bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential expression of phospholipase D1 in the developing retina
Authors: Lee E.‐J. , Min D. S. , Lee M.‐Y. , Chung J.‐W. , Chun M.‐H. , Oh S.‐J. 
Published: March 2003

AbstractExpression patterns of phospholipase D1 (PLD1) in the developing rat retina were investigated using immunocytochemistry and Western blot analysis and compared with the expression patterns of glutamine synthetase. PLD1 immunoreactivity appeared first in a few neuroblasts in the middle of the mantle zone of the primitive retina by embryonic (E) day 13. PLD1‐immunoreactive primitive ganglion cells were characterized in the ganglion cell layer by E17. Faint immunoreactivity at E17 profiled radially orientated cells and this pattern appeared up to postnatal (P) day 7. In the ganglion cell layer at P3, displaced amacrine cells and ganglion cells were classified. At P5, presumptive horizontal cells and amacrine cells were identified. By P7, a thin outermost layer of newly formed segments of the photoreceptor cells was also PLD1 immunoreactive. PLD1 immunoreactivity at P8 was limited to radial Müller cells and the outer segment layer of the photoreceptor cells, and the expression pattern was conserved to adulthood. Western blot analysis showed relatively high amounts of PLD1 protein at E17 and P3, a decrease at P7, and moderate amounts from P8 onward. Co‐expression of PLD1 with glutamine synthetase in the retina appeared first after birth in differentiating neurons and in Müller cells by P8; thereafter the pattern was maintained. The expression pattern of the PLD1 during development of the retina suggests that PLD1 plays important roles in glutamate‐associated differentiation of both specific neurons and radial glial cells, and in glutamate‐mediated cellular signalling in Müller cells.
Morphological and pharmacological evidence for the role of peripheral prostaglandins in the pathogenesis of neuropathic pain
Authors: Ma Weiya , Eisenach James C. 
Published: March 2003

AbstractInflammatory mediators produced in the injured nerve have been proposed as contributing factors in the development of neuropathic pain. Prostaglandins (PGs) are probably included in these important inflammatory mediators. In the present study, 2 and 4 weeks following partial sciatic nerve ligation (PSNL), we observed a dramatic increase in the prostaglandin synthesizing enzyme cyclooxygenase (COX)2‐immunoreactive (IR) cell profiles in the injury site and adjacent region. Some of these COX2‐IR cells were identified as macrophages because they coexpressed ED1. None of these COX2‐IR cell profiles coexpressed the Schwann cell marker S100. In the contralateral sciatic nerve and sciatic nerve from normal rats, we failed to observe any of these COX‐IR cell profiles. We also observed COX1‐IR cell profiles (presumably Langerhans cells) in the epidermis of the footpad of both normal and PSNL rats. Interestingly, a greater number of COX1‐IR cell profiles were observed in the epidermis of the ipsilateral footpad of PSNL rats. Local injection of ketorolac, a nonselective COX inhibitor, into the ipsilateral plantar side or into the injury site of the sciatic nerve, effectively reversed the tactile allodynia induced by PSNL for > 5 days. Intraperitoneal or intramuscular injection of ketorolac had a similar but shorter antiallodynic effect. Intraplantar or peri‐neural injection of ketorolac dramatically suppressed the PSNL‐induced increase in the phosphorylation of a transcription factor cAMP response element binding protein (CREB) in the ipsilateral dorsal horn of L4 and L5 spinal cord of PSNL rats. Intraplantar or peri‐neural injection of ketorolac at the time of lesion did not prevent mechanical hypersensitivity but reduced it with a slow onset 3 weeks after lesion. Our data suggest that PSNL induces over‐production of PGs in peripheral tissues and that PGs probably sensitize nociceptors and are involved in central plasticity and sensitization at the spinal cord level, thus contributing to the maintenance of tactile allodynia.
Memory traces for inflectional affixes as shown by mismatch negativity
Authors: Shtyrov Yury , Pulvermüller Friedemann 
Published: March 2003

