuronal afferents. In the SCNDM, Per1 mRNA was initially expressed at the most dorsomedial region along the third ventricle (SCNDMPV, periventricular part of the dorsomedial compartment of the SCN) at CT0, and then spread laterally to the central dorsomedial region (SCNDMCe, central part of the dorsomedial compartment of the SCN), reaching peaks at subjective day and troughs at subjective night. In contrast, in the SCNVL, Per1 expression showed a weak, two‐peak pattern in one circadian cycle. Per2 expression was also robust in the SCN, showing very similar circadian profiles among these three subdivisions with a slightly earlier phase in SCNDMPV than that in SCNDMCe. We also investigated the Per1 and Per2 expression in response to a light exposure at early subjective night. The light pulse induced both Per1 and Per2 expression, which was restricted in the SCNVL neurons. The present findings suggest that the phase and amplitude of the circadian expression of clock genes are not uniform, and there are topographic neuron groups that have different properties in the SCN.
Excitotoxic lesions of the rhinal cortex in the baboon differentially affect visual recognition memory, habit memory and spatial executive functions
Authors: Chavoix C. , Blaizot X. , Meguro K. , Landeau B. , Baron J.C. 
Published: March 2003

AbstractTo specify the functional role of the rhinal cortex, baboons with bilateral excitotoxic lesions of the rhinal cortex (RH group) were tested on a series of computerized memory and learning tasks. Preoperatively, they were trained to and then tested on a delayed nonmatching‐to‐sample (DNMS) task with trial‐unique stimuli. Postoperatively, this visual recognition memory task was given twice. As compared to a sham‐operated group, the RH group showed good retention of rule learning and were unimpaired on the Delay memory subtest. Performance on the List Length memory subtest was, however, severely impaired at both postoperative evaluations, with a significant negative correlation between cognitive performance and neuronal loss in rhinal areas. Visual habit memory and spatial working memory were assessed postoperatively only, using a concurrent discrimination learning task and both a delayed‐response task (with a two‐ and four‐location choice) and a delayed alternation task, respectively. The RH group was unimpaired on the first two tasks and was even faster than the controls in learning the delayed‐response task with four locations. Finally, most RH baboons failed to learn the delayed alternation task within the limits of testing. These results indicate that neuronal loss in the rhinal cortex is sufficient to impair visual recognition memory, and extend the implication of this area to spatial executive functions. Furthermore, the observation of impaired recognition memory and executive processes with preserved procedural memory and retrograde memory suggests that damage to the rhinal cortex probably participates in the cognitive deficits typical of the early stages of Alzheimer's disease.
Age‐related changes of anandamide metabolism in CB1 cannabinoid receptor knockout mice: correlation with behaviour
Authors: Maccarrone Mauro , Valverde Olga , Barbaccia Maria L. , Castañé Anna , Maldonado Rafael , Ledent Catherine , Parmentier Marc , Finazzi‐Agrò Alessandro 
Published: March 2003

AbstractAnandamide (N‐arachidonoylethanolamine, AEA) and 2‐arachidonoylglycerol (2‐AG) are the most active endocannabinoids at brain (CB1) cannabinoid receptors. CD1 mice lacking the CB1 receptors (‘knockout’[KO] mutants) were compared with wildtype (WT) littermates for their ability to degrade AEA through an AEA membrane transporter (AMT) and an AEA hydrolase (fatty acid amide hydrolase, FAAH). The age dependence of AMT and FAAH activity were investigated in 1‐ or 4‐month‐old WT and KO animals, and found to increase with age in KO, but not WT, mice and to be higher in the hippocampus than in the cortex of all animals. AEA and 2‐AG were detected in nmol/mg protein (µm) concentrations in both regions, though the hippocampus showed approximately twice the amount found in the cortex. In the same regions, 2‐AG failed to change across groups, while AEA was significantly decreased (≈ 30%) in hippocampus, but not in cortex, of old KO mice, when compared with young KO or age‐matched WT animals. In the open‐field test under bright light and in the lit‐dark exploration model of anxiety, young KO mice, compared with old KO, exhibited a mild anxiety‐related behaviour. In contrast, neither the increase in memory performance assessed by the object recognition test, nor the reduction of morphine withdrawal symptoms, showed age dependence in CB1 KO mice. These results suggest that invalidation of the CB1 receptor gene is associated with age‐dependent adaptive changes of endocannabinoid metabolism which appear to correlate with the waning of the anxiety‐like behaviour exhibited by young CB1 KO mice.
Timecourse of object‐related neural activity in the primate prefrontal cortex during a short‐term memory task
Authors: Rainer Gregor , Miller Earl K. 
Published: March 2003

