bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Temperature and Calcium on the Binding Properties of the AMPA Receptor in Frozen Rat Brain Sections
Authors: Tocco G. , Massicotte G. , Standley S. , Thompson R. F. , Baudry M. 
Published: April 2006

AbstractThe elucidation of the mechanisms regulating the properties of the α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionate (AMPA) subtype of glutamate receptors is important for understanding glutamatergic transmission. Here we report that qualitative as well as quantitative analysis of tritiated ligand binding to the AMPA receptor on thin frozen rat brain tissue sections reveals the existence of several mechanisms regulating the binding properties of AMPA receptors. Preincubation of tissue sections at 35°C results in a decreased amount of [3H]AMPA binding as compared to that measured following preincubation at 0°C. The decrease in binding appears to be mainly localized to cell bodies as evaluated by autoradiography, and could be due to proteolysis. Preincubation with calcium at 35°C produces increased levels of [3H]AMPA binding. The effect of calcium is mimicked by manganese and to a lesser extent by magnesium; it is concentration‐dependent with a 50% effective concentration for calcium of ∼150 μM, time‐dependent and temperature‐dependent. The calcium‐induced increase in [3H]AMPA binding is different among various brain structures, being larger in area CA1 of the hippocampus and in the superficial layers of the cerebral cortex. The effect of calcium is partly reduced by preincubation with the calpain inhibitor leupeptin and potentiated by preincubation with purified calpain II. The calcium‐induced increase in [3H]AMPA binding is associated with a decrease in the binding of an antagonist of AMPA receptors, [3H]6‐nitro‐7‐cyanoquinoxaline‐2,3‐dione. The results indicate that the binding properties of the AMPA receptor are rapidly regulated by calcium‐dependent processes, and possibly by calcium‐dependent proteases. They suggest that modulation of the binding properties involves changes in the configuration of the receptor, producing opposite changes in the affinities of the receptor for agonists and antagonists. Finally, these results strengthen the hypothesis that changes in the properties of AMPA receptors might underlie various forms of synaptic plasticity.
Learning‐dependent Changes in the Responses to Visual Stimuli of Neurons in a Recognition Memory System
Authors: McLennan J. G. , Horn G. 
Published: April 2006

AbstractWhen young chicks are trained by exposing them to a conspicuous object they learn its characteristics. The learning process is known as imprinting. In the present study neuronal activity in a region crucial for imprinting was shown to be affected by training and by the object on which the chicks had been trained. The region is the intermediate and medial part of the left hyperstriatum ventrale (left IMHV). No such effects were found in a visual projection area, the left hyperstriatum accessorium. Domestic chicks were imprinted on either a rotating red box (n= 7 chicks) or a rotating blue box (n= 8). When the chicks were ∼48 h old they were anaesthetized and multiple‐unit activity was recorded in simultaneous, single penetrations through each of the two regions. Records were also made from eight dark‐reared chicks. Whilst recording, the red or blue box, placed in front of the contralateral eye, was switched on to give a total of 20 rotations, the interval between each rotation being 10 s. The alternative stimulus was then presented 20 times. Unit activity in the 3 s before and after stimulus onset was compared and the data for each of the 20 presentations were combined. In the left IMHV 18 out of a total of 115 recording sites (16%) responded significantly to the stimuli; in the left hyperstriatum accessorium 39 out of 126 recording sites (26%) did so. Measures of unit activity at each recording site were combined for a given penetration to provide a ‘mean penetration response’. The response to the red box differed from the response to the blue box in the left IMHV of dark‐reared chicks. After training with the blue box the response to both boxes was similar to the response to the blue box in dark‐reared birds. After training with the red box the response to both boxes was similar to the response to the red box in dark‐reared birds. No significant effects were found in the left hyperstriatum accessorium. The two training boxes were virtually identical apart from the differences in colour and brightness. Training appeared to stabilize the response of the visually naive left IMHV to the training stimulus whilst changing its response to the alternative, but similar stimulus. That is, one consequence of training is that the two stimuli are placed in the same category, and this neural change may provide a basis for stimulus generalization. The underlying neural system is modelled and a mechanism that allows such stimuli to be discriminated is proposed.
Somatic Acetylcholine Release in Rabbit Nodose Ganglion
Authors: Palouzier‐Paulignan B. , Chamoin M.‐C. , Ternaux J.‐P. 
Published: April 2006

