bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Cerebral Cortex and Parafascicular Thalamic Nucleus Facilitate In vivo Acetylcholine Release in the Rat Striatum through Distinct Glutamate Receptor Subtypes
Authors: Consolo Silvana , Baldi Gianni , Giorgi Susanna , Nannini Luca 
Published: April 2006

AbstractElectrical stimulation (ten pulses of 0.5 ms, 10 V applied over 10 s at 10 Hz, 140 pA) delivered bilaterally to the prefrontal cortex or the parafascicular thalamic nucleus of freely moving rats facilitated acetylcholine release in dorsal striata, assessed by trans‐striatal microdialysis. The facilitatory effects were blocked by coperfusion with 5 μM tetrodotoxin, suggesting that the release was of neuronal origin. The response of the striatal cholinergic neurons to prefrontal cortical stimulation was short‐lived and required a longer period of stimulation (20 min) than the response to thalamic stimulation (4 min) to reach maximal effect. The α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA)/kainate glutamatergic receptor antagonist 6,7‐dinitroquinoxaline‐2,3‐dione [DNQX; 12 nmol per side, intracerebroventricularly (i.c.v.)] and the AMPA antagonist 6‐nitro‐7‐sulphamoylbenzo(f)quinoxaline‐2,3‐dione (NBQX; 12 nmol per side, i.c.v. or 12.8 μM infused into the striatum), but not the NMDA‐type receptor antagonist MK‐801 (0.2 mg/kg, i.p.), abolished the facilitatory effect on striatal acetylcholine release evoked by stimulation of the prefrontal cortex. By contrast, DNQX or NBQX did not prevent the increase in striatal acetylcholine release evoked by parafascicular nucleus stimulation, but MK‐801, in accordance with previous results, did so. MK‐801 by itself lowered striatal acetylcholine output while DNQX and NBQX did not. The results provide in vivo evidence that the cerebral cortex facilitates cholinergic activity in the dorsal striatum apparently through the non‐tonic activation of AMPA‐type glutamatergic receptors while the parafascicular nucleus does this through tonic activation of NMDA receptors. Both glutamate receptor types are probably located in the striatum. The overall results suggest that the two pathways operate independently to regulate striatal cholinergic activity through distinct mechanisms.
Localization of the Serotonin Transporter in Rat Spinal Cord
Authors: Sur Cyrille , Betz Heinrich , Schloss Patrick 
Published: April 2006

AbstractThe spinal cord is richly innervated by serotoninergic fibres originating from the raphe nuclei. The localization of the terminating component of serotoninergic neurotransmission, the serotonin transporter SERT1, was found in both the dorsal and ventral horns, especially at the level of the cervical and lumbar segments. Within the thoracic region, we observed a heavily labelled bundle in the intermediolateral nucleus of lamina VII. A low density of stained fibres was encountered in the sacral spinal cord. In contrast to homogeneous staining of motor nuclei, a differential labelling of laminae was seen in the dorsal horn, with laminae I, III and IV exhibiting a higher density of immunopositive terminals than the medial part of lamina II. High magnification revealed a preferential accumulation of serotonin transporter staining within nerve endings and varicosities of thin fibres. Double immunofluorescence staining demonstrated a co‐localization of serotonin and its uptake system within these varicosities. These results show that the serotonin transporter is highly expressed in the rat spinal cord and that its distribution parallels the serotoninergic innervation. They also reinforce the view that varicosities are important neuronal structures, which modulate the function of dorsal and ventral horn neurons by releasing serotonin.
Hippocampal Lesions Cause Forgetting in a Spatial Response Task
Authors: Baylis Gordon C. , Moore Beth O. 
Published: April 2006