AbstractWe studied the timecourse of neural activity in the primate (Macacca mulatta) prefrontal (PF) cortex during an object delayed‐matching‐to‐sample (DMS) task. To assess the effects of experience on this timecourse, we conducted the task using both novel and highly familiar objects. In addition, noise patterns containing no task‐relevant information were used as samples on some trials. Comparison of average PF ensemble activity relative to baseline activity generated by objects and noise patterns revealed three distinct activity periods. (i) Sample onset elicited a transient sensory visual response. In this sensory period, novel objects elicited stronger average ensemble activity than both familiar objects and noise patterns. (ii) An intermediate period of elevated activity followed, which began before sample offset, and continued well into the delay period. In the intermediate period, activity was elevated for noise patterns and novel objects, but near baseline for familiar objects. (iii) Finally, after average ensemble activity reached baseline activity at the end of the intermediate period, a reactivation period occurred late in the delay. Experience had little effect during reactivation, where activity was elevated for both novel and familiar objects compared to noise patterns. We show that the ensemble average resembles the activity timecourse of many single prefrontal neurons. These results suggest that PF delay activity does not merely maintain recent sensory input, but is subject to more complex experience‐dependent dynamics. This has implications for how delay activity is generated and maintained.
Neural cells from primary human striatal xenografts migrate extensively in the adult rat CNS
Authors: Hurelbrink Carrie B. , Armstrong Richard J. E. , Dunnett Stephen B. , Rosser Anne E. , Barker Roger A. 
Published: March 2003

AbstractPrimary neural cells do not appear to migrate significantly following transplantation into the adult rodent CNS, which is in contrast to expanded neural precursor cells where migration is well‐documented. However, most transplant studies of primary neural tissue have been performed in an allograft situation in which it is difficult to identify graft‐derived cells. We have, therefore, used a xenograft paradigm to investigate the potential for cells derived from grafts of primary human fetal striatal tissue (gestational age of 66–72 days) to migrate following intrastriatal transplantation in an athymic adult rat model of Huntington's disease. The use of an antibody specific to human nuclear antigen enabled clear identification of graft‐derived cells within the host brain, and specific neural phenotypes were determined using human‐specific tau for neurons, glial fibrillary acidic protein for mature astrocytes and Ki67 for proliferative cells. At 6 weeks, the graft mass was very dense with a high proliferative index, few cells had migrated away from the graft, and the cells that had differentiated both within and away from the graft were mainly neurons. In contrast, at 6 months, the graft core was dispersed significantly more and a large number of graft‐derived cells had migrated throughout the brain as far rostral as the olfactory bulb and as caudal as the substantia nigra. Cells had differentiated into both neurons and astrocytes and the level of proliferation was significantly lower within the graft. These results demonstrate that primary neural xenografts contain proliferative cells that possess the ability to migrate and differentiate into both neurons and astrocytes, and suggest that these cells could contribute to normal graft function. This property may be a consequence of the xenograft situation and could potentially be exploited to provide the opportunity to target regions of distant pathology in neurodegenerative diseases using xenotransplantation of embryonic neural tissue.
Effect of halothane on neuronal excitation in the superficial dorsal horn of rat spinal cord slices: evidence for a presynaptic action
Authors: Asai Tatsuya , Kusudo Kei , Ikeda Hiroshi , Takenoshita Makoto , Murase Kazuyuki 
Published: March 2003

