bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cerebral Achromatopsia in Monkeys
Authors: Heywood C. A. , Gaffan D. , Cowey A. 
Published: April 2006

AbstractIn human cerebral achromatopsia, extrastriate cortical damage produces a severe or complete loss of colour vision, with relative sparing of non‐chromatic vision. The critical lesion appears to be in a medial occipito‐temporal area, occupying the lingual and caudal fusiform gyri; positron emission tomography has shown that this cortical region is one of several activated in normal human observers during colour vision tasks. Attempts to find an analogous ‘colour centre’ in the cortex of monkeys have not been successful. In particular, ablation of cortical area V4, sometimes thought on physiological grounds to be more involved in wavelength and colour coding than any other visual cortical area, produces only mild impairments in colour discrimination. In the present study we tested the colour vision of monkeys after cortical ablations that mainly or entirely spared area V4. One group of monkeys (group AT) received ablations in the temporal lobe anterior to area V4, and a second group (group MOT) received ablations in a medial occipito‐temporal area roughly corresponding in cranial location to the lesion that produces human cerebral achromatopsia. The animals in group MOT showed no impairment of their colour vision. Group AT, in contrast, had a severe impairment in chromatic vision, with a relative sparing of non‐chromatic vision. Their behaviour was indistinguishable from that of a human patient with total cerebral achromatopsia who had been tested on the same tasks. These results show that area V4 in macaque monkeys is not analogous, and probably not homologous, to the human colour centre. Instead, they suggest that the area of the monkey's brain corresponding to the colour area in the human brain is in the temporal cortex, anterior to area V4.
Peripheral Myelin Protein‐22 is Expressed in Rat and Mouse Brain and Spinal Cord Motoneurons
Authors: Parmantier E. , Cabon F. , Braun C. , D'Urso D. , Müller H. W. , Zalc B. 
Published: April 2006

AbstractPeripheral myelin protein PMP‐22 is expressed by Schwann cells and is a constituent of peripheral nervous system (PNS) myelin. Two PMP‐22 transcripts, SR73 and CD25, differing in their 5’non‐coding sequences have been described. SR73 is present both in the PNS and in non‐neural tissue, whereas CD25 mRNA is almost exclusively expressed in Schwann cells. PMP‐22 mRNA is also present in the central nervous system (CNS), but at much lower levels than in the PNS. We have investigated the regional distribution of PMP‐22 mRNA in the rat and mouse CNS by the reverse transcriptase‐polymerase chain reaction method, using oligonucleotide primers specific for the SR73 or CD25 transcripts. SR73 mRNA was detected in all the CNS regions analysed, whereas the CD25 message was present only in the brainstem and the spinal cord. Localization of the PMP‐22 transcripts, determined by in situ hybridization in 21 day‐old animals, showed selective expression in the motor nuclei. The PMP‐22 signal was very weak in the nuclei of the oculomotor and trochlear nerves and absent in the nucleus of the abducens nerve. A strong PMP‐22 signal was observed in the motor nuclei of the trigeminal, facial, ambigus, vagus, hypoglossal and accessory spinal nerves and in the ventral horn of the spinal cord. The PMP‐22‐positive cells were identified as motoneurons on the basis of topographic and morphological criteria, as well as immunolabelling with neuron‐specific antibodies. Immunostaining with specific anti‐PMP‐22 antibodies demonstrated that neurons expressing the PMP‐22 message also expressed the corresponding protein in their cell bodies and axons. In contrast, neurons in the sensory nuclei of cranial nerves and dorsal root ganglion neurons were PMP‐22‐negative. In the trembler mouse, a PNS dysmyelinating mutant with a missense mutation in PMP‐22, the motoneuronal expression of PMP‐22 mRNA was either normal or increased.
Long‐lasting Potentiation of a Direct Central Connection between Identified Motor Neurons in the Locust
Authors: Parker David 
Published: April 2006