AbstractMonkeys with lesions to the hippocampus and overlying cortex were impaired in making a spatially selective response on the basis of a spatial cue. Their impairment was even more severe on a task in which they were required to make spatial responses on the basis of cues which are not spatially distinct. A second experiment showed that once lesioned monkeys had been trained on a task with spatially distinct stimuli, they were initially able to perform accurately if the spatial distinctiveness of the cue was reduced. However, their performance declined to chance over four to six trials. These results suggest that lesions to the hippocampus and overlying cortex may cause impairments in memory for the arrangement of visual scenes, including the spatial location of responses.
Synaptic Connections Between Spiny Neurons of the Direct and Indirect Pathways in the Neostriatum of the Rat: Evidence from Dopamine Receptor and Neuropeptide Immunostaining
Authors: Yung K. K. L. , Smith A. D. , Levey A. I. , Bolam J. P. 
Published: April 2006

AbstractThe flow of cortical information through the basal ganglia occurs through the so‐called ‘direct pathway’ and ‘indirect pathways’. The object of the present work was to attempt to determine whether spiny neurons in the neostriatum that give rise to the direct pathway (i.e. the striatonigral/entopeduncular pathway) and those giving rise to the indirect pathways (i.e. striatopallidal pathway) are synaptically interconnected. The approach was to carry out double immunocytochemistry at the electron microscopic level using antibodies against peptides or dopamine receptor subtypes that are selectively associated with the neurons that give rise to the direct (substance P or D1 receptors) and indirect pathways (enkephalin or D2 receptors). Sections of perfuse‐fixed rat neostriatum were immunostained to reveal both substance P immunoreactivity and D2 receptor immunoreactivity or enkephalin and D1 receptor immunoreactivity, respectively. Double peroxidase methods were employed using different chromogens that were distinguishable at both the light and electron microscopic levels. In the electron microscope substance P‐immunoreactive terminals were seen in synaptic contact with dendritic structures that displayed immunoreactivity for D2 receptor. Similarly, enkephalin‐immunoreactive terminals were seen in synaptic contact with D1‐immunoreactive dendritic structures. Thus, axon collaterals of neurons giving rise to the direct pathway form synaptic contacts with neurons that give rise to the indirect pathway and axon collaterals of neurons giving rise to the indirect pathway form synaptic contact with neurons that give rise to the direct pathway. These results indicate that the two pathways of information flow through the basal ganglia are synaptically linked at the level of the neostriatum.
Neuronal Differentiation in the Rat Hippocampus Involves a Stage‐specific Reorganization of Subnuclear Structure both In Vivo and In Vitro
Authors: Santama Niovi , Dotti Carlos G. , Lamond Angus I. 
Published: April 2006

AbstractPyramidal neurons from the hippocampus undergo a well characterized programme of differentiation in vitro involving five distinct stages (1–5). While some important aspects of the dynamic organization of cell cytoplasmic structure that underlie neuronal polarization have been elucidated, little is known about corresponding changes in nuclear organization. Here we identify major changes affecting nuclear structure and gene expression during late stages of differentiation. At stage 4 a sustained increase in global transcriptional activity occurs. This is followed at stage 5 by proliferation of coiled bodies, i.e. subnuclear organelles containing splicing factors, which form a novel domain around the nucleolus that we refer to as the rosette. Both the morphology and timing of rosette formation are identical in neurons in vitro and in situ in the developing hippocampus in rat brain. Long‐term synaptic inhibition in vitro or growth at low density does not prevent either nuclear reorganization, enhanced transcriptional activity or the formation of pre‐synaptic specializations. These data indicate that stage‐specific changes in nuclear structure and function, similar to distinct rearrangements of cytoplasmic components, are pre‐programmed aspects of the neuronal differentiation pathway in the hippocampus.
Chronic Dizocilpine Maleate (MK‐801) Treatment Suppresses the Effects of Nigrostriatal Dopamine Deafferentation on Enkephalin but not on Substance P Expression in the Rat Striatum
Authors: Hajji Moulay Driss , Salin Pascal , Goff Lydia Kerkerian‐Le 
Published: April 2006