AbstractThe action of the volatile anaesthetic halothane on optically recorded neuronal excitation in juvenile rat spinal cord slices was investigated. Prolonged neuronal excitation lasting ≈ 100 ms was evoked in the superficial dorsal horn after single‐pulse dorsal root stimulation that activated both A‐ and C‐fibres. Halothane depressed the neuronal excitation in a concentration‐dependent manner (IC50 0.21 mm, Imax 28%). In Ca2+‐free solution, dorsal root stimulation induced excitation with a short duration of several tens of milliseconds, in which the excitation of the postsynaptic component was largely eliminated. Under these conditions, halothane also depressed the excitation concentration‐dependently (IC50 0.46 mm, Imax 60%). Most of the suppression occurred within 5 min of halothane application, and the effect of halothane was fully reversible upon washout of the anaesthetic. Application of bicuculline and strychnine or picrotoxin, or reduction of extracellular Cl– concentration ([Cl–]o), had no effect on halothane inhibition. Applications of K+ channel blockers tetraethyl ammonium, 4‐aminopyridine, Cs+ or Ba2+ either had no effect or augmented the inhibitory effect of halothane. On the other hand, the degree of inhibition by halothane was found to be dependent on [K+]o; the higher [K+]o, the larger the depression. In addition, decreases in [Na+]o and [Mg2+]o reduced the excitation similar to that of halothane treatment, and the degree of halothane inhibition became larger with lower [Mg2+]o. These results lead to a hypothesis that halothane suppresses the excitation of presynaptic elements by inhibiting presynaptic Na+ channels by shifting the steady‐state inactivation curve in the hyperpolarizing direction.
Adenosine depresses a Ca2+‐independent step in transmitter exocytosis at frog motor nerve terminals
Authors: Huang Shu‐Ming , Kitamura Atsuko , Akita Tenpei , Narita Kazuhiko , Kuba Kenji 
Published: March 2003

AbstractThe depressant action of adenosine on acetylcholine release at frog motor nerve terminals was studied by intracellular recording and Ca2+‐imaging techniques. Adenosine (200 µm) quickly and reversibly decreased the amplitude and quantal content of end‐plate potentials (EPPs) with no change in quantal size in a low‐Ca2+, high‐Mg2+ solution, and EPP amplitude in normal Ringer containing d‐tubocurarine. Likewise, adenosine (200 µm) reduced miniature EPP (MEPP) frequency, but not amplitude, in a high‐K+ (6 mm) solution. Adenosine (40–200 µm), however, did not affect single or repetitive impulse(s)‐induced rises in Ca2+ in the nerve terminals or its basal level. Adenosine (100–200 µm) reduced the Ca2+‐independent enhancement of MEPP frequency caused by hypertonicity. EPPs induced by tetanic stimulation (33 Hz) in Ringer with d‐tubocurarine initially increased in amplitude within 10 stimuli and then declined to the minimum. Adenosine (200 µm) decreased EPP amplitude in the initial phase of the tetanus, but enhanced it in the middle phase, thus prolonging the decay of EPP amplitude. The total sum of these EPPs, reflecting the readily releasable pool of vesicles and its refilling, however, was not changed. The results suggest that adenosine inhibits a Ca2+‐independent step of transmitter exocytosis at frog motor nerve terminals.
Expression of BCL‐2 via adeno‐associated virus vectors rescues thalamic neurons after visual cortex lesion in the adult rat
Authors: Caleo Matteo , Cenni Maria Cristina , Costa Mario , Menna Elisabetta , Zentilin Lorena , Giadrossi Sara , Giacca Mauro , Maffei Lamberto 
Published: March 2003

AbstractLesions of the mammalian visual cortex cause the retrograde degeneration of the thalamic neurons projecting to the damaged cortex. The proto‐oncogene bcl‐2 is known to inhibit neuronal apoptosis induced by a variety of noxious stimuli and preserve the functional integrity of the injured cells. Here we have tested whether the overexpression of bcl‐2 via adeno‐associated virus (AAV) vectors is able to protect the neurons in the lateral geniculate nucleus after visual cortex ablation in adult rats. Recombinant AAV vectors encoding Bcl‐2 (AAV‐Bcl‐2) or green fluorescent protein (AAV‐GFP) as a control were stereotaxically injected into the geniculate. Three weeks after vector injection, the ipsilateral visual cortex was removed by aspiration, and cell survival was assessed 2 weeks later. We found that 20% of the geniculate neurons were transduced by the Bcl‐2 vector. These cells were completely protected from death following cortical ablation. Delivery of AAV‐GFP transduced an identical number of geniculate neurons but had no effect on cell survival after lesion. The total number of surviving geniculate neurons was found to be significantly higher in animals injected with AAV‐Bcl‐2 than in rats injected with AAV‐GFP or in control lesioned rats. These data indicate that Bcl‐2 gene therapy with AAV vectors represents an effective treatment to promote neuronal survival after central nervous system insults.
Classical eyeblink conditioning in decerebrate guinea pigs
Authors: Kotani Sadaharu , Kawahara Shigenori , Kirino Yutaka 
Published: March 2003