AbstractMismatch negativity (MMN), an index of experience‐dependent memory traces, was used to investigate the processing of grammatical affixes in the human brain. The MMN was elicited by either a verb stem or an inflected verb form, phonetic contrasts being identical in both conditions. The topography of the mismatch responses showed clear left‐hemispheric laterality in both conditions. However, the MMN to the inflected form occurred later than that for the stem. Furthermore, the inflected stimulus produced MMN maximal in centroparietal sites, whereas stem‐elicited MMN was more profound at more frontal sites. We suggest that these features of the MMN to inflected form indicate delayed activation of left‐lateralized perisylvian cell assemblies that function as cortical memory traces of inflectional affixes.
Neuronal activation and corticotropin‐releasing hormone expression in the brain of obese (fa/fa) and lean (fa/?) Zucker rats in response to refeeding
Authors: Timofeeva Elena , Picard Frédéric , Duclos Martine , Deshaies Yves , Richard Denis 
Published: March 2003

AbstractThe present study was conducted to investigate the pattern of neuronal activation and corticotropin‐releasing hormone (CRH) expression in fed, food deprived and refed lean (Fa/?) and obese (fa/fa) Zucker rats. The pattern of neuronal activation was studied by measuring the expression of the immediate‐early gene c‐fos. Expression of c‐fos and CRH mRNA was determined by in situ hybridization histochemistry. In both lean and obese rats, one hour of refeeding led to a transient increase in c‐fos mRNA levels which was detected in the paraventricular hypothalamic nucleus (PVH), the dorsomedial hypothalamic nucleus, the supraoptic nucleus, the paraventricular thalamic nucleus, the central nucleus of amygdala (CeA), the lateral and medial parabrachial nuclei, the nucleus of the solitary tract, and the area postrema. In addition, refeeding led to strong activation of the arginine‐vasopressin neurons located in the magnocellular part of the PVH. Following 24 h of food deprivation, CRH expression in the parvocellular division of the PVH was significantly higher in obese rats compared to lean animals. During refeeding, PVH CRH mRNA levels in obese rats decreased to reach control values. The decrease in CRH expression in obese rats was accompanied by the alleviation of the hypercorticosteronemia that characterized obese Zucker rats. CRH mRNA levels in the central nucleus of the amygdala were significantly higher in lean rats than in obese animals, when the rats were fed ad libitum During food deprivation, CeA CRH mRNA levels decreased in lean rats and gradually returned to predeprivation values during refeeding. In refed obese rats, CeA levels of CRH mRNA were higher than those of ad libitum fed or food‐deprived obese mutants. In the perifornical region of the lateral hypothalamic area (LHA), the expression of CRH mRNA rose significantly in response to refeeding in lean rats, but not in obese animals. Following the first hour of refeeding, the number of neurons expressing CRH mRNA in the LHA in lean rats almost doubled. The present results demonstrate that refeeding has a stimulating effect in obese Zucker rats in a pattern of activation similar to that seen in lean Fa/? rats. They also demonstrate differences in CRH expression between Fa/? and fa/fa rats after refeeding. The most apparent of these differences was seen in the lateral hypothalamus in which refeeding failed to up‐regulate CRH expression in obese rats.
Transistor array with an organotypic brain slice: field potential records and synaptic currents
Authors: Besl Brigitte , Fromherz Peter 
Published: March 2003

AbstractLinear transistor arrays on a silicon chip were used to map evoked extracellular field potentials in organotypic brain slices of rat hippocampus. The shape and amplitude of the transients were similar to those from records with micropipette electrodes. The spatial resolution was 21 and 4.6 µm. The sampled profile of the field potential showed a wide and shallow trough of transients in the stratum radiatum and a narrow but higher ridge in the stratum pyramidale. Due to the high resolution, the profile could be interpreted quantitatively in terms of synaptic currents. Transistor chips may become a novel tool for neurophysiological and pharmacological studies in brain slices.
Sub‐chronic treatment with classical but not atypical antipsychotics produces morphological changes in rat nigro‐striatal dopaminergic neurons directly related to ‘early onset’ vacuous chewing
Authors: Marchese Giorgio , Casu Maria Antonietta , Bartholini Francesco , Ruiu Stefania , Saba Pierluigi , Gessa Gian Luigi , Pani Luca 
Published: March 2003

