bluuebunny/crossref_metadata_2025_split huggingface dataset:
Contribution of endogenously formed arachidonic acid in the presynaptic facilitatory effects of NMDA and carbachol on dopamine release in the mouse striatum
Authors: L'hirondel M. , Chéramy A. , Artaud F. , Godeheu G. , Glowinski J. 
Published: March 2003

AbstractArachidonic acid stimulated the release of [3H]‐dopamine from striatal microdiscs in a concentration‐dependent and partially calcium‐dependent manner. Inhibitors of cytosolic and membrane‐bound phospholipase A2 were used to determine whether endogenously formed arachidonic acid also contributes to the release of [3H]‐DA (previously taken up in tissues or endogenously synthesized from [3H]‐tyrosine) evoked by N‐methyl‐d‐aspartate (NMDA) and carbachol alone or in combination. In the presence of magnesium, carbachol was found to remove the magnesium block of NMDA receptors and to facilitate the NMDA‐evoked release of [3H]‐DA from striatal microdiscs and synaptosomes. In addition, in the absence of magnesium, synergistic responses were induced by both agonists on microdiscs but not on synaptosomes. Responses induced by NMDA, carbachol or both agonists on microdiscs were reduced by phospholipase A2 inhibitors, the most striking effects being observed with mepacrine. Mepacrine was also shown to reduce the oxotremorine, but neither the nicotine‐ nor the potassium‐evoked release of [3H]‐DA. Tetrodotoxin decreased the release of [3H]‐DA evoked by the co‐application of NMDA and carbachol on microdiscs, but mepacrine still decreased this tetrodotoxin‐resistant response. Similarly, mepacrine still decreased the release of [3H]‐DA evoked by NMDA and carbachol on synaptosomes. Altogether, these results indicate that arachidonic acid which is formed in striatal neurons, and to a lesser extent in DA fibres, under stimulation of NMDA and muscarinic receptors, partially contributes to the presynaptic facilitation of DA release evoked by NMDA and carbachol.
Auditory activation of cortical visual areas in cats after early visual deprivation
Authors: Yaka Rami , Yinon Uri , Wollberg Zvi 
Published: March 2003

AbstractAuditory activation of the primary visual cortex (area 17) and two extrastriate visual cortical areas – the anterolateral lateral suprasylvian area (ALLS) and anteromedial lateral suprasylvian area (AMLS), was investigated in visually impaired cats. Impairment was accomplished shortly after birth by bilateral eyelid suturing (binocularly deprived cats, BD) or bilateral enucleation (binocularly enucleated cats, BE). In BE cats, the optic nerve and chiasm were entirely degenerated. No cortical atrophy or cytoarchitectural malformation was noticed in either BD or BE cats. In both normal and impaired cats we found auditory‐responsive cells in the ALLS and AMLS, areas that are considered strictly visual. The most remarkable finding was an increase in the relative number of these auditory cells in the BD and BE cats, which was more prominent in the latter. Some auditory‐responsive cells were also found in area 17 of BE cats. On the basis of formal calculation, it is tempting to suggest that the increase in relative number of auditory cells in these areas reflects the transformation of all the visual cells in the ALLS of BD and BE cats into auditory cells. In BE cats, all bimodal cells and an appreciable percentage of non‐responsive cells also had transformed to auditory cells. In the AMLS of BD cats, it is primarily the bimodal cells that become auditory cells, whereas in BE cats all the visual and bimodal cells as well as non‐responsive cells undergo this transformation. This assumption, however, is one possible interpretation of our results but not the only one. Other modes of neuronal plasticity that might yield similar results in the visually deprived cats can not be ruled out.
Glucocorticoid receptor activation in the rat nucleus of the solitary tract facilitates memory consolidation: involvement of the basolateral amygdala
Authors: Roozendaal Benno , Williams Cedric L. , McGaugh James L. 
Published: March 2003