AbstractThe plasticity of the direct central connection between the fast extensor and the posterior fast flexor tibiae motor neurons in the locust (Schistocerca gregaria) metathoracic ganglion was studied. An action potential in the fast extensor results in a monosynaptic excitatory postsynaptic potential (EPSP) in the flexor motor neuron. Antidromic stimulation of the fast extensor at 100 Hz for 3.5 s resulted in a long‐lasting potentiation of the EPSP amplitude. The potentiation was not dependent on feedback caused by movement of the tibia, and was associated with an increase in the input resistance of the flexor motor neuron. The potentiation was heterosynaptic, and was not affected by bath application of the N‐methyl‐D‐aspartate receptor antagonist 2‐amino‐5‐phosphonovaleric acid. The potentiation was voltage dependent, as hyperpolarizing the flexor motor neuron during the stimulation blocked the development of the potentiation whereas depolarizing the flexor in the absence of presynaptic activity caused potentiation of subsequent fast extensor‐evoked EPSPs. The depolarization‐induced potentiation was calcium dependent. Antidromic stimulation of the fast extensor at 100 Hz for 3.5 s also caused modulation of the presynaptic action potential. The spike duration was increased and the amplitude of the afterhyperpolarization reduced. These effects were dependent on movement of the tibia. Bath application of the 5‐hydroxytryptamine (5‐HT) receptor antagonist ketanserin blocked the changes in the presynaptic spike. The modulation was probably due to the release of 5‐HT from proprioceptive afferents that monitor movement of the tibia about the femur. The modulation of the presynaptic action potential increases transmitter release onto the flexor motor neurons, and this acts in synergy with the postsynaptic modulation to potentiate the connection.
Synaptic Vesicle Depletion in Reticulospinal Axons is Reduced by 5‐hydroxytryptamine: Direct Evidence for Presynaptic Modulation of Glutamatergic Transmission
Authors: Shupliakov O. , Pieribone V. A. , Gad H. , Brodin L. 
Published: April 2006

Abstract5‐hydroxytryptamine (5‐HT; serotonin) is known to depress glutamatergic synaptic transmission in the spinal cord of vertebrates. To test directly whether 5‐HT inhibits synaptic glutamate release, we examined its effect on the ultrastructure of synaptic vesicle clusters in giant reticulospinal axons in a lower vertebrate (lamprey; Lampetra fluviatilis). The size of these axons makes it possible to selectively expose only a part of the presynaptic element to 5‐HT, while another part of the same axon is maintained in control solution. Action potential stimulation at 20 Hz for 20 min caused a marked reduction in the number of synaptic vesicles in active zones maintained in control solution, while in the part exposed to 5‐HT (20 μM) the number of synaptic vesicles per active zone was ‐3‐fold higher. In contrast, 5‐HT had no effect on the number of vesicles in resting axons. To examine whether 5‐HT acts by reducing presynaptic Ca2+ influx, intra‐axonal recordings of Ba2+ potentials were performed. No reduction of the axonal Ba2+ potential could be detected after application of 20 or 200 pM 5‐HT. The present results show that 5‐HT reduces the rate of synaptic exocytosis in reticulospinal axons. The effect appears to be mediated by a mechanism distinct from the presynaptic Ca2+ channels.
Trans‐synaptic Modulation of Striatal ACh Release In Vivo by the Parafascicular Thalamic Nucleus
Authors: Baldi Gianni , Russi Giovanni , Nannini Luca , Vezzani Annamaria , Consolo Silvana 
Published: April 2006

AbstractElectrical stimulation of the parafascicular but not the ventrolateral or dorsomedial thalamic nucleus (ten 0.5 ms, 10 V pulses, 140 pA) of freely moving rats induced a frequency‐dependent (2.5, 5,10 and 20 Hz) increase in the extracellular acetylcholine (ACh) content of the dorsal striatum, assessed by trans‐striatal microdialysis. The time‐dependent effect of 10 Hz stimulation was studied. The peak increase, 39% above baseline, was attained during 4 min of stimulation. This was blocked by coperfusion with 5 pM tetrodotoxin, indicating that the release we measured represents a physiological process. The facilitatory effect of parafascicular nucleus stimulation does not appear to be associated with indirect action through the cerebral frontal cortex because acute lesion of the excitatory corticostriatal afferents, which by itself reduced basal ACh release by 40%, did not modify the effect of 10 Hz stimulation. The possible involvement of the fasciculus retroflexus in the facilitation of ACh release was also ruled out. The non‐competitive NMDA‐type receptor antagonist MK‐801, applied by reversed dialysis (30 pM) or systemically injected (0.2 mg/kg), significantly reduced the basal ACh output and prevented the tetanus‐evoked increase in ACh release. The results provide in vivo evidence that the activity of the cholinergic neurons in the dorsal striatum is trans‐synaptically modulated by parafascicular nucleus excitatory afferents through activation of the NMDA subtype of glutamate receptors that is probably located in the striatum.
Comparing Localization of Conventional Functional Magnetic Resonance Imaging and Magnetoencephalography
Authors: Beisteiner R. , Gomiscek G. , Erdler M. , Teichtmeister C. , Moser E. , Deecke L. 
Published: April 2006

