bluuebunny/crossref_metadata_2025_split huggingface dataset:
Release of classical transmitters and nitric oxide in the rat olfactory bulb, evoked by vaginocervical stimulation and potassium, varies with the oestrus cycle
Authors: Guevara‐Guzmán Rosalinda , Barrera‐Mera Baltazar , De La Riva Carlos , Kendrick Keith M. 
Published: March 2003

AbstractIn vivo microdialysis was used to investigate the effects of ovariectomy and the oestrus cycle on vaginocervical stimulation‐evoked classical transmitter and nitric oxide release in the olfactory bulb of anaesthetized (urethane) and conscious rats. During pro‐oestrus/oestrus, vaginocervical stimulation (1 or 10 min) significantly increased concentrations of glutamate, aspartate, GABA, noradrenaline, dopamine and nitric oxide (citrulline) but failed to do so in met‐oestrus/di‐oestrus or following ovariectomy. Potassium chloride‐evoked GABA, noradrenaline and nitric oxide release in the olfactory bulb was also significantly enhanced during pro‐oestrus/oestrus. The effects of vaginocervical stimulation on olfactory bulb transmitter release during pro‐oestrus/oestrus were significantly reduced by pelvic or vagus nerve section. Basal concentrations of classical transmitters and nitric oxide in the olfactory bulb did not vary across the oestrus cycle although noradrenaline and dopamine levels were reduced following ovariectomy. These results confirm our previous electrophysiological data showing that the olfactory bulb mitral cells are only excited by vaginocervical stimulation during pro‐oestrus/oestrus. They also suggest that sex hormones acting primarily at the level of the olfactory bulb dramatically enhance the ability of vaginocervical stimulation to evoke release of both classical transmitters and nitric oxide in this region. Such alterations in neurochemical release in the olfactory bulb may be important for mediating plasticity changes underlying olfactory recognition of mates or offspring.
Distinct immunohistochemical localization of two isoforms of Ca2+/calmodulin‐dependent protein kinase kinases in the adult rat brain
Authors: Sakagami Hiroyuki , Umemiya Masashi , Saito Sachiko , Kondo Hisatake 
Published: March 2003

AbstractCa2+/calmodulin‐dependent protein kinase IV (CaM‐KIV) is thought to be involved in regulating gene expression by phosphorylating various transcriptional factors. CaM‐KIV as well as CaM‐KI are activated upon phosphorylation by two distinct isoforms of Ca2+/calmodulin‐dependent protein kinase kinases, CaM‐KKs α and β. In this study, we raised isoform‐specific monoclonal antibodies against CaM‐KKs and examined the immunohistochemical localization of CaM‐KKs in the rat brain, compared with that of CaM‐KIV. CaM‐KK α‐immunoreactivity was rather widely distributed in neurons throughout the brain, except cerebellar cortex. The highest levels of CaM‐KK α‐immunoreactivity were observed in the cerebral cortex, facial nucleus and motor neurons of the spinal cord. Moderate CaM‐KK α‐immunoreactivity was observed in the hippocampal formation, pontine nuclei and various brain stem nuclei including trigeminal, vestibular, cochlear and hypoglossal nuclei. In contrast, CaM‐KK β‐immunoreactivity was relatively restricted in some neuronal populations. The highest levels of CaM‐KK β‐immunoreactivity were observed in the cerebellar granule cell layer, and moderate immunoreactivity was observed in the cerebral cortex, hippocampal formation, caudate putamen, pontine nuclei, cochlear nucleus and molecular layer of the cerebellum. In contrast to the prominent nuclear localization of CaM‐KIV, both isoforms of CaM‐KKs were localized in the perikaryal cytoplasm, dendrites and nerve terminals, but not in the cell nuclei. The distinct localization of two isoforms of CaM‐KKs suggests that the complicated mechanisms for activation of CaM‐KIV by CaM‐KKs may be exerted in region‐specific manners as well as intracellularly.
Neurotrophins from dorsal root ganglia trigger allodynia after spinal nerve injury in rats
Authors: Zhou X. ‐F. , Deng Y. ‐S. , Xian C. J. , Zhong J. ‐H. 
Published: March 2003

AbstractInjury to peripheral nerves often results in chronic pain which is difficult to relieve. The mechanism underlying the pain syndrome remains largely unknown. In previous studies we showed that neurotrophins are up‐regulated in satellite cells around sensory neurons following sciatic nerve lesion. In the present study, we have examined whether the neurotrophins in the dorsal root ganglia play any role in allodynia after nerve injury. Antibodies to different neurotrophins, directly delivered to injured dorsal root ganglia, significantly reduced (with different time sequences) the percentage of foot withdrawal responses evoked by von Frey hairs. The antibodies to nerve growth factor acted during the early phase but antibodies to neurotrophin‐3 and brain‐derived neurotrophic factor were effective during the later phase. Exogenous nerve growth factor or brain‐derived neurotrophic factor, but not neurotrophin‐3, directly delivered to intact dorsal root ganglia, trigger a persistent mechanical allodynia. Our results showed that neurotrophins within the dorsal root ganglia after peripheral nerve lesion are involved in the generation of allodynia at different stages. These studies provide the first evidence that ganglia‐derived neurotrophins are a source of nociceptive stimuli for neuropathic pain after peripheral nerve injury.
Mechanisms of human motion perception: combining evidence from evoked potentials, behavioural performance and computational modelling
Authors: Patzwahl Dieter R. , Zanker Johannes M. 
Published: March 2003

AbstractBased on single cell recordings in monkey, it has been suggested that neural activity can be related directly to psychophysically measured threshold behaviour. Here, we investigated in humans whether evoked potentials correlate with behavioural measurements like discrimination thresholds and reaction time. Subjects were asked to report the perceived direction of object motion stimuli which contained variable amounts of coherent motion. Simultaneously, we recorded evoked potentials with a multielectrode array, or measured the reaction time. We show here that motion coherence had a strong influence on both amplitude and latency of the evoked potential. Stronger motion signals evoked stronger and faster cortical responses. The latency reduction of the motion onset response with increasing coherence correlated very well with the concurrent decrease in reaction time. Taken together, these results suggest that temporal integration is an important step in analysing motion signals to generate a reliable behavioural response. We stimulated a two‐dimensional array of correlation‐type motion detectors with the same motion sequences, and analysed the distribution of local motion signals according to signal detection theory. Performance resembled that of human subjects when the decision strategy was optimized so as to exclude small signals and, in particular, when the ideal observer had some knowledge about a region of interest in which the object was to be expected.
Cellular and synaptic effect of substance P on neonatal phrenic motoneurons
Authors: Ptak Krzysztof , Konrad Martin , Di Pasquale Eric , Tell Fabien , Hilaire Gérard , Monteau Roger 
Published: March 2003

AbstractExperiments were carried out on the in vitro brainstem–spinal cord preparation of the newborn rat to analyse the effects of substance P (SP) on phrenic motoneuron (PMN) activity. In current‐clamp mode, SP significantly depolarized PMNs, increased their input resistance, decreased the rheobase current and shifted the firing frequency–intensity relationships leftwards, but did not affect spike frequency adaptation or single spike configuration. The neurokinin receptor agonist NK1 had SP‐mimetic effects, whereas the NK3 and NK2 receptor agonists were less effective and ineffective, respectively. In a tetrodotoxin‐containing aCSF, only SP or the NK1 receptor agonist were still active. No depolarization was observed when the NK1 receptor agonist was applied in the presence of muscarine. In voltage‐clamp mode, SP or the NK1 receptor agonist produced an inward current (ISP) which was not significantly reduced by extracellular application of tetraethylammonium, Co2+, 4‐aminopyridine or Cs+. In aCSF containing tetrodotoxin, Co2+ and Cs+, ISP was blocked by muscarine. No PMN displayed any M‐type potassium current but only a current showing no voltage sensitivity over the range −100 to 0 mV, reversing near the expectedEK+, hence consistent with a leak current. SP application to the spinal cord only (using a partitioned chamber) significantly increased the phrenic activity. Pretreatment with the NMDA receptor antagonist dl‐2‐amino‐5‐phosphonovaleric acid (AP5) decreased the C4 discharge duration and blocked the effect of SP, thus exhibiting an NMDA potentiation by SP. In conclusion, SP modulates postsynaptically the response of phrenic motoneurons to the inspiratory drive through the reduction of a leak conductance and the potentiation of the NMDA component of the synaptic input.
Neurophysiological correlates of face gender processing in humans
Authors: Mouchetant‐Rostaing Yolande , Giard Marie‐Hélène , Bentin Shlomo , Aguera Pierre‐Emmanuel , Pernier Jacques 
Published: March 2003

AbstractEvent‐related potentials (ERPs) were recorded while subjects were involved in three gender‐processing tasks based on human faces and on human hands. In one condition all stimuli were only of one gender, preventing any gender discrimination. In a second condition, faces (or hands) of men and women were intermixed but the gender was irrelevant for the subject's task; hence gender discrimination was assumed to be incidental. In the third condition, the task required explicit gender discrimination; gender processing was therefore assumed to be intentional. Gender processing had no effect on the occipito‐temporal negative potential at ≈ 170 ms after stimulation (N170 component of the ERP), suggesting that the neural mechanisms involved in the structural encoding of faces are different from those involved in the extraction of gender‐related facial features. In contrast, incidental and intentional processing of face (but not hand) gender affected the ERPs between 145 and 185 ms from stimulus onset at more anterior scalp locations. This effect was interpreted as evidence for the direct visual processing of faces as described in Bruce and Young's model [Bruce, V. & Young, A. (1986) Br. J. Psychol., 77, 305–327]. Additional gender discrimination effects were observed for both faces and hands at mid‐parietal sites around 45–85 ms latency, in the incidental task only. This difference was tentatively assumed to reflect an early mechanism of coarse visual categorization. Finally, intentional (but not incidental) gender processing affected the ERPs during a later epoch starting from ≈ 200 ms and ending at ≈ 250 ms for faces, and ≈ 350 ms for hands. This later effect might be related to attention‐based gender categorization or to a more general categorization activity.
Bone morphogenetic protein‐7 enhances dendritic growth and receptivity to innervation in cultured hippocampal neurons
Authors: Withers G. S. , Higgins D. , Charette M. , Banker G. 
Published: March 2003

AbstractMembers of the bone morphogenetic protein (BMP) family of growth factors are present in the central nervous system during development and throughout life. They are known to play an important regulatory role in cell differentiation, but their function in postmitotic telencephalic neurons has not been investigated. To address this question, we examined cultured hippocampal neurons following treatment with bone morphogenetic protein‐7 (BMP‐7, also referred to as osteogenic protein‐1). When added at the time of plating, BMP‐7 markedly stimulated the rate of dendritic development. Within 1 day, the dendritic length of BMP‐7‐treated neurons was more than twice that of controls. By three days the dendritic arbors of BMP‐7‐treated neurons had attained a level of branching similar to that of 2‐week‐old neurons cultured under standard conditions. Several findings indicate that BMP‐7 selectively enhances dendritic development. While dendritic length was significantly increased in BMP‐7‐treated neurons, the length of the axon was not. In addition, the mRNA encoding the dendritic protein MAP2 was significantly increased by BMP‐7 treatment, but the mRNA for tubulin was not. Finally, BMP‐7 did not enhance cell survival. Because dendritic maturation is a rate‐limiting step in synapse formation in hippocampal cultures, we examined whether BMP‐7 accelerated the rate at which neurons became receptive to innervation. Using two separate experimental paradigms, we found that the rate of synapse formation (assessed by counting synapsin I‐positive presynaptic vesicle clusters) was increased significantly in neurons that had been exposed previously to BMP‐7. Because BMP‐7 and related BMPs are expressed in the hippocampus in situ, these factors may play a role in regulating dendritic branching and synapse formation in both development and plasticity.
Intrathecally injected neurotrophins and the release of substance P from the rat isolated spinal cord
Authors: Malcangio Marzia , Ramer Matt S. , Boucher Tim J. , McMahon Stephen B. 
Published: March 2003

AbstractThe aim of this study was to investigate the effects of intrathecally delivered trophic molecules nerve growth factor (NGF), neurotrophin‐3 (NT‐3) and glial cell line‐derived neurotrophic factor (GDNF) on substance P (SP) release and content in the rat spinal cord and SP content in sciatic nerve. SP release was assayed with an in vitro dorsal roots‐attached spinal cord preparation, in which the roots were stimulated at A‐ or C‐fibre strength, and SP levels were measured by radioimmunoassay (RIA). NGF but not NT‐3 and GDNF treatment caused a significant increase in basal SP outflow; NGF, NT‐3 but not GDNF increased C‐fibre stimulation‐evoked SP release, and capsaicin superfusion‐induced SP release. The increase in C‐fibre stimulation‐evoked SP release over basal outflow was greater in NGF‐ than NT‐3‐treated cords, and nociceptive threshold testing showed that intrathecal NGF, but not NT‐3 or GDNF treatment was associated with thermal hyperalgesia. There was no detectable A‐fibre stimulation‐induced SP release from any group as well as no change in SP content in the sciatic nerve and spinal cord. Systemic treatment with the NGF‐sequestering fusion protein trkA‐IgG significantly inhibited electrically or capsaicin‐evoked SP release without affecting basal outflow and SP content in spinal cord and sciatic nerve. These results suggest that: (i) NGF tonically regulates the central synaptic function of SP‐containing primary afferents; (ii) increased SP‐release from the spinal cord is not necessarily associated with behavioural hyperalgesia as in NT‐3‐treated rats there was increased SP release but no detectable hyperalgesia; and (iii) because A‐fibre stimulation failed to increase SP release in any group, these neurotrophins are unlikely to be responsible for the de novo upregulation of SP in large afferents seen after peripheral inflammation or nerve injury.
Endogenous and exogenous nitric oxide enhance the DNA strand scission induced by tert‐butylhydroperoxide in PC12 cells via peroxynitrite‐dependent and independent mechanisms, respectively
Authors: Sestili Piero , Clementi Emilio , Guidarelli Andrea , Sciorati Clara , Cantoni Orazio 
Published: March 2003

AbstractA short‐term exposure to tert‐butylhydroperoxide (tB‐OOH) promoted a concentration‐dependent formation of DNA single‐strand breaks in PC12 cells. These events were paralleled by an increase in the cytosolic concentration of Ca2+ that was in part cleared by the mitochondria. Unlike the extent of Ca2+ mobilization and/or mitochondrial Ca2+ clearance, the DNA strand scission evoked by the hydroperoxide was markedly reduced by the nitric oxide (NO) scavenger 2‐phenyl‐4,4,5,5‐tetramethylimidazolin‐1‐oxyl‐3‐oxide (PTIO) or by the NO synthase inhibitor N‐nitro‐l‐arginine methylester (L‐NAME). Inhibitors of electron transport (rotenone and myxothiazol), ruthenium red (RR, a polycation which inhibits the calcium uniporter of mitochondria), or peroxynitrite scavengers (Trolox and l‐methionine) were as effective as PTIO or L‐NAME in inhibiting the DNA‐damaging response mediated by tB‐OOH. Rotenone, RR or peroxynitrite scavengers did not further reduce the residual DNA cleavage observed following treatment with tB‐OOH in L‐NAME‐supplemented cells. Exogenous NO also increased the DNA damage caused by tB‐OOH in L‐NAME‐supplemented cells and this response was blunted by RR or by inhibitors of electron transport but was insensitive to peroxynitrite scavengers. We conclude that both endogenous and exogenous NO enhance the DNA cleavage generated by tB‐OOH in PC12 cells. However, only endogenous NO set the bases for an involvement of peroxynitrite in this DNA‐damaging response.
Differential signalling of the chemokine receptor CXCR4 by stromal cell‐derived factor 1 and the HIV glycoprotein in rat neurons and astrocytes
Authors: Lazarini Françoise , Casanova Philippe , Tham To Nam , De Clercq Erik , Arenzana‐Seisdedos Fernando , Baleux Françoise , Dubois‐Dalcq Monique 
Published: March 2003

AbstractCXCR4 is the Gi protein‐linked seven‐transmembrane receptor for the alpha chemokine stromal cell‐derived factor 1 (SDF‐1), a chemoattractant for lymphocytes. This receptor is highly conserved between human and rodent. CXCR4 is also a coreceptor for entry of human immunodeficiency virus (HIV) in T cells and is expressed in the CNS. To investigate how these CXCR4 ligands influence CNS development and/or function, we have examined the expression and signalling of this chemokine receptor in rat neurons and astrocytes in vitro. CXCR4 transcripts and protein are synthesized by both cell types and in E15 brain neuronal progenitors. In these progenitors, SDF‐1, but not gp120 (the HIV glycoprotein), induced activation of extracellular signal regulated kinases (ERKs) 1/2 and a dose‐dependent chemotactic response. This chemotaxis was inhibited by Pertussis toxin, which uncouples Gi proteins and the bicyclam AMD3100, a highly selective CXCR4 antagonist, as well as by an inhibitor of the MAP kinase pathway. In differentiated neurons, both SDF‐1 and the glycoprotein of HIV, gp120, triggered activation of ERKs with similar kinetics. These effects were significantly inhibited by Pertussis toxin and the CXCR4 antagonist. Rat astrocytes also responded to SDF‐1 signalling by phosphorylation of ERKs but, in contrast to cortical neurons, no kinase activation was induced by gp120. Thus neurons and astrocytes can respond differently to signalling by SDF‐1 and/or gp120. As SDF‐1 triggers directed migration of neuronal progenitors, this alpha chemokine may play a role in cortex development. In differentiated neurons, both natural and viral ligands of CXCR4 activate ERKs and may therefore influence neuronal function.
Spontaneous and locomotor‐related GABAergic input onto primary afferents in the neonatal rat
Authors: Fellippa‐Marques Silvia , Vinay Laurent , Clarac François 
Published: March 2003

AbstractThe in vitro brain stem–spinal cord preparation of neonatal rats (0–5 days old) was used to examine the contribution of GABAA (γ‐aminobutyric acid) receptors to the spontaneous and locomotor‐related antidromic firing in the dorsal roots of neonatal rats. Spontaneous bursts of antidromic discharges were generated by the underlying afferent terminal depolarizations reaching spiking threshold. The number of antidromic action potentials increased significantly in saline solution with Cl– concentration reduced to 50% of control. Bath application of the GABAA receptor antagonist bicuculline, at low concentrations (1–2 μm), or picrotoxin blocked the antidromic discharges in the dorsal roots almost completely. The increase in Cl– conductance was therefore mediated by an activation of GABAA receptors. Increasing the concentration of bicuculline to 10–20 μm never blocked these discharges further. On the contrary, in half of the preparations, the number of antidromic action potentials was higher in the presence of high concentrations of bicuculline (10–20 μm) than in the presence of picrotoxin or low concentrations of bicuculline. This suggests that bicuculline, at high concentrations, may have other effects, in addition to blocking GABAA receptors. Dorsal root firing was observed during fictive locomotion induced by bath application of excitatory amino acids and serotonin. A rhythmical pattern was often demonstrated. Bicuculline at low concentrations caused a decrease of the antidromic discharge whereas, at high concentrations, bursts of discharges appeared. A double‐bath with a barrier built at the L3 level was then used to separate the mechanisms which generate locomotion from those mediating primary afferent depolarizations. Excitatory amino acids and serotonin were perfused in the rostral pool only. Decreasing the concentration of chloride in the caudal bath caused a sharp increase in the number of antidromic action potentials recorded from the L5 dorsal root. These discharges, which were modulated in phase with the locomotor rhythm, were blocked by bicuculline. These data demonstrate the existence of a locomotor‐related GABAergic input onto primary afferent terminals in the neonatal rat.
Evaluation of simple and complex sensorimotor behaviours in rats with a partial lesion of the dopaminergic nigrostriatal system
Authors: Barnéoud Pascal , Descombris Eric , Aubin Nadine , Abrous Djoher N. 
Published: March 2003

AbstractWe have examined the behavioural consequences of a partial unilateral dopaminergic denervation of the rat striatum. This partial lesion was obtained by an intrastriatal 6‐hydroxy‐dopamine injection (6‐OHDA, 20 or 10 μg divided between two injection sites) and was compared with a unilateral complete lesion resulting from an injection of 6‐OHDA (2 × 6 μg) into the medial forebrain bundle. Quantification of striatal dopamine (DA) and its metabolites, and the immunohistochemical evaluation of the nigrostriatal DA system confirmed the complete and partial lesions. Animals with complete striatal denervation displayed both apomorphine‐ and amphetamine‐induced rotations whereas the partial denervation elicited amphetamine‐induced rotations only. However, the rates of amphetamine‐induced rotation were not correlated with the size of the lesion. In contrast, the paw‐reaching impairments were significantly correlated with the striatal dopaminergic depletion. When evaluated in the staircase test, animals with partial denervation were impaired exclusively for the paw contralateral to the side of the lesion. This motor deficit (50–75%) included all components of the skilled paw use (i.e. attempt, motor coordination and success) and was observed at least 12 weeks after the lesion. However, these animals were able to perform normal stepping adjustments with the impaired paw, indicating that the partial lesion induced a coordination deficit of the paw rather than a deficit of movement initiation. After a complete lesion, stepping adjustments of the contralateral paw were dramatically impaired (by 80%), an akinesia which almost certainly accounted for the great deficit in skilled paw use. The paw‐reaching impairments resulting from the partial striatal denervation are proposed as a model of the early symptoms of Parkinson's disease and may be useful for the development of restorative therapies.