bluuebunny/crossref_metadata_2025_split huggingface dataset:
NMDA Receptor‐dependent Transient Homo‐ and Heterosynaptic Depression in Picrotoxin‐treated Hippocampal Slices
Authors: Bashir Zafar I. , Collingridge Graham L. 
Published: April 2006

AbstractExtracellular recording was used to study the effects of high‐frequency (tetanic) stimulation on excitatory synaptic transmission in the CA1 region of rat hippocampal slices in the presence of the γ‐aminobutyric acid (GABA) type A antagonist, picrotoxin (50 γM). Under these conditions tetanic stimulation (100 Hz, 1 s) at the test intensity resulted in homosynaptic long‐term potentiation (LTP). In contrast, tetanic stimulation of higher intensity (100 Hz, 1 s, double test intensity) resulted in homo‐ and heterosynaptic depression which recovered within 45 min. A transient (1–3 min) negative shift in DC potential and a transient (5–10 min) depression of the homosynaptic fibre volley occurred immediately following the higher intensity tetanus. The DC shift, induction of homo‐ and heterosynaptic depression and depression of the fibre volley were reversibly prevented by the N‐methyl‐d‐aspartate (NMDA) receptor antagonist, d‐2‐amino‐5‐phosphonopentanoate (AP5; 20 γM) but were not prevented by a variety of L‐type calcium channel antagonists. Transient (30 ‐ 45 min) synaptic depression of pharmacologically isolated NMDA receptor‐mediated field excitatory postsynaptic potentials also occurred following tetanic stimulation (100 Hz, 1 s) at double test intensity. These results demonstrate an NMDA receptor‐dependent form of reversible synaptic depression in the CA1 region of the hippocampus.
Memory Formation in Day‐old Chicks Requires NMDA but not Non‐NMDA Glutamate Receptors
Authors: Burchuladze Rusudan , Rose Steven P. R. 
Published: April 2006

AbstractThe non‐competitive N‐methyl‐D‐aspartate (NMDA) antagonist MK‐801, injected intraperitonealy at 0.1 mg/kg, at times between 1 h before and 5 min after training chicks on a one‐trial passive avoidance task, resulted in amnesia for the task on test 3 or 24 h subsequently. No amnesia was apparent at 24 h if chicks were injected between 1 and 6 h after training. Amnesia did not develop immediately; it was not apparent 30 min after training in chicks injected 5 min after training. At this dose of MK‐801 no other effects on motor or pecking behaviour of the birds were observed. Bilateral or unilateral intracerebral injections of 1.5 nM MK‐801 5 min after training produced a similar amnesia at 3 h to that of intraperitonealy injected MK‐801; no hemispheric differences were observed, presumably because of the ready diffusion of the MK‐801. By contrast, intracerebral injections of the non‐NMDA glutamate antagonists 6‐cyano‐7‐nitroquinoxaline‐2, 3‐dione (CNQX), 6,7‐dinitroquinoxaline‐2,3‐dione (DNQX) and 6,7‐nitro‐7‐sulphamoyl‐benzoquinoxaline‐2,3‐dione (NBQX) (0.066 μM) 5 min after training, despite producing severe if transient behavioural disturbances, were without effect on retention for the avoidance response in chicks tested 3 h subsequently. We interpret these results as pointing to a requirement for NMDA, but not kainate or quisqualate, receptor activation as an early enabling event in the biochemical cascade required for long‐term memory formation for passive avoidance in the chick.
Cellular Localization of Brain‐derived Neurotrophic Factor and Neurotrophin‐3 mRNA Expression in the Early Chicken Embryo
Authors: Hallböök Finn , Ibáñez Carlos F. , Ebendal Ted , Persson Håkan 
Published: April 2006