AbstractThe present study examined the effects of chronic treatment with dizocilpine maleate (0.2 mg/kg i.p., twice a day for 8 days) alone or in combination with unilateral 6‐hydroxydopamine‐induced lesion of the nigrostriatal dopaminergic neurons on substance P and enkephalin expression in the rat striatum. This was done by means of quantitative in situ hybridization histochemistry and immunocytochemistry. As reported previously, the unilateral dopaminergic lesion resulted in marked decreases in substance P mRNA expression and immunoreactivity in the ipsilateral striatum, while enkephalin mRNA expression and Met‐enkephalin immunoreactivity were considerably increased in this structure. Blockade of NMDA receptors by chronic dizocilpine maleate treatment alone resulted in decreased levels of striatal substance P mRNA without significant change in substance P immunoreactivity versus controls. Enkephalin mRNA levels were also decreased in the striatum, matched by parallel reductions in Met‐enkephalin immunoreactivity. These observations indicate that NMDA receptor activity may exert tonic excitatory effects on substance P and enkephalin expression in the striatum. The same chronic treatment with dizocilpine maleate started 12 days after the 6‐hydroxydopamine injection suppressed the lesion‐induced up‐regulation of enkephalin expression without significantly affecting the down‐regulation of substance P expression. These data provide evidence that NMDA receptor‐mediated mechanisms contribute to the alteration of striatal enkephalin expression associated with dopaminergic depletion in hemiparkinsonian rat models.
Contrasting Effects of Chronic Clozapine, SeroquelTM (ICI 204,636) and Haloperidol Administration on ΔFosB‐like Immunoreactivity in the Rodent Forebrain
Authors: Vahid‐Ansari F. , Nakabeppu Y. , Robertson G. S. 
Published: April 2006

AbstractWe have recently demonstrated that specific neuroanatomical patterns of Fos‐like immunoreactivity are predictive of atypical antipsychotic activity. However, the fact that neuroleptics must be administered chronically in order to generate both extrapyramidal side effects and an optimal therapeutic response calls into question the relevance of acute changes in Fos‐like immunoreactivity for these slowly developing events. Fos‐like immunoreactivity cannot be used to identify neurons activated by chronic neuroleptic administration because the increase in Fos‐like immunoreactivity produced by an acute antipsychotic injection is dramatically reduced following repeated neuroleptic administration. In contrast, expression of the immediate‐early gene product ΔFosB is persistently elevated in the striatum by chronic haloperidol administration. This suggests that ΔFosB‐like immunoreactivity may be used to identify neurons activated by chronic antipsychotic administration. Since typical and atypical neuroleptics elevate Fos‐like immunoreactivity in different regions of the forebrain acutely, the purpose of the present study was to determine whether typical (haloperidol) and atypical (clozapine, ICI 204,636) antipsychotics produce distinct patterns of elevated ΔFosB‐like immunoreactivity in the forebrain after chronic administration. Administration of haloperidol (2 mg/kg/day) to rats for 19 days induced a homogeneous elevation of neurons which displayed ΔFosB‐like immunoreactivity in the ventral, medial and dorsolateral aspects of the striatum. Chronic haloperidol administration did not enhance ΔFosB‐like immunoreactivity in the prefrontal cortex and lateral septal nucleus. Repeated administration of clozapine (20 mg/kg/day) and ICI 204,636 (20 mg/kg/day) for 19 days elevated ΔFosB‐like immunoreactivity not only in the ventral striatum but also in the prefrontal cortex and lateral septal nucleus. However, these compounds had weak effects on ΔFosB‐like immunoreactivity in the dorsolateral striatum. These results suggest that a preferential action on limbic structures such as the prefrontal cortex, ventral striatum and lateral septal nucleus may account for the ability of chronic clozapine and ICI 204,636 administration to reduce the symptoms of schizophrenia without generating extrapyramidal side effects.
Brain Rhythms of Language: Nouns Versus Verbs
Authors: Pulvermüller Friedemann , Preissl Hubert , Lutzenberger Werner , Birbaumer Niels 
Published: April 2006

AbstractElectrocortical activity was recorded from scalps of human subjects reading nouns and verbs. Current source density analysis of EEG signals and calculation of spectral responses revealed differences between word categories in the 30 Hz range. Verbs elicited stronger 30 Hz activity at recording sites over the motor cortices, while nouns elicited stronger responses at sites over visual cortices in the occipital lobes. Behavioural testing indicated that, at the cognitive level, this double dissociation corresponds to motor and visual associations prompted by verbal stimuli. These results suggest that local high‐frequency brain responses can be indicators of conscious processing of motor and visual associations of verbal material. Furthermore, the results provide additional evidence that nouns and verbs have distinct neuronal generators in the intact human brain.
Synaptogenesis in the Occipital Cortex of Macaque Monkey Devoid of Retinal Input From Early Embryonic Stages
Authors: Bourgeois Jean‐Pierre , Rakic Pasko 
Published: April 2006