AbstractIn the rabbit, as in various other species, the presence of a cholinergic vagal afferent contingent has been demonstrated previously using biochemical and immunohistological approaches at the nodose ganglion level, where vagal afferent cell bodies are located. This structure is completely devoid of synaptic contacts. In the present study, somatic acetylcholine release is demonstrated on different types of in vitro rabbit nodose ganglion preparations (fragments of nodose tissue or isolated cell bodies) using chemiluminescent detection. Acetylcholine endogenous content was measured and was shown to be greater in the right nodose ganglion compared to the left. This difference was also observed when spontaneous and potassium chloride‐evoked acetylcholine release was measured in extracellular fluid after a 15‐min incubation of nodose ganglion fragments. Calcium removal totally blocked this somatic release. A kinetic study of acetylcholine release was also performed by placing the samples (nodose ganglion fragments or isolated cell bodies) directly in front of the photomultiplier, allowing the direct monitoring of (acetylcholine + choline) and choline effluxes. The net acetylcholine release was then deduced by subtraction. Identical kinetics was obtained with the two different nodose ganglion preparations used. This somatic release is calcium‐dependent. The occurrence of acetylcholine release at the nodose ganglion level is discussed in comparison with the events occurring in the cholinergic nerve endings. These mechanisms could be implicated in the premodulation of the vagal afferent messages conveyed from the periphery to the central nervous system.
An Electromyographic Study of the Hindlimb Locomotor Movements in the Acute Thalamic Rat
Authors: Goudard I. , Orsal D. , Cabelguen J.‐M. 
Published: April 2006

AbstractIn this paper we have analysed the patterns of muscular activities that underlie hindlimb locomotor movements in the acute thalamic rat. Electromyographic activities of muscles representative of the functional muscle groups of the hindlimbs were recorded bipolarly during locomotion in acute thalamic rats. Locomotor movements occurred spontaneously, but could also be induced by electrical stimulation (0. 1 ms pulses; 30–70 Hz; 75–300 μA) of the lateral hypothalamic area. The two hindlimbs displayed a wide variety of coordination patterns during both types of locomotion. However, alternated coordination of the hindlimbs occurred more frequently during induced than during spontaneous locomotion. Correspondingly, the duration of the spontaneous step cycles had a tendency to be shorter than that of the evoked step cycles, although they had a quite similar range. The patterns of muscular activities within one hindlimb were similar during spontaneous and induced locomotion. During each step cycle, (i) the hip and ankle flexors usually displayed a single burst in alternation with that displayed by the hip, knee and ankle extensors, (ii) a double bursting pattern was sometimes observed in flexors during fast locomotor movements, (iii) within flexors and extensors, muscles were recruited sequentially, and (iv) the activation of other muscles (semitendinosus, rectus femoris, extensor and flexor digitorum longus) consisted of single or double bursting patterns.
Early Development of Olivocerebellar Projections in the Fetal Rat Using CGRP Immunocytochemistry
Authors: Chedotal Alain , Sotelo Constantino 
Published: April 2006