AbstractThese experiments examined the involvement of glucocorticoid receptors (GRs or type II) located in the A2‐noradrenergic cell group of the rat nucleus of the solitary tract (NTS) in modulating memory storage. Bilateral intra‐NTS infusions (0.5 μL) of the specific GR agonist RU 28362 (11β, 17β‐dihydroxy‐6,21‐dimethyl‐17α‐pregna‐4,6‐trien‐20yn‐3‐one), in doses ranging from 0.01 to 10.0 ng, immediately after inhibitory avoidance training produced a dose‐dependent enhancement of 48 h retention performance. Infusions of 0.1 or 1.0 ng of the agonist enhanced retention, whereas lower or higher doses were ineffective. Post‐training infusions of the GR antagonist RU 38486 [17β‐hydroxy‐11β‐(4‐dimethylaminophenyl)‐17α‐(1‐propynyl)‐oestra‐4,9‐dien‐3‐one, 0.01–10.0 ng] into the NTS did not significantly affect retention performance, but shifted the dose–response effects of post‐training systemic injections of the synthetic glucocorticoid dexamethasone to the right. These results indicate that activation of GRs in the NTS can influence memory formation for inhibitory avoidance training, and suggest that the effects of circulating glucocorticoids on memory are mediated, in part, by an activation of GRs in the NTS. Additionally, pretraining infusions of the β1‐adrenergic antagonist atenolol (0.5 μg in 0.2 μL) into the basolateral nucleus of the amygdala (BLA), a brain structure which receives noradrenergic projections from the NTS and is implicated in memory storage modulation, blocked the memory‐enhancing effects of the GR agonist (1.0 ng) infused into the NTS. These findings provide evidence that memory storage is modulated by glucocorticoid binding to GRs in noradrenergic cell bodies in the NTS and suggest that these modulatory effects are conveyed by ascending projections to the BLA.
Platelet‐activating factor receptor is not required for long‐term potentiation in the hippocampal CA1 region
Authors: Kobayashi Katsunori , Ishii Satoshi , Kume Kazuhiko , Takahashi Tomoyuki , Shimizu Takao , Manabe Toshiya 
Published: March 2003

From pharmacological studies, platelet‐activating factor (PAF) has been proposed as a retrograde messenger for long‐term potentiation (LTP) in the hippocampal CA1 region. We re‐examined a possible contribution of PAF to LTP with a more specific approach using mice deficient in the PAF receptor. The PAF receptor‐deficient mice exhibited normal LTP and showed no obvious abnormality in excitatory synaptic transmission. We also performed pharmacological experiments on the wild‐type mice. Two structurally different antagonists of PAF receptors had no effects on LTP. Furthermore, the application of PAF itself caused no detectable changes in excitatory synaptic transmission. Thus, we conclude that the PAF receptor is not required for LTP in the CA1 region.Introduction
Excitatory amino acids and synaptic transmission in embryonic rat brainstem motoneurons in organotypic culture
Authors: Launey Thomas , Ivanov Anton , Kapus Gàbor , Ferrand Nadine , Tarnawa Istvan , Gueritaud Jean‐Patrick 
Published: March 2003

AbstractWe used brainstem motoneurons recorded in organotypic slice co‐cultures maintained for more than 18 days in vitro, together with multibarrel ionophoretic applications of glutamate receptor agonists and bath applications of specific blocking agents, to study the responses of rat brainstem motoneurons to glutamate receptor activation, and the contribution of these receptors to synaptic transmission. Differentiated brainstem motoneurons in vitro are depolarized by glutamate, N‐methyl‐d‐aspartate (NMDA) and dl‐α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole‐propionic acid (AMPA) iontophoresis, and express NMDA, AMPA and also specific kainate receptors, as evidenced by (+/–)2‐amino‐5‐phosphonovaleric acid (APV)‐ and (–)1‐(4‐aminophenyl)‐3‐methyl‐carbamoyl‐4‐methyl‐7,8‐methylenedioxy‐3,4‐dihydro‐5H‐2,3‐benzo‐diazepine [GYKI 53784 (LY303070)]‐resistant depolarizations. Electrical stimulations applied to the dorsal part of the explant trigger excitatory synaptic potentials with latencies distributed in three regularly spaced groups. Excitatory postsynaptic potentials (EPSPs) in the earliest group have a similar latency and time course and correspond to monosynaptic activation. EPSPs in later groups have more scattered latencies and time courses and correspond to polysynaptic activation. Monosynaptic EPSPs are insensitive to the specific NMDA blocker APV, and are completely and reversibly suppressed by the non‐competitive AMPA receptor antagonist GYKI 53784 (LY303070). Detailed analysis of the spontaneous excitatory synaptic activity shows that APV decreases the frequency of spontaneous EPSPs without modifying their shape or amplitude. We conclude that excitatory synapses on brainstem motoneurons in vitro are mainly activated through AMPA receptors (AMPA‐Rs). NMDA receptors (NMDA‐Rs) are present in the membrane, but are located either at extrasynaptic sites or silent synapses, and are not directly involved in synaptic transmission on motoneurons. On the contrary, NMDA receptors contribute to synaptic transmission within the premotor interneuronal network.
Unexpected localization of the Na+/Cl–‐dependent‐like orphan transporter, Rxt1, on synaptic vesicles in the rat central nervous system
Authors: Masson J. , Riad M. , Chaudhry F. , Darmon M. , Aïdouni Z. , Conrath M. , Giros B. , Hamon M. , Storm‐Mathisen J. , Descarries L. , Mestikawy S. El 
Published: March 2003