AbstractIn the present work, we investigated if an impairment of dopaminergic neurons after subchronic haloperidol treatment might be a possible physiopathologic substrate of the ‘early onset’ vacuous chewing movements (VCMs) in rats. For this purpose, different antipsychotics were used to analyse a possible relationship between VCMs development and morphological alterations of tyrosine‐hydroxylase‐immunostained (TH‐IM) neurons.    Rats treated twice a day with haloperidol displayed a significant increase of VCMs that was both time‐ (2–4 weeks) and dose (0.1–1 mg/kg) dependent. Immunocytochemical analysis showed a shrinkage of TH‐IM cell bodies in substantia nigra pars compacta and reticulata and a reduction of TH‐immunostaining in the striatum of haloperidol treated rats with the arising of VCMs. No differences were observed in TH‐IM neurons of ventral tegmental area and nucleus accumbens vs. control rats. The atypical antipsychotics risperidone (2 mg/kg, twice a day), amisulpride (20 mg/kg, twice a day) and clozapine (10 mg/kg, twice a day) did not produce any nigro‐striatal morphological changes or VCMs. TH‐IM nigro‐striatal neuron morphological alterations and VCMs were still present after three days of withdrawal in rats treated for four weeks with haloperidol (1 mg/kg). Both the main morphological changes and the behavioural correlate disappeared after three weeks of withdrawal. These results suggest that haloperidol induces a morphological impairment of the dopaminergic nigro‐striatal neurons which is directly associated with the arising, permanency and disappearance of VCMs in rats.
Contribution of amygdala neurons containing peptides and calcium‐binding proteins to fear‐potentiated startle and exploration‐related anxiety in inbred Roman high‐ and low‐avoidance rats
Authors: Yilmazer‐Hanke Deniz M. , Faber‐Zuschratter Heidi , Linke Rüdiger , Schwegler Herbert 
Published: March 2003

AbstractThe purpose of this study was to investigate amygdala‐related fear and anxiety in two inbred rat lines differing in emotionality (RHA/Verh and RLA/Verh), and to relate the behaviour of the animals to neuronal types in different nuclei of the amygdala. The behavioural tests used were the motility test, elevated plus‐maze and fear‐potentiated startle response. The neurons investigated were immunoreactive for the anxiogenic peptide corticotropin‐releasing factor (CRF‐ir), the anxiolytic peptide neuropeptide Y (NPY‐ir), and the calcium‐binding proteins parvalbumin (PARV‐ir) and calbindin (CALB‐ir). The NPY‐ir, PARV‐ir and CALB‐ir neurons studied were subpopulations of GABAergic neurons. RLA/Verh rats, which showed a significant fear‐potentiation of the acoustic startle response, had more CRF‐ir projection neurons in the central nucleus of the amygdala. The same RLA/Verh rats were either less or equally anxious in the motility test (similar to open field) and elevated plus‐maze as compared with RHA/Verh rats. In accordance with this behaviour, the RLA/Verh rats had more NPY‐ir neurons in the lateral, and more PARV‐ir neurons in basal nuclei of the amygdala than RHA/Verh rats, but no differences were detected in the number of CRF‐ir and CALB‐ir neurons of the basolateral complex. In conclusion, the RLA/Verh rats displayed an opposite behaviour in the fear‐potentiated startle model and the exploratory tests measuring anxiety based on choice behaviour. Thus, the anxiogenic systems in the central nucleus and anxiolytic systems in the basolateral complex of the amygdala might be differentially involved in the fear‐potentiated startle paradigm and exploratory tests in the Roman rat lines.
Glycinergic and GABAergic calcium responses in the developing lateral superior olive
Authors: Kullmann Paul H. M. , Ene F. Aura , Kandler Karl 
Published: March 2003

AbstractThe lateral superior olive (LSO), a binaural nucleus involved in sound localization, receives tonotopically organized inhibitory inputs from the medial nucleus of the trapezoid body (MNTB). During development, the tonotopic organization of this glycinergic/GABAergic MNTB–LSO pathway is established by activity‐dependent axonal reorganization. However, the underlying mechanisms by which this reorganization takes place have remained largely unknown. As cytosolic calcium is one of the most important second messengers responsible for inducing synaptic plasticity and reorganization, we examined whether and how activity in the MNTB–LSO pathway changes the intracellular calcium concentration ([Ca2+]i) in developing LSO neurons. By applying calcium imaging techniques to Fura‐2‐labelled slices from neonatal rats and mice, we found that glycine and GABA (γ‐aminobutyric acid) affect [Ca2+]i in LSO neurons in an age‐dependent manner; during the first postnatal week, the period at which glycine and GABA are depolarizing in the LSO, glycine and GABA always increased [Ca2+]i. However, in 2‐week‐old animals, the time around hearing onset when glycine and GABA are hyperpolarizing, glycine and GABA slightly decreased [Ca2+]i. Calcium responses could also be elicited by stimulation of afferent fibres from the MNTB, and these synaptic responses were mediated by glycine and GABAA receptors. Furthermore, GABA, which is a neurotransmitter only in the immature MNTB–LSO pathway, played a major role in generating MNTB‐elicited Ca2+ responses. The direct link of glycinergic/GABAergic synaptic activity to intracellular calcium signalling during the period of inhibitory synaptic plasticity could be one of the mechanisms by which tonotopic MNTB–LSO connections become established.
Seizure‐dependent modulation of mitochondrial oxidative phosphorylation in rat hippocampus
Authors: Kudin Alexei P. , Kudina Tatiana A. , Seyfried Jan , Vielhaber Stefan , Beck Heinz , Elger Christian E. , Kunz Wolfram S. 
Published: March 2003