AbstractThe expression of calcitonin gene‐related peptide (CGRP) immunoreactivity in certain inferior olivary neurons is transient and developmentally regulated. Labelled neurons begin to appear at embryonic day 16 (E16), and reach their maximal extent by postnatal day 2 (P2). The extinction of the labelling occurs between P13 and P16. Expression of CGRP immunoreactivity is also observed in a few cerebellar fibres from E17, when axons in the restiform bundle begin to enter medially the cerebellar parenchyma. Their maximal extent is reached by P6, and thereafter they slowly disappear following a precise pattern, although fibre extinction is not complete. The spatio‐temporal changes in the olivary distribution of the labelled neurons and the changes in the cerebellar labelled fibres follow the known pattern of topographic arrangement of the olivocerebellar system in adult rats. Moreover, the developmental phases of the CGRP‐labelled fibres in postnatal rats correspond to those known for climbing fibre phenotypic acquisition. Thus, CGRP immunocytochemistry identifies in the fetal rat a subset of inferior olivary neurons and their corresponding cerebellar climbing fibres. Using this approach, we have analysed some of the initial events leading to the formation of the olivocerebellar projection, and obtained the following information: (i) Olivocerebellar axons are not randomly distributed in the restiform bundle before they enter the cerebellum. (ii) In the presence of a large spectrum of choices at the surface of the rostral half of the cerebellar plate the labelled olivary axons begin to enter the cerebellum at a precise medial point to abut a region composed solely of migrating Purkinje cells, and establish contacts with their targets before these neurons reach their final cortical location. (iii) From E18 to E19, the bundle of labelled fibres loses its superficial location, being bypassed by migrating Purkinje cells, to occupy a region corresponding to the prospective white matter. This translocation is coincident with the occurrence of a second axonal entry point, somewhat more lateral than the previous one, and with the appearance of a new lateral stripe of labelled fibres. (iv) Both the early and the late appearing labelled stripes remain confined from the time of their formation in precise cerebellar territories, indicating that only some clusters of Purkinje cells are contacted by the CGRP fibres. The results obtained imply that there is neither a waiting period nor an initial phase of randomness in the formation of the olivocerebellar projection map. This absence of chaotic cerebellar invasion, and the high selectivity of the entry points, suggest that the orientation of CGRP‐positive olivocerebellar fibres towards their targets is regulated by positional information shared between subsets of olivary neurons and clusters of Purkinje cells. The result of this process would be the formation of a precocious coarse topography that would need further refinement.
Long‐term Potentiation and Field EPSPs in the Lateral and Medial Perforant Paths in the Dentate Gyrus In Vitro: a Comparison
Authors: Hanse Eric , Gustafsson Bengt 
Published: April 2006

AbstractThe entorhinal cortex projects monosynaptically to the granule cells in the dentate gyrus via the lateral and medial perforant paths. These two subdivisions of the perforant path differ with respect to synaptic properties, and recent studies suggest that they also differ with respect to long‐term potentiation (LTP). In the present study, using the in vitro slice preparation of the guinea‐pig hippocampus, field excitatory postsynaptic potentials (EPSPs) and LTP in the lateral and medial perforant paths were compared. The two pathways were distinguished on the basis of their different termination in the dendritic layer, their different pharmacology and short‐term synaptic facilitation. The field EPSP [obtained in the presence of γ‐aminobutyric acid (GABA) A and B receptor antagonists] consisted of a non‐N‐methyl‐d‐aspartate (NMDA) component with different time characteristics in the two pathways, the decay being monoexponential in the lateral perforant path and biexponential in the medial one. In addition, the field EPSP in both pathways contained a small NMDA‐mediated component that could also be observed after complete blockade of the non‐NMDA one. LTP induction in both lateral and medial perforant paths was facilitated by blockade of GABAA inhibition, showed associative properties, and was blocked by NMDA receptor antagonists. Following the induction event, LTP in both pathways developed to a peak value within 30–40 s, and the stability of LTP was correlated with the amount of postsynaptic, but not presynaptic, activity during the induction event. During blockade of GABAA inhibition the opioid receptor antagonist naloxone and the β‐adrenergic antagonist timolol had no effect on the magnitude or stability of LTP. It is concluded that LTP in the lateral and medial perforant paths does not differ with respect to induction mechanisms and early temporal characteristics.
The Effect of Apomorphine and Buspirone on Regional Cerebral Blood Flow During the Performance of a Cognitive Task—Measuring Neuromodulatory Effects of Psychotropic Drugs in Man
Authors: Grasby P. M. , Friston K. J. , Bench C. J. , Frith C. D. , Paulesu E. , Cowen P. J. , Liddle P. F. , Frackowiak R. S. J. , Dolan R. 
Published: April 2006