AbstractThe role of input from the retina on the development of synaptic organization in the primate striate cortex was examined in macaque monkeys enucleated at embryonic (E) day 67 and E59. Both the prenatally operated animals and their age‐matched controls were delivered at term (E165) and killed either at 3 months (at the end of the rapid phase of synaptogenesis) or 3 years (at the end of the plateau phase of synaptogenesis). As expected, in the operated animals the striate cortex had a smaller surface area but a normal thickness and complement of layers. The present study revealed that the mean densities of synaptic contacts per unit area and volume of neuropil in the striate cortex of the two operated animals were similar to those of age‐matched controls (∼30/100 μm2 or 100/100 μm3 of neuropil). Thus, the absence of retinal input via the lateral geniculate nucleus did not affect the schedule and magnitude of synaptogenesis. Likewise, the ratio of symmetrical versus asymmetrical synapses and mean lengths of synaptic junctions were within the normal range of variation in both group of animals. The proportions of synaptic contacts situated on dendritic spines and shafts were also similar in supra‐ and infragranular cortical layers of normal and enucleated animals. However, the ratio of synapses situated on dendritic spines and shafts in the sublayers IVAB and IVC, which normally become reversed during late adolescence, were not reversed in the enucleates. Therefore, our study indicates that certain parameters of synaptic development, such as the density of contacts per unit volume of neuropil and the proportion of basic types and their size, in the supra‐ and infragranular layers of the striate cortex develop to an optimal normal level in the absence of both retinae from early embryonic stages. However, in the thalamorecipient sublayers the details of the synaptic circuits, such as their localization on dendritic spines or shafts, fail to mature properly in the absence of normal functional input from the periphery.
Involvement of Na+–Ca2+ Exchanger in Reperfusion‐induced Delayed Cell Death of Cultured Rat Astrocytes
Authors: Matsuda Toshio , Takuma Kazuhiro , Nishiguchi Emi , Asano Shoichi , Hashimoto Hitoshi , Azuma Junichi , Baba Akemichi 
Published: April 2006

AbstractIn some cells, Ca2+ depletion induces an increase in intracellular Ca2+ ([Ca2+]i) after reperfusion with Ca2+‐containing solution, but the mechanism for the reperfusion injury is not fully elucidated. Using an antisense strategy we studied the role of the Na+‐Ca2+ exchanger in reperfusion injury in cultured rat astrocytes. When astrocytes were perfused in Ca2+‐free medium for 15–60 min, a persistent increase in [Ca2+]i was observed immediately after reperfusion with Ca2+‐containing medium, and the number of surviving cells decreased 3–5 days latter. The increase in [Ca2+]i was enhanced by low extracellular Na+ ([Na+]o) during reperfusion and blocked by the inhibitors of the Na+‐Ca2+ exchanger amiloride and 3,4‐dichlorobenzamil, but not by the Ca2+ channel antagonists nifedipine, Cd2+ and Ni2+. Treatment of astrocytes with antisense, but not sense, oligodeoxynucleotide to the Na+‐Ca2+ exchanger decreased Na+–Ca2+ exchanger protein level and exchange activity. The antisense oligomer attenuated reperfusion‐induced increase in [Ca2+]i and cell toxicity. The Na+‐Ca2+ exchange inhibitors 3,4‐dichlorobenzamil and ascorbic acid protected astrocytes from reperfusion injury partially, while the stimulators sodium nitroprusside and 8‐bromo‐cyclic GMP and low [Na+]o exacerbated the injury. Pretreatment of astrocytes with ouabain and monensin caused similar delayed glial cell death. These findings suggest that Ca2+ entry via the Na+–Ca2+ exchanger plays an important role in reperfusion‐induced delayed glial cell death.
Activation of Meningeal 5‐HT2B Receptors: An Early Step in the Generation of Migraine Headache?
Authors: Schmuck Karin , Ullmer Christoph , Kalkman Hans O. , Probst Alphonse , Lübbert Hermann 
Published: April 2006