AbstractThe technique of functional magnetic resonance imaging (FMRI) allows the measurement of functional cerebral blood flow changes occurring with specific tasks. However, the spatial relationship between neuronal activity and functional cerebral blood flow changes is not kno'wn yet. This study compares the centre of neuronal activation (measured by magnetoencephalography) with that of the blood flow response (measured by FMRI) to unilateral motor stimulation in eight subjects. The results show a mean localization difference of 1.6 cm and demand application of methodological improvements as recently suggested.
Involvement of Serotonin in Developmental Plasticity of Kitten Visual Cortex
Authors: Gu Qiang , Singer Wolf 
Published: April 2006

AbstractDuring a critical period of postnatal development, neuronal connections in the kitten visual cortex are susceptible to experience‐dependent modifications. These modifications are facilitated by the neuromodulators noradrenaline and acetylcholine. To address the question of whether serotonin (5‐hydroxytryptamine; 5‐HT), the other major neuromodulator in the cerebral cortex, also plays a role in developmental plasticity, we investigated whether interference with serotoninergic transmission in the kitten visual cortex affects ocular dominance (OD) plasticity. The serotonin neurotoxin 5,7‐dihydroxytryptamine or the serotonin receptor blockers ketanserin and methysergide were infused into the visual cortex of kittens undergoing monocular deprivation. We found that both methods of disrupting serotoninergic transmission reduced OD plasticity. However, to be effective, the receptor blockers ketanserin and methysergide had to be applied in combination, suggesting that coactivation of serotonin receptor subtypes of both the 5‐HT1 and 5‐HT2 families have a permissive function in OD plasticity. Since activation of 5‐HT2 receptors stimulates phosphoinositide hydrolysis, our data suggest that second messengers from the phospholipid pathway may play an important role in developmental plasticity of visual cortex.
Failure of Axon Regeneration in Postnatal Rat Entorhino‐hippocampal Slice Coculture is Due to Maturation of the Axon, not that of the Pathway or Target
Authors: Li D. , Field P. M. , Raisman G. 
Published: April 2006

AbstractHorizontal slices which included the entorhinal area in continuity with the hippocampus were taken from the ventral levels of the cerebral hemispheres of rat pups from two age groups, from the 6th to the 8th postnatal days (‘young') and the 12th to the 15th days (‘old’). The slices were divided into an entorhinal part and a hippocampal part (which consisted of the hippocampus proper, dentate gyrus and subiculum) by a knife cut passing through the deep white matter of the entorhinal area. The slices were recombined in their normal orientation by matching the cut edges in the following age combinations: young/young, old/old, young/old and old/young. After 14 days in culture, crystals of biocytin were placed on the superficial layers of the entorhinal area. In the young/young combination the same placement of biocytin simultaneously labelled projections passing in both directions across the interface, i.e. (i) orthograde transport of biocytin taken up by entorhinal projection neurons resulted in labelling of axons passing from the entorhinal area across the interface between the cocultures to reach the correct terminal zone in the outer molecular layer of the dentate gyrus, and (ii) retrograde transport of biocytin taken up by axons and their terminals in the entorhinal area labelled the slender subicular and adjacent hippocampal field CA1 pyramidal cells whose axons project to the entorhinal area. In the old/old cocultures there were no projections in either direction. In the mixed age combinations, young entorhinal cortical tissue projected correctly across the interface to old dentate gyrus, but old entorhinal tissue did not project to young dentate gyrus. Conversely, the pyramids of young subicular tissue projected across the interface to old entorhinal tissue, but old subicular tissue did not project to young entorhinal cortex. Therefore, the crucial factor in the age‐related failure of the formation of projections was the age of the axons of the projecting neurons. The fail‐age for the formation of entorhino‐dentate projections was the same as that for the formation of the subiculo‐entorhinal projections passing in the opposite direction across the same interface. Thus the greater age of the pathway and the target fields did not prevent the younger axons from successfully finding their routes through the tissue and recognizing the correct terminal fields. General tissue factors, such as the formation of scar tissue and the onset of myelination (which occurs in the perforant path around the 10th day of life), also did not affect the outcome, since in the young/old and old/young combinations the projection failed in one direction across the interface while it succeeded in the opposite direction across the same interface.
5′‐Nucleotidase Activates and an Inhibitory Antibody Prevents Neuritic Differentiation of PC12 Cells
Authors: Heilbronn Alev , Zimmermann Herbert 
Published: April 2006