AbstractDegenerate primers from conserved regions in nerve growth factor, brain‐derived neurotrophic factor (BDNF) and neurotrophin‐3 (NT‐3) were used in the polymerase chain reaction to isolate DNA fragments from the chicken BDNF and NT‐3 genes. A genomic clone coding for chicken NT‐3 was isolated and the structure of the chicken NT‐3 mature protein was subsequently deduced from nucleotide sequence analysis of the isolated chicken NT‐3 gene. Comparison of the chicken BDNF and NT‐3 with the corresponding rat molecules showed that the avian molecules are very similar to their mammalian homologues. Northern blot analyses of messenger RNA (mRNA) from chicken embryos from embryonic day 3.5 (E3.5), E4.5, E8, E12 and E18 showed that expression of both BDNF and NT‐3 mRNA peaked at E4.5 and decreased at later stages of development. Both probes revealed two transcripts; larger mRNAs of 4.5 kilobases (kb) for BDNF and 4.0 kb for NT‐3 predominated over the smaller transcripts of 1.4 and 1.3 kb, respectively. The cellular localization of BDNF and NT‐3 mRNA in the E4 and E6 embryos was studied by in situ hybridization. In the E4 embryo, labelling for BDNF was seen over cells in restricted parts of the epithelium of the otic vesicle. Analysis of adjacent sections for the low‐affinity nerve growth factor receptor mRNA showed that regions in the otic vesicle epithelium which labelled for BDNF mRNA also labelled for low‐affinity nerve growth factor receptor mRNA. No labelling for NT‐3 was detected in the otic vesicle. Labelling for BDNF mRNA was also found over mesenchyme dorsal to the wing bud, in the wing bud and in the splanchnopleural lining of the stomach. Labelling for NT‐3 mRNA was found at E4 over the epidermis on the ventral side in the region of the branchial arches. The labelling extended up the maxillary processes to Rathke's pouch. The closely located infundibulum was weakly labelled for NT‐3 mRNA. NT‐3 mRNA was also detected in the mesenchyme surrounding the oesophagus and lung buds. The regional expression pattern is in agreement with the established role for BDNF and NT‐3 as target‐derived neurotrophic factors, but the results also suggest that BDNF may be an intrinsic factor important for the development of the inner ear. The results support the emerging view that neurotrophic factors can play a role in early differentiation of both neuronal and non‐neuronal tissues.
Formation of Specific Efferent Connections in Organotypic Slice Cultures from Rat Visual Cortex Cocultured with Lateral Geniculate Nucleus and Superior Colliculus
Authors: Novak Nino , Bolz Jürgen 
Published: April 2006

AbstractCells in the cerebral cortex project to many distant regions in the brain. Each cortical target receives input from a specific population of cells which have a characteristic morphology and which are located in a distinct cortical layer. In an attempt to learn about the mechanisms by which this stereotypic output pattern is generated during development, we have studied the formation of cortical projections in an in vitro system. Slices from developing rat visual cortex were cocultured with slices from the superior colliculus, the major target of cells in layer 5, and the lateral geniculate nucleus, the major target of cells in layer 6. Cortical neurons which established connections with tectal and thalamic explants were retrogradely labelled with fluorescent dyes. It was found that, in vitro, different populations of neurons project to these two targets, and that the laminar position and cellular morphology of the projecting cells were similar to their in vivo counterparts. These specific connections were established when the target explants were placed either next to the white matter or next to the pial side of cortical slice cultures. The axons of cells projecting to ectopic positioned explants reoriented their trajectories and grew through the cortical grey matter directly towards their targets. Thus subcortical targets exert an orienting effect specifically on their innervating cells and attract growing axons of the appropriate cells at a distance. These results suggest that different targets release different molecules that act selectively on specific populations of neurons. Therefore, chemotropic guidance is likely to play a significant role in the development of specific connections between cortical neurons and their target areas.
Injury‐induced Regulation of Ciliary Neurotrophic Factor mRNA in the Adult Rat Brain
Authors: Ip Nancy Y. , Wiegand Stanley J. , Morse Joanne , Rudge John S. 
Published: April 2006

AbstractCiliary neurotrophic factor (CNTF) is a pleiotropic molecule that acts as a neurotrophic factor for a wide range of embryonic neurons as well as a differentiation factor for sympathetic neuroblasts and O2A progenitor cells in culture. CNTF messenger RNA (mRNA) is present at very low levels in the normal adult rat central nervous system (CNS), but is dramatically up‐regulated after an aspiration lesion of dorsal hippocampus and overlying cortex, in the area coincident with glial scar. The increased level of CNTF mRNA in lesioned hippocampus is maximal by 3 days and is sustained for up to 20 days, the longest time point examined. In contrast, mRNA levels for brain‐derived neurotrophic factor (BDNF) and neurotrophin‐3 (NT‐3) were slightly decreased during the same period. In situ hybridization experiments revealed that cells expressing CNTF mRNA were concentrated at the margin of the wound, and also present within the gelfoam which filled the lesion cavity. This distribution of CNTF‐expressing cells corresponded very closely to that of cells expressing high levels of glial fibrillary acidic protein mRNA at the wound site. Paralleling the observed increase in CNTF mRNA, increased levels of CNTF‐like neurotrophic activity were apparent in soluble extracts of the lesioned tissues. This neurotrophic activity for ciliary ganglion neurons was completely blocked by the addition of neutralizing antiserum against CNTF. Basic fibroblast growth factor, which has been shown by others to increase after a similar lesion paradigm (Frautschy et al., Brain Res., 553, 291–299, 1991), does not contribute appreciably to this trophic activity. We conclude that CNTF is markedly increased as a function of injury to the CNS and that its expression is most likely restricted to reactive astrocytes in the glial scar.
The L2/HNK‐1 Carbohydrate Mediates Adhesion of Neural Cells to Laminin
Authors: Hall Heike , Liu Li , Schachner Melitta , Schmitz Brigitte 
Published: April 2006

AbstractThe L2/HNK‐1 carbohydrate epitope shared by several neural adhesion molecules has been implicated in cell‐to‐cell and cell‐to‐laminin adhesion (Keilhauer et al., Nature, 316, 728–730, 1985; Künemund et al., J. Cell Biol., 106, 213–223, 1988). As demonstrated previously for chicken retinal ganglion cells (Cole et al., Neurosci. Lett., 93, 170–175, 1988), cerebral cortex astrocytes or cerebellar neurons could not be shown to adhere to the substrate‐bound L2/HNK‐1 carbohydrate. The cell‐bound L2/HNK‐1 carbohydrate, however, was a potent mediator of astrocytic and neuronal cell adhesion to laminin, which was strongly reduced in the presence of the L2/HNK‐1 carbohydrate‐carrying glycolipids or Fab fragments of a monoclonal antibody against it. Inhibition of adhesion could not be observed in the presence of the negatively charged gangliosides or sulphatide, but in the presence of heparin. To investigate whether the L2/HNK‐1 carbohydrate and heparin use the same or different binding sites on laminin, adhesion of cells to laminin was determined in the presence of heparin and Fab fragments of a monoclonal L2 antibody, which gave an additive value of inhibition as compared to the inhibition caused by the single compounds. This result, as well as studies of the binding of the L2/HNK‐1 glycolipids to laminin in the presence of heparin, indicates that the L2/HNK‐1 carbohydrate and heparin are implicated in different aspects of neural cell adhesion to laminin.
Optical Recording of Neuronal Activity in the Insect Central Nervous System: Odorant Coding by the Antennal Lobes of Honeybees
Authors: Lieke Edmund E. 
Published: April 2006

AbstractVoltage‐sensitive dyes and activity‐dependent intrinsic optical signals were used to study the spatio‐temporal activity in the antennal lobes of honeybees. The intrinsic signals are somewhat slower than the dye signals but show a 10‐fold larger intensity change. These intrinsic signals consist of at least two components—one is wavelength‐independent and the other strongly wavelength‐dependent, with a maximum at ∼500 nm. Local inhibitory connections within the antennal lobes were examined by recording the activity elicited by an electrical stimulus to the antennal nerve of a slice preparation before and after applying picrotoxin to manipulate GABAergic inhibitory synapses. The inhibition starts with a delay of ∼10 ms after onset of the response and has at least two components. The spatial distribution of the inhibition is extremely inhomogeneous, with areas of small inhibition adjacent to areas of large inhibition. Thus inhibitory interactions in the antennal lobes are not evenly distributed among the glomerular organization. Stimulation of an in vivo preparation with an odour yields a spatially restricted activity. However, the spatial map appears highly dynamic in time because the size of the activated area is a function of the time during and after the stimulus.
Currents Activated by GABA and their Modulation by Zn2+ in Cerebellar Granule Cells in Culture
Authors: Kilic Gordan , Moran Oscar , Cherubini Enrico 
Published: April 2006

AbstractWhole‐cell and single‐channel currents evoked by γ‐aminobutyric acid (GABA) were recorded from rat cerebellar granule cells in culture. The electro‐physiological properties of these currents were studied in control condition and in the presence of external Zn2+ (10 – 30μM). GABA (10 μM) induced bicuculline‐sensitive whole‐cell currents which desensitized. The desensitization was more rapid for higher concentrations of GABA (30 – 300 μM). The current – voltage relation of GABA currents was linear from – 70 to +50 mV. Two different types of cells were found with respect to the stoichiometry for agonist binding, one with Hill coefficient 1.5 and another one with coefficient 1. The half‐maximum concentration displayed more variability, with values varying from 10 to 50 μM. The time constant of recovery from desensitization (Tr) was estimated to be 36 s. Zn2+ (30 μM) blocked GABA‐activated whole‐cell currents in a non‐competitive and voltage‐independent way without a significant change in the current kinetics. In excised outside‐out patches, GABA (0.5 μM) activated single‐channel events of 19 and 31 pS. Kinetic analysis yielded two mean shut times (Tc1= 2.70 ms, Tc2= 205 ms) and one mean open time (To= 3.64 ms). Zn2+ (10 μM) did not affect single‐channel conductances and mean open and shut times, but significantly reduced the probability of opening from 0.17 to 0.06. It is probable that Zn2+ binds to a site located on the extracellular part of the GABAA receptor channel complex.
Regeneration of Hypoglossal Nerve Axons Following Blockade of the Axotomy‐induced Microglial Cell Reaction in the Rat
Authors: Svensson M. , Aldskogius H. 
Published: April 2006

AbstractThe aim of the present study was to examine whether inhibition of the microglial cell reaction around axotomized motoneurons affects the subsequent regeneration process of the injured axons. The microglial cell reaction in the hypoglossal nucleus of the rat was blocked by infusion of cytosine‐arabinoside (ARA‐C) into the ventricular system. Axon regeneration was evaluated by determining the number and size distribution of myelinated axons at a defined level distal to the crush site, the number of neurons which could be retrogradely labelled from the distal stump as well as the number of motor endplates in the tongue at various times following injury. No significant difference was observed for any of these parameters between ARA‐C‐treated and untreated animals. Therefore, it is concluded that the microglial cell reaction is not necessary for peripheral nerves to regenerate and restore target contact at a normal rate and to a normal extent.
Cellular Localization of Interleukin 6 mRNA and Interleukin 6 Receptor mRNA in Rat Brain
Authors: Schöbitz Bernd , de Kloet E. Ronald , Sutanto Win , Holsboer Florian 
Published: April 2006

AbstractThe distribution of interleukin 6 (IL‐6) mRNA and IL‐6 receptor (IL‐6R) mRNA in the brain of adult male rats was studied at the light microscope level by in situ hybridization histochemistry using 35S‐labelled oligonucleotides. The transcripts of both genes were localized in the pyramidal neurons and in the granular neurons of the hippocampus, in neurons of the habenular nucleus as well as in the dorsomedial and ventromedial hypothalamus, in the piriform cortex, in scattered neurons of the cortex and in granular cells of the cerebellum. The medial preoptic nucleus and the anterior tip of the lateral ventricle contained mRNA encoding IL‐6 and its receptor. Moreover, white matter areas, such as the internal capsule, which consist of only fibres and glial cells, were found to have autoradiographic signals above background. The mRNAs for IL‐6 and IL‐6R in hippocampus and cerebellum are not different, as shown by Northern blot analyses of RNA isolated from these tissues. We postulate that the cytokine IL‐6 is expressed constitutively in discrete regions of the CNS and that it is involved in the mechanisms coordinating metabolic, behavioural and neuroendocrine changes not only during illness but also under normal physiological conditions. Our results suggest that IL‐6 mRNA and IL‐6R mRNA are colocalized, thus supporting a role of the cytokine in autocrine and paracrine communication.
Endogenous Histamine in Cultured Bovine Adrenal Chromaffin Cells
Authors: Tuominen Raimo K. , Karhunen Tuula , Panula Pertti , Yamatodani Atsushi 
Published: April 2006

AbstractHistamine releases catecholamines and opioids in primary cultured bovine adrenal medullary (BAM) chromaffin cells. We have studied whether histamine is synthesized and localized in BAM cells, and whether it can be released upon activation with secretagogues. In BAM cells histamine is immunohistochemically co‐localized with tyrosine hydroxylase in 45 ± 8% of all cells. Only histamine immunoreactivity was observed in 8 ± 2% of all BAM cells. No mast‐cell‐like cells were observed in our system. Histamine can be released from BAM cells by high potassium (56 mM K+) in a calcium‐dependent manner. Compound 48/80 did not release histamine from BAM cells but nicotine caused a dose‐dependent liberation of the amine. Cultured BAM cells have histidine decarboxylase activity which is inhibited by α‐fluoromethylhistidine. These results indicate that endogenous histamine is synthesized, stored and released in BAM chromaffin cells in vitro.
Regional Distribution of Amyloid β‐Protein Precursor, Growth‐associated Phosphoprotein‐43 and Microtubule‐associated Protein 2 Messenger RNAs in the Nigrostriatal System of Normal and Weaver Mutant Mice and Effects of Ventral Mesencephalic Grafts