AbstractSeveral pharmaceuticals are frequently dispensed to prevent or reduce the occurrence of migraine attacks. The prophylactic effect of these drugs has been suggested to be caused through blockade of serotonin (5‐HT) receptors of type 5‐HT2B or 5‐HT2C. To elucidate which of these receptors is involved, we first used radioligand binding assays to determine the pharmacological profile of the human and rat 5‐HT2B receptor. Furthermore, the potency of drugs used in migraine prophylaxis to stimulate or inhibit 5‐HT2B or 5‐HT2C receptor‐mediated phosphatidyl inositol hydrolysis was measured. All these drugs were found to block both human receptors. Correlation of the receptor affinities with the potencies used in migraine prophylaxis showed significant correlations, which were better for the 5‐HT2B (P= 0.001) than for the 5‐HT2C receptor (P= 0.005). Migraine headache is thought to be transmitted by the trigeminal nerve from the meninges and their blood vessels. Using the reverse transcription–polymerase chain reaction, the expression patterns of all cloned G‐protein‐coupled serotonin receptors were analysed in various human meningeal tissues. All tissues expressed 5‐HT1Dβ, 5‐HT2A, 5‐HT2B, 5‐HT4 and 5‐HT7 mRNAs. Only trace amounts of 5‐HT2C receptor mRNA were found. With organ bath experiments we showed that the 5‐HT2B receptor stimulated the relaxation of the pig cerebral artery via the release of nitric oxide. Our data support the hypothesis that 5‐HT2B receptors located on endothelial cells of meningeal blood vessels trigger migraine headache through the formation of nitric oxide.
Origin of Aspartate‐induced Responses in Rat Cerebellar Purkinje Cells
Authors: Renard A. , Crépel F. 
Published: April 2006

AbstractThe effects of glutamate, aspartate and N‐methyl‐d‐aspartate (NMDA) on Purkinje cells and interneurons were investigated in cerebellar slice cultures using the whole‐cell configuration of the patch‐clamp technique. l‐Glutamate and l‐aspartate induced inward currents in Purkinje cells voltage‐clamped at ‐60 mV. In standard external solution, the amplitude of the responses induced by these two amino‐acids was a linear function of the membrane potential. l‐Aspartate‐induced currents were inhibited by 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX), a selective antagonist of non‐NMDA receptors. NMDA, a selective agonist of NMDA receptors, had no effect of its own on the excitability of Purkinje cells, but was effective in blocking the responses induced by aspartate in Purkinje cells in a voltage‐independent manner. In contrast, d‐(–)‐2‐amino‐5‐phosphonovaleric acid (d‐APV), a selective antagonist of NMDA receptors, had no effect on aspartate‐induced responses. d‐Aspartate also induced responses in Purkinje cells, and the amplitude of these responses was a linear function of the membrane potential. Currents induced by l‐ and d‐aspartate were inhibited by dihydrokainate, a glutamate uptake blocker. In sodium‐free external solution, glutamate still induced outward currents in Purkinje cells, whereas l‐ and d‐aspartate no longer evoked any current. When sodium was replaced by lithium in the external medium, no change in the holding current could be detected in Purkinje cells maintained at ‐60 mV; moreover, in this bathing medium l‐aspartate no longer evoked any current whereas glutamate‐induced responses were still present. In contrast, interneurons were sensitive to both NMDA and aspartate applications, and these responses were antagonized by d‐APV. In addition, aspartate still induced an outward current in sodium‐free external solution. This study presents rather direct evidence in favour of l‐aspartate as being a very selective NMDA receptor agonist in the cerebellum. l‐Aspartate‐induced currents in Purkinje cells are not due to activation of mixed NMDA/non‐NMDA receptors, but are probably due to the release of l‐glutamate induced by aspartate through glutamate uptake.