AbstractPsychopharmacological activation, in conjunction with positron emission tomographic measurements of regional cerebral blood flow (rCBF), was used to investigate the neurotransmitter basis of a specific cognitive function in man. Monoaminergic neurotransmission was pharmacologically manipulated during performance of auditory – verbal memory tasks. Statistical parametric mapping was used to identify the brain sites of interaction between memory‐induced increases in rCBF and active drugs. Memory task‐induced increases in rCBF in the left prefrontal cortex were attenuated by apomorphine, a non‐selective dopamine agonist, whilst buspirone, a serotonin1A partial agonist, augmented rCBF increases in this area. In addition, apomorphine and buspirone augmented memory‐induced increases in rCBF centred in the posterior cingulate cortex, whilst buspirone alone attenuated rCBF increases in the retrosplenial cortex and posterior parahippocampal gyrus. These regionally selective interactions may represent neuromodulatory effects of monoaminergic neurotransmission on a specific cognitive function in man.
The Effect of Removing Superior Temporal Cortical Motion Areas in the Macaque Monkey: I. Motion Discrimination Using Simple Dots
Authors: Cowey Alan , Marcar Valentine L. 
Published: April 2006

AbstractWe compared the pre‐ and postoperative performance of macaque monkeys on visual discrimination tasks entailing the perception of differences in the motion of two luminous spots. Animals in which area MT and adjacent regions had been surgically removed were not significantly impaired as long as there were differences in the temporal frequency of the two stimuli. When the latter were eliminated the postoperative performance of the MT animals was significantly impaired compared to their preoperative performance and compared to the animals in the control groups. The same animals were also impaired at perceiving which of two moving dots, presented in the dark, changed its direction.
The Effect of Removing Superior Temporal Cortical Motion Areas in the Macaque Monkey: II. Motion Discrimination Using Random Dot Displays
Authors: Marcar Valentine L. , Cowey Alan 
Published: April 2006

AbstractNine macaque monkeys were trained to discriminate between a display in which all the dots moved randomly (visual dynamic noise) and an adjacent display in which a proportion of the dots oscillated coherently from side to side. Two monkeys in which area MT (middle temporal visual area) and adjacent regions were surgically removed were unable to perform even the simplest version of this task where the coherent motion was not masked by any visual dynamic noise. The other seven animals tolerated between 60% and 65% of random movement in the otherwise coherently oscillating display before they failed to discriminate between the two displays. In contrast, shape discrimination tasks containing luminance boundaries were unaffected by the removal of area MT. However, the removal of area MT did impair the animals' ability to use a kinetic boundary as the basis for shape discrimination. Their performance with a kinetic boundary between a moving and a stationary random dot field and a kinetic boundary between two random dot fields moving in opposite directions was the most severely impaired. Their performance with a kinetic boundary defined by two random dot fields moving orthogonally to each other was unimpaired. None of the animals from either group was able to use the kinetic boundary defined by coherent motion and visual dynamic noise as the basis for shape discrimination. The ease with which the control animals were able to employ the different types of kinetic boundaries to perform the shape discrimination reflected previously published proportions of cells in area MT that are specialized for detecting the different types of kinetic boundaries.
Spontaneous Gaze Shifts in Intact Head‐free Rats and Following Inferior Olive and Cerebellar Lesions
Authors: Tempia Filippo , Ghirardi Mirella , Dotta Michele , Strata Piergiorgio 
Published: April 2006

AbstractRecent experiments have shown that after lesions of the inferior olive or of the flocculus and paraflocculus of the cerebellum, in the pigmented rat, spontaneous saccades made when the head is completely restrained are followed by a large postsaccadic drift. The aims of the present paper were to study (i) the strategies and the characteristics of spontaneous eye – head coordinated gaze shifts in intact pigmented rats and to compare them with those described in other mammals, (ii) how they are affected by inferior olive and flocculus – paraflocculus lesions, and (iii) whether in these groups of animals the stability of the gaze is more deficient when the head is free to rotate in the horizontal plane (head‐free condition) relative to the head‐fixed condition. Three types of gaze shift strategy of intact rats are described and characterized. Following inferior olive or flocculus – paraflocculus lesion the dynamic parameters of such gaze shifts (the main sequences of head, gaze and eye and the timing of eye and head movement onset) are not significantly affected. The main deficits of lesioned animals affect the stability of gaze at the end of gaze shifts. After inferior olive lesion the amplitude of the postsaccadic drift of the gaze is 43.2% of the gaze saccade in the head‐fixed condition, which is reduced to 22.9% in the head‐free condition. Following flocculus – paraflocculus lesion the postsaccadic drift of gaze is even more reduced than after inferior olive lesion, changing from 39.2% in the head‐fixed condition to only 9.7% in the head‐free condition.
Tunicamycin Dissociates Depolarization‐induced Calcium Entry From Transmitter Release. Involvement of Glycosylated Protein(s) in the Process of Neurosecretion in PC‐12 Cells
Authors: Schwartz Lydia , Diamant Sophia , Barhanin Jacques , Atlas Daphne 
Published: April 2006