AbstractNumerous features of its primary structure demonstrate that the orphan transporter Rxt1 belongs to the Na+/Cl–‐dependent neurotransmitter plasma membrane transporter superfamily, which includes the dopamine, norepinephrine, serotonin and γ‐aminobutyric acid (GABA) transporters. Initial immunocytochemical investigations with affinity‐purified antibodies have established that Rxt1 is localized, almost exclusively, in axon terminals of glutamatergic neurons and subsets of GABAergic neurons in the CNS. Further studies were carried out to determine its subcellular distribution. In a first series of experiments, PC‐12 cells were transfected with plasmids encoding either the dopamine transporter or Rxt1. Immunofluorescence experiments showed that the dopamine transporter was expressed in these cells, and, as expected, addressed to their plasma membrane. Surprisingly, this was never the case with Rxt1, which was targeted to the same subcellular compartment as synaptophysin, a vesicular protein. In a second set of experiments, subcellular fractionation of rat striatum showed that Rxt1, but not the dopamine transporter, was relatively abundant in the purified synaptic vesicle fraction. Finally, electron microscopic immunocytochemistry with anti‐Rxt1 antibodies showed peroxidase as well as pre‐ and post‐embedding immunogold labelling confined to the intracellular compartment in various brain regions. Moreover, quantitative analysis of post‐embedding experiments demonstrated that the immunogold particles corresponding to Rxt1 immunoreactivity were mostly localized to small synaptic vesicles. These data indicate that, in contrast with the other members of the Na+/Cl–‐dependent neurotransmitter transporter superfamily, which are targeted to the plasma membrane, Rxt1 is distributed as a vesicular protein in the CNS.
Absence of the dopamine D2 receptor leads to a decreased expression of GDNF and NT‐4 mRNAs in restricted brain areas
Authors: Bozzi Yuri , Borrelli Emiliana 
Published: March 2003

AbstractNeurotrophic factors (NTFs) control the metabolic and electrophysiological properties of dopaminergic neurons in the brain. At the level of the substantia nigra, NTFs have been proposed to control dopamine release by regulating the firing rate of dopaminergic cells. This function is normally controlled by presynaptic dopaminergic autoreceptors. Dopamine has also been proposed to regulate the expression of NTFs and their receptors in the nigrostriatal pathway. Thus, an interaction between the signalling cascades activated by NTFs and dopamine receptors might possibly influence the physiology of dopaminergic neurons. Among dopamine receptors, D2 receptors (D2R) are the most abundant on dopaminergic neurons, where they exert autoreceptor functions. To test for an interaction between the NTF and dopaminergic pathways we have analysed the expression of NTFs and their receptors in D2R‐deficient (D2R –/–) mice. Our study shows that the mRNA levels of brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 and their corresponding receptors are not modified in the dopaminergic system of D2R –/– adult mice compared with wild‐type littermates. However, a marked reduction of glial cell line‐derived neurotrophic factor (GDNF) and neurotrophin‐4 (NT‐4) mRNAs is observed in the striatum and parietal cortex of D2R –/– mice, respectively. These results implicate dopamine, acting through D2 receptors, in the local control of specific NTF expression. The down‐regulation of GDNF and NT‐4 expression might also contribute to the locomotor phenotype of D2R –/– mice.
Distribution of synaptic vesicle proteins in the mammalian retina identifies obligatory and facultative components of ribbon synapses
Authors: Von Kriegstein Katharina , Schmitz Frank , Link Egenhard , Südhof Thomas C. 
Published: March 2003