AbstractMitochondrial function is a key determinant of both excitability and viability of neurons. Here, we demonstrate seizure‐dependent changes in mitochondrial oxidative phosphorylation in the epileptic rat hippocampus. The intense pathological neuronal activity in pilocarpine‐treated rats exhibiting spontaneous seizures resulted in a selective decline of the activities of NADH–CoQ oxidoreductase (complex I of the respiratory chain) and cytochrome c oxidase (complex IV of respiratory chain) in the CA3 and CA1 hippocampal pyramidal subfields. In line with these findings, high‐resolution respirometry revealed an increased flux control of complex I on respiration in the CA1 and CA3 subfields and decreased maximal respiration rates in the more severely affected CA3 subfield. Imaging of mitochondrial membrane potential using rhodamine 123 showed a lowered mitochondrial membrane potential in both pyramidal subfields. In contrast to the CA1 and CA3 subfields, mitochondrial oxidative phosphorylation was unaltered in the dentate gyrus and the parahippocampal gyrus. The changes of oxidative phosphorylation in the epileptic rat hippocampus cannot be attributed to oxidative enzyme modifications but are very likely related to a decrease in mitochondrial DNA copy number as shown in the more severely affected CA3 subfield and in cultured PC12 cells partially depleted of mitochondrial DNA. Thus, our results demonstrate that seizure activity downregulates the expression of mitochondrial‐encoded enzymes of oxidative phosphorylation. This mechanism could be invoked during diverse forms of pathological neuronal activity and could severely affect both excitability and viability of hippocampal pyramidal neurons.
The role of hippocampal dopamine receptors in prepulse inhibition
Authors: Ellenbroek Bart A. , Lubbers Luuk J. , Cools Alexander R. 
Published: March 2003

AbstractAlthough it has long been realized that the hippocampal formation receives a projection from the midbrain dopaminergic cell groups and contains mRNA for all five dopamine receptors, the functional role of this dopaminergic projection has not been studied so far. The present study aimed to investigate the role of dopamine receptors in the dorsal CA1 area of the hippocampus in prepulse inhibition. The results show that local application of amphetamine reduced prepulse inhibition without affecting the baseline startle amplitude. This effect of amphetamine could be reversed by coadministration of the D1 antagonist SCH23390. Moreover, local application of the D1 agonist SKF81297 also disrupted prepulse inhibition without altering basal startle amplitude. These data clearly suggest that the hippocampal D1 receptor plays an important role in prepulse inhibition. The effects of amphetamine could not be reversed by coadministration of the D2 antagonist sulpiride. Interestingly, the D2/3 agonist quinpirole did reduce prepulse inhibition, again without affecting basal startle amplitude. Because quinpirole has a much higher affinity for the D3 receptor than does sulpiride, it is suggested that the D3 receptor might be involved in this effect.
Opposing effects of head position on sound localization in blind and sighted human subjects
Authors: Lewald Jörg 
Published: March 2003

AbstractUp to now, there is an unsolved contradiction between the view that the development of an auditory spatial representation needs calibration by vision and the psychophysical demonstration of quite precise sound localization in early blind humans. The present study provides a link between these two competing conceptions. Two experiments were conducted with congenitally or early blind subjects and sighted controls. In the first experiment, subjects pointed with their head to actual sound sources located in the azimuthal plane. In the second experiment, lateralization of dichotic sound stimuli, presented via headphones, was investigated with variation of head‐to‐trunk position. The results showed opposing systematic errors of sound localization or lateralization, depending on head position, made by blind and sighted subjects. These differences suggest that audiomotor feedback replaces vision so as to calibrate auditory space in blind individuals. That is, in contrast to the widespread opinion of compensation of visual loss by a general sharpening of audition, compensatory plasticity in the blind may specifically be related to enhanced processing of proprioceptive and vestibular information with the auditory spatial input.
Intrinsic GABA neurons inhibit proenkephalin gene expression in slice cultures of rat neostriatum
Authors: Mörl Franz , Gröschel Michael , Leemhuis Jost , Meyer Dieter K. 
Published: March 2003