AbstractThe process of regulated secretion in PC‐12 cells is tightly coupled to calcium entry, which is absolutely dependent on extracellular Ca2+([Ca2+]ex). Tunicamycin treatment of the cells dissociated depolarization‐triggered Ca2+ influx from depolarization (high K+)‐induced transmitter release into two distinct and independent phases. Deplarization‐evoked Ca2+ influx was not affected by tunicamycin treatment (1 μg/ml, 72 h), whereas depolarization‐evoked transmitter release was strongly inhibited (>60%), suggesting at least a two‐step process, and the participation of glycosylated protein(s) in the actual fusion/secretion step. Similarly, bradykinin‐mediated transmitter release was linearly related to and absolutely dependent on Ca2+ entry, and was inhibited by tunicamycin treatment (>80%), whereas bradykinin‐evoked Ca2+ entry was not impaired, indicating that glycosylated protein(s) are essential for bradykinin‐evoked release at a step subsequent to Ca2+ influx. The heavily glycosylated α2 subunit of the dihydropyridine‐sensitive channel, which was used to monitor tunicamycin inhibition of glycosylation, was not expressed in the tunicamycin‐treated cells, as shown by Western blot analysis. This observation allowed us to conclude that the a, subunit of the heteromeric dihydropyridine voltage‐sensitive Ca2+ channel, which is responsible for Ca2+ entry, is also fully functional when not assembled with its corresponding α2 subunit. The molecular properties of the α2 subunit, whose role in the complex structure of the channel is not yet understood, are shown for the first time for the L‐type Ca2+ channel of PC‐12 cells. Similar to cardiac and skeletal muscle cells, the α2 subunit appears to be a glycosylated polypeptide of molecular weight 170 kD and to display a characteristic mobility shift to 140 kD under reducing conditions.
Kynurenic Acid in the Quinolinate‐lesioned Rat Hippocampus: Studies In Vitro and In Vivo
Authors: Wu Hui‐Qiu , Baran Halina , Ungerstedt Urban , Schwarcz Robert 
Published: April 2006

AbstractThe present study was designed to examine the cellular localization and biosynthetic machinery of the broad‐spectrum excitatory amino acid receptor antagonist kynurenic acid in the lesioned rat hippocampus. Seven days after an intrahippocampal injection of 120 nmol quinolinic acid, which causes massive neurodegeneration in the dorsal hippocampus, kynurenic acid tissue levels and the activity of kynurenic acid's anabolic enzyme, kynurenine aminotransferase, were increased by 92% and 67%, respectively, as compared to controls. The steady‐state levels of extracellular kynurenic acid, examined by microdialysis in unanaesthetized rats, were also increased in the lesioned tissue (from 93.6 ± 10.2 to 207.6 ± 18.6 fmol/30 μl dialysate). Using microdialysis, three compounds which are known to decrease kynurenic acid production from its bioprecursor l‐kynurenine in brain slices and in vivo were tested for their ability to reduce the levels of endogenous kynurenic acid. In unlesioned tissue, aminooxyacetic acid (300 μM), veratridine (50 μM) and glutamate (5 mM), all administered through the dialysis probe, decreased extracellular kynurenic acid concentrations by 30 – 40%, i.e. to a lesser degree than in previous experiments in which kynurenine was used as a bioprecursor. Only the effect of veratridine was abolished in the quinolinate‐lesioned hippocampus. These data indicate that kynurenic acid is produced in and liberated from astrocytes, and that aminooxyacetic acid and glutamate (but not veratridine) exert their action by directly affecting glial kynurenic acid biosynthesis. The results also suggest the existence of two distinct intracellular kynurenic acid pools, which are responsible for kynurenic acid storage and rapid kynurenic acid mobilization, respectively. Taken together, these features of kynurenic acid neurobiology may be of relevance in the control of excitatory amino acid receptor function under physiological and pathological conditions.