AbstractThe mammalian retina contains two synaptic layers. The outer plexiform layer (OPL) is primarily composed of ribbon synapses while the inner plexiform layer (IPL) comprises largely conventional synapses. In presynaptic terminals of ribbon synapses, electron‐dense projections called ribbons are present at the synaptic plasma membranes. Ribbons bind synaptic vesicles and guide them to the synaptic membrane for fusion. In this manner, ribbons are thought to accelerate the delivery of vesicles for continuous exocytosis. In recent years, a large number of synaptic proteins has been described but it is not known if these protein colocalize in the same types of synapses. In previous studies, several proteins essential for synaptic function were not detected in ribbon synapses, suggesting that the mechanism of synaptic vesicle exocytosis may be very different in ribbon and conventional synapses. Using confocal laser scanning microscopy, we have now systematically investigated the protein composition of ribbon synapses. Our results show that, of the 19 synaptic proteins investigated, all except synapsin and rabphilin are obligatorily present in ribbon synapses. For example, rab3 which was reported to be absent from ribbon synapses, was found in bovine, rat and mouse ribbon synapses using multiple independent antibodies. In addition, we found staining in these synapses for PSD‐95 and NMDA receptors, which suggested a similar design for the postsynaptic component in ribbon and conventional synapses. Our data show that ribbon synapses are more conventional in composition than reported, that most synaptic proteins are colocalized to the same type of synapse, and that synapsin and rabphilin are likely to be dispensible for basic synaptic functions.
The isolated mammalian brain: an in vivo preparation suitable for pathway tracing
Authors: Von Bohlen Oliver , Halbach Und 
Published: March 2003

AbstractAn in vitro preparation of complete brain is presented which allows successful tracing with fast axonal tracers for at least 2 days after in vitro preparation. A simple procedure is used, by which the isolated brain is submerged in oxygenated artificial cerebrospinal fluid, enabling maintenance of adequate integrity without perfusion the vascular system. The use of an isolated brain has many advantages: virtually all brain areas are easily accessible; tracer applications are possible without problems of animal survival; and the tracers are be translocated by blood circulation. The viability of this isolated brain preparation was validated by successful recording of extracellular field potentials 1 day later.
Visual experience alters the molecular profile of NMDA‐receptor‐mediated sensory transmission
Authors: Binns K. E. , Turner J. P. , Salt T. E. 
Published: March 2003

AbstractN‐methyl‐d‐aspartate (NMDA) receptors (NMDArs) may facilitate experience‐dependent changes in the visual system. Early sensory experience has an influence over the production of the molecular components from which NMDArs are assembled, and thereby alters the properties of functional receptors. Using the antagonists d‐2‐amino‐5‐phosphonovalerate (AP5) and 3‐(2‐carboxypiperazin‐4‐yl)‐propyl‐1‐phosphonate (CPP), which have some selectivity for different variants of the NMDAr, we demonstrate that visual deprivation (by dark rearing) has functional consequences for NMDArs in the superior colliculus. An increase in the sensitivity of visual responses to AP5 in dark‐reared rats indicated that NMDArs were more important for visual transmission in these individuals. We also observed a relative change in the efficacy of the antagonists against the visual responses of normal versus dark‐reared rats. AP5 reduced the visual responses of both groups, but CPP was ineffective against visual responses after dark rearing. In the same neurons, CPP blocked NMDA induced activity indicating that molecular adaptations of NMDArs are specific to those synapses mediating visual activity.
Contralateral trigeminal nerve lesion reduces polyneuronal muscle innervation after facial nerve repair in rats
Authors: Angelov Doychin N. , Skouras Emmanouil , Guntinas‐Lichius Orlando , Streppel Michael , Popratiloff Anastas , Walther Michael , Klein Johannes , Stennert Eberhard , Neiss Wolfram F. 
Published: March 2003

AbstractFunctional recovery after facial nerve surgery is poor. Axotomized motoneurons (hyperexcitable upon intracellular current injections, but unable to discharge upon afferent stimulation) outgrow supernumerary branches which are misrouted towards improper muscles. We hypothesized that alterations in the trigeminal input to axotomized electrophysiologically silent facial motoneurons might improve specificity of reinnervation. To test this we compared, in the rat, behavioural, electrophysiological, and morphological parameters after transection and suture of the buccal facial nerve (buccal–buccal anastomosis, BBA) with those after BBA plus excision of the ipsi‐ or contralateral infraorbital nerve (ION). After BBA, the mystacial vibrissae dropped and remained motionless until 18–21 days post operation (days PO). After BBA plus ipsilateral ION excision, there was no recovery of vibrissae whisking at all. Following BBA plus contralateral ION excision, full restoration of whisking occurred at 7–10 days PO. Electromyography of whiskerpad muscles showed normal waveform and amplitude was also most rapidly restored after BBA plus contralateral ION excision. Neuron counts after retrograde tracing showed that the intact buccal nerve contained axons of the superior (91%) and inferior (9%) buccolabial nerves. After BBA, the superior nerve comprised 56%, the inferior 21%, and 23% of the motoneurons projected within both nerves. After BBA plus ipsilateral ION excision, misdirection worsened and values changed to 48, 39 and 13%, respectively. After BBA plus contralateral ION excision, portions improved to 69, 23 and 8%. We conclude that, by reducing the redundant axon branching, lesion of contralateral ION provides the best conditions for recovery of vibrissae rhythmical whisking after reconstructive surgery on the facial nerve.
Distribution of fibroblast growth factor‐5 in rat hypothalamus, and its possible role as a regulator of feeding behaviour
Authors: Li Ai‐Jun , Ozawa Kazuo , Tsuboyama Hiroyuki , Imamura Toru 
Published: March 2003