AbstractEcto‐5′‐nucleotidase catalyses the hydrolysis of AMP at the surface of a variety of cells whereas it is absent from others. In addition to its catalytic activity, a function in neural development and also its interaction with extracellular matrix proteins has been reported. In order to further elucidate the biological function of ecto‐5′‐nucleotidase we have investigated the effect of 5′‐nucleotidase on nerve growth factor‐induced differentiation of PC12 cells. Furthermore, we compared the effect of an inhibitory versus a non‐inhibitory monospecific antibody against the enzyme on neuritic differentiation and survival of PC12 cells that constitutively express the enzyme. When coverslips are coated with the soluble form of ecto‐5′‐nucleotidase in addition to collagen, there is a considerable increase in nerve growth factor‐induced neurite length during the first 24 h of culture. Addition of an antibody to a culture medium that inhibits 5′‐nucleotidase activity to 33% of control values dramatically reduces the number of neurites per cell within 3 days of culture. The cells round up, cluster and eventually die. On the contrary, another antibody that had no significant effect on enzyme activity affected neither nerve growth factor‐induced neurite formation nor survival of PC12 cells. Addition of adenosine (200 nM, 10 or 20 μM) to the culture medium did not influence PC12 cell differentiation. The effects induced by the inhibitory antibody could be only partially prevented by simultaneous application of adenosine. Our results suggest that 5′‐nucleotidase is essential for nerve growth factor‐induced neurite outgrowth and survival of PC12 cells. The results obtained cannot be simply explained on the basis of the availability and extracellular production of adenosine.
Response to Novelty and its Rapid Habituation in Locus Coeruleus Neurons of the Freely Exploring Rat
Authors: Vankov Andrey , Hervé‐Minvielle Anne , Sara Susan J. 
Published: April 2006

AbstractActivity of single units of the noradrenergic nucleus locus coeruleus was recorded in rats during active exploration of a novel environment. Novelty was controlled by the placement of objects in given holes in a hole board. The basic protocol included a habituation session in which the holes were empty and an object session in which a novel object was placed in one of the two holes. During the habituation session, when the whole environment was unfamiliar, there was a phasic response the first time the rat visited any hole, which habituated after one visit. During the second session, when one of the holes contained an object, the cell fired when the rat encountered the novel object. There was no response to empty holes in this session. The neuronal response was markedly diminished or entirely absent on the second and subsequent visits to object‐containing holes, indicative of rapid habituation. In some rats it was possible to run a second object session, when a new object was introduced into a previously empty hole. Visits to this hole elicited a robust response, which again habituated after one single visit. The results show that the responses of locus coeruleus to novelty or change, which has been demonstrated in formal learning situations, occurs in freely behaving rats while they are learning about a new environment. Moreover, the response to novelty and change in the environment is short‐lived, rapidly habituating after one or two encounters with the stimulus.This research was supported by grants from the Ministere de la Recherche et de la Technologie (MRT; 91C0956) and the CNRS Cognisciences Programme (ATIPE) to S. J. S., and by a collaborative grant from the European Neuroscience Programme of the European Science Foundation. A. V. is a visiting scientist from the Brain Research Institute of the Bulgarian Academy of Sciences, Sofia, and was supported by postdoctoral fellowships from the Fondation Pour La Recherche Medicale and from the CNRS. A. H. M. was supported by a predoctoral fellowship from the MRT. Gerard Dutrieux provided technical assistance in the development of the hole board apparatus.
Glycine‐ and GABA‐activated Currents in Identified Glial Cells of the Developing Rat Spinal Cord Slice
Authors: Pastor Andrea , Chvátal Alexandr , Syková Eva , Kettenmann Helmut 
Published: April 2006