AbstractIn the neostriatum, the proenkephalin gene is expressed in medium spiny GABA neurons, which project to the globus pallidus. The expression is activated by glutamatergic projections from the neocortex via NMDA receptors. In these experiments we have used slice cultures of rat neostriatum to study the role of GABA in proenkephalin gene expression. Our results show that GABA is released from neostriatal neurons and negatively regulates the proenkephalin gene expression induced by NMDA receptor stimulation. The GABAA receptors involved seem to be colocalized with NMDA receptors on the projection neurons, which express the proenkephalin gene. In further experiments, we have found that the proenkephalin gene expression is not only activated by neocortical projection neurons but also by intrinsic striatal neurons as well as by projections from the thalamus. All these glutamatergic afferents enhance the proenkephalin gene expression via NMDA receptors. Their efficacy is regulated by endogenous GABA.
The histaminergic system in human thalamus: correlation of innervation to receptor expression
Authors: Jin C. Y. , Kalimo H. , Panula P. 
Published: March 2003

AbstractThe mRNA expression of three histamine receptors (H1, H2 and H3) and H1 and H3 receptor binding were mapped and quantified in normal human thalamus by in situ hybridization and receptor binding autoradiography, respectively. Immunohistochemistry was applied to study the distribution of histaminergic fibres and terminals in the normal human thalamus. mRNAs for all three histamine receptors were detected mainly in the dorsal thalamus, but the expression intensities were different. Briefly, H1 and H3 receptor mRNAs were relatively enriched in the anterior, medial, and part of the lateral nuclei regions; whereas the expression level was much lower in the ventral and posterior parts of the thalamus, and the reticular nucleus. H2 receptor mRNA displayed in general very low expression intensity with slightly higher expression level in the anterior and lateropolar regions. H1 receptor binding was mainly detected in the mediodorsal, ventroposterolateral nuclei, and the pulvinar. H3 receptor binding was detected mainly in the dorsal thalamus, predominantly the periventricular, mediodorsal, and posterior regions. Very high or high histaminergic fibre densities were observed in the midline nuclear region and other nuclei next to the third ventricle, ventroposterior lateral nucleus and medial geniculate nucleus. In most of the core structures of the thalamus, the fibre density was very low or absent. The results suggest that histamine in human brain regulates tactile and proprioceptory thalamocortical functions through multiple receptors. Also, other, e.g. visual areas and those not making cortical connections expressed histamine receptors and contained histaminergic nerve fibres.
Preferential alterations in the mesolimbic dopamine pathway of heterozygous reeler mice: an emerging animal‐based model of schizophrenia
Authors: Ballmaier Martina , Zoli Michele , Leo Giuseppina , Agnati Luigi Francesco , Spano PierFranco 
Published: March 2003

AbstractBased on a number of neuroanatomical and behavioural similarities, recent evidence suggests that heterozygous reeler mice, haploinsufficient for reelin expression, represent a useful model of psychosis vulnerability. As brain mesolimbic dopamine pathways have been proposed to be associated with the pathophysiology of psychotic disorders, we thought it would be of interest to examine whether these animals present disturbances in the mesolimbic dopamine system. To this end we studied by immunocytochemical, in situ hybridization procedures and receptor autoradiography, several markers of the mesotelencephalic dopamine pathway in heterozygous reeler mice and controls. We report that heterozygous reeler mice exhibit a reduction in the number of tyrosine hydroxylase‐immunoreactive cell bodies and tyrosine hydroxylase mRNA levels in the ventral tegmental area, as well as a reduction of tyrosine hydroxylase and dopamine transporter immunoreactivity in the dopamine terminal fields of the limbic striatum. In these areas we also observed a reduction of dopamine D2 receptor mRNA. Finally, a marked increase in D3 receptor mRNA levels was observed concomitant with a significant increase in D3 binding sites. On the contrary, the nigrostriatal pathway did not show any significant alteration in heterozygous reeler mice with regards to the dopaminergic markers examined in substantia nigra cell bodies and dorsal striatum dopamine terminal fields. These results suggest a specific link between reelin‐related neuronal pathology and dopamine involvement in the pathophysiology of psychotic disorders.