AbstractA decerebrate guinea pig preparation was used to test the hypothesis that brainstem–cerebellar circuitry is sufficient for classical delay eyeblink conditioning. Delay conditioning was carried out using a tone conditioned stimulus (CS) paired with a co‐terminating, periorbital shock unconditioned stimulus (US). Decerebrate animals readily acquired the conditioned response (CR), while pseudoconditioning yielded no signs of learning. When a longer tone CS was used, the learning became slower. These CRs were adaptive and appropriately timed relative to the US. Subsequent CS‐alone trials caused extinction of the CR. These characteristics of the eyeblink conditioning were similar to those reported previously in various species, suggesting that the cerebellum and brainstem are sufficient for this type of learning.
Neuronal activity in the monkey motor thalamus during bicuculline‐induced dystonia
Authors: Macia F. , Escola L. , Guehl D. , Michelet Th. , Bioulac B. , Burbaud P. 
Published: March 2003

AbstractRecent data suggest that a decreased basal ganglia output may occur in dystonia, resulting in an increased thalamic drive to the mesial premotor cortex. In a previous work we found that injection of the GABAA antagonist bicuculline into the rostral motor thalamus induced contralateral dystonic postures, whereas myoclonic jerks were frequent after injection into the caudal motor thalamus. In the present study, we performed electrophysiological recordings in the rostral and caudal parts of the ventrolateral thalamus of two cynomolgus monkeys before and after bicuculline injections or saline injections. Discharge frequencies of thalamic neurons were increased after bicuculline injections vs. controls. Their discharge pattern was more bursty in the caudal part in which bursts of neuronal activity were correlated with myoclonic jerks. After bicuculline injection, neurons responded more frequently and less selectively to passive limb movements in both parts of the motor thalamus. Conversely, the response to microstimulation increased after bicuculline injection, particularly in the caudal part. Our data show that acute bicuculline‐induced dystonia is associated with a reversible overactivity and disorganization of neuronal activity in the motor thalamus. Such a phenomenon might induce an overspreading of cortical activity leading to dystonia. We postulate that the distinct clinical syndromes observed after bicuculline injections into the rostral and caudal motor thalamus are due to differences both in the neuronal circuitry within each thalamic nucleus and in segregated cortical projections.
Increased hypothalamic expression of prolactin in lactation: involvement in behavioural and neuroendocrine stress responses
Authors: Torner Luz , Toschi Nicola , Nava Gabriel , Clapp Carmen , Neumann Inga D. 
Published: March 2003

AbstractProlactin (PRL) has recently been shown to exert an anxiolytic effect in male and virgin female rats, as well as an inhibitory tone on hypothalamic‐pituitary‐adrenal (HPA) axis activity. Reduced emotional and neuroendocrine stress responses have been described in lactation, a time of high blood PRL levels. Here we tested brain PRL‐receptor (PRL‐R)‐mediated effects on anxiety, maternal behaviour, HPA axis and oxytocin stress responses in lactating rats. Chronic intracerebroventricular (i.c.v.) infusion of antisense oligonucleotides against the long form of the PRL‐R (AS; osmotic minipump, 0.5 µg/0.5 µL/h) in order to downregulate brain PRL‐R expression increased the anxiety‐related behaviour on the elevated plus maze (P < 0.01) compared with mixed bases‐ and vehicle‐treated rats. Also, PRL‐R AS treatment impaired maternal behaviour (P < 0.05), whereas physiological parameters of lactation (weight gain of the litter, number of milk ejection reflexes during a 20‐min suckling period) were not affected. PRL‐R AS treatment further evoked an increase (P < 0.05) in the stress‐induced adrenocorticotropin release, demonstrating an inhibitory role of PRL on HPA axis responses in lactation. Inhibition of stress responses of the oxytocin system by brain PRL was evidenced by higher stress‐induced (P < 0.05) plasma oxytocin concentration in PRL‐R AS‐treated lactating rats and, in contrast, decreased stress‐induced oxytocin release (P < 0.01) in chronic i.c.v. ovine PRL‐treated (1 µg/0.5 µL/h) virgin rats. Finally, an increased expression of the hypothalamic PRL gene was seen by RT‐PCR in pregnancy and lactation, suggesting an activated state of the brain PRL system during the peripartum period. In summary, activation of the brain PRL system in the peripartum period significantly contributes to emotional and neuroendocrine adaptations, including downregulation of the responsiveness of the HPA axis and oxytocin systems to stressors seen at this time.