AbstractIn the neonatal rat spinal cord, four types of glial cells, namely astrocytes, oligodendrocytes and two types of precursor cells, can be distinguished based on their membrane current patterns and distinct morphological features. In the present study, we demonstrate that these cells respond to the inhibitory neurotransmitters glycine and GABA, as revealed with the whole‐cell recording configuration of the patch‐clamp technique. All astrocytes and glial precursor cells and a subpopulation of oligodendrocytes responded to glycine. The involvement of glycine receptors was inferred from the observation that the response was blocked by strychnine and that the induced current reversed close to the Cl‐ equilibrium potential. GABA induced large membrane currents in astrocytes and precursor cells while oligodendrocytes showed only small responses. The GABA‐activated current was due to the activation of GABAA receptors since muscimol mimicked and bicuculline blocked the response; moreover, the reversal potential was close to the Cl‐ equilibrium potential. Besides the increase in a Cl‐ conductance, GABAA receptor activation also induced a block of the resting K+ conductance, as observed previously in Bergmann glial cells. Our experiments show that while glial GABAA receptors are found in many brain regions and the spinal cord, glial glycine receptors have so far been detected only in the spinal cord. The restricted coexpression of glial and neuronal glycine receptors in a defined central nervous system grey matter area implies that such glial receptors may be involved in synaptic transmission.
Effects of Nigrostriatal Denervation and L‐Dopa Therapy on the GABAergic Neurons of the Striatum in MPTP‐treated Monkeys and Parkinson's Disease: An In Situ Hybridization Study of GAD67 mRNA
Authors: Levy R. , Herrero M. T. , Ruberg M. , Villares J. , Faucheux B. , Guridi J. , Guillen J. , Luquin M. R. , Javoy‐Agid F. , Obeso J. A. , Agid Y. , Hirsch E. C. 
Published: April 2006

AbstractThe effects of nigrostriatal denervation and L‐dopa therapy on GABAergic neurons were analysed in patients with Parkinson's disease and in monkeys rendered parkinsonian by MPTP intoxication. The expression of the messenger RNA coding for the 67 kDa isoform of glutamic acid decarboxylase (GAD67 mRNA), studied by quantitative in situ hybridization, was used as an index of the GABAergic activity of the striatal neurons. A significant increase in GAD67 mRNA expression, generalized to all GABAergic neurons, was observed in MPTP‐treated monkeys compared to control monkeys in the putamen and caudate nucleus (+44 and +67% respectively), but not in the ventral striatum. L‐Dopa therapy significantly reduced GAD67 mRNA expression in the putamen and caudate nucleus to levels similar to those found in control monkeys. However, the return to normal of GAD67 mRNA expression was not homogeneous across all neurons since it was followed by an increase of labelling in one subpopulation of GABAergic neurons and a decrease in another. These data suggest that in MPTP‐treated monkeys the degeneration of nigrostriatal dopaminergic neurons results in a generalized increase in GABAergic activity in all the GABAergic neurons of the striatum, which is partially reversed by L‐dopa therapy. As the expression of GAD67 mRNA is less intense in the ventral than in the dorsal striatum, this increase in striatal GABAergic activity may be related to the severity of nigrostriatal denervation. In parkinsonian patients who had been chronically treated with L‐dopa, GAD67 mRNA expression was significantly decreased in all GABAergic neurons, in the caudate nucleus (by 44%), putamen (by 43.5%) and ventral striatum (by 26%). The opposite variation of GAD67 mRNA in patients with Parkinson's disease, compared with MPTP‐treated monkeys, might be explained by the combination of chronic nigrostriatal denervation and long‐term L‐dopa therapy.