AbstractWe previously reported that a transcript of fibroblast growth factor‐5 (FGF‐5) was more abundant in the brain of postnatal and adult mice than in the embryonic brain. This suggested that FGF‐5 plays some role in the mature brain. Here, we have investigated the spatiotemporal expression and function of FGF‐5 in the adult rat hypothalamus with the emphasis on feeding behaviour. In situ hybridization experiments demonstrated that, in both adequately fed and fasted (20 h) rats, FGF‐5 transcripts were present within several nuclei in the hypothalamus (viz. the magnocellular part of the paraventricular nucleus, supraoptic nucleus, arcuate nucleus, median eminence, and ventromedial hypothalamic nucleus), but not in the lateral hypothalamic area. Quantitative detection of FGF‐5 mRNA in the hypothalamus (especially in the paraventricular nucleus) indicated that food deprivation (20 h) reduced the expression of this gene to almost one‐half of that seen in the control (fed) rats. The expression recovered to the control level after 1 h re‐feeding, and this recovery persisted for several hours. Furthermore, FGF‐5, when infused into the third ventricle, consistently reduced food intake, water intake and body weight gain, all in a dose‐dependent manner. These results suggest that FGF‐5 in the hypothalamus acts as a physiological regulator of feeding behaviour, and that its decreased expression during food deprivation may be important in stimulating appetite.
Effects of unilateral cochlear removal on dendrites in the gerbil medial superior olivary nucleus
Authors: Russell F. Anne , Moore David R. 
Published: March 2003

AbstractFor most neurons, dendrites serve as the major pathway for incoming activity from other neurons. It might therefore be expected that dendrites are particularly sensitive to variations in the level of afferent input they receive. In the auditory brainstem, this expectation has been confirmed in neurons of the medial superior olivary nucleus (MSO). The MSO is uniquely suited to studies of afferent influences on dendrites, as lateral and medial dendrites of MSO neurons receive inputs almost exclusively from the ipsilateral and contralateral ears, respectively. Thus, the effects of unilateral afferent manipulations may be compared between defined dendrites on the same neurons. We have used unilateral deafening (by surgical destruction of the cochlea) in immature [postnatal day 18 (P18)] and adult gerbils to study the late maturation and effect of peripheral deafferentation on the dendrites of MSO neurons. In semi‐thin, frontal sections from unoperated animals, we found a change between P18 and adulthood from a lateral to a medial bias in the symmetry of MSO dendrites. Cochlear removal in adulthood led to a reduction in the density of dendritic profiles on the side of the ablation in both MSOs. Cochlear removal at P18 led to a rapid (< 3 days) and sustained dendritic atrophy that was most marked in the caudal part of the nucleus. Electron microscope (EM) measurements in the sagittal plane on MSO dendrite profiles of animals unilaterally deafened at P18 showed a reduction in the number, but not in the area, of profiles on the side of the deafened ear. These results demonstrate a developmental change in the symmetry of MSO medial and lateral dendrites, and a rapid and long‐lasting reduction in the number of distal dendrites produced by unilateral deafening either in infancy or adulthood.
Ca2+ activation of hSlo K+ channel is suppressed by N‐terminal GFP tag
Authors: Meyer Elisabeth , Fromherz Peter 
Published: March 2003

AbstractThe human slow poke (hSlo) K+ channel was tagged with GFP (green fluorescent protein) at the N‐terminus of its α‐subunit. The fusion protein was expressed transiently in HEK293 cells; it formed functional voltage‐gated channels as shown by whole cell patch‐clamp measurements. However, the tag lowered the voltage dependence of gating and it suppressed the typical left‐shift of gating by intracellular binding of Ca2+. The location of the GFP‐tagged N‐terminus was confirmed to be on the extracellular side by application of a monoclonal antibody to nonpermeabilized cells. Structural interpretations of the effects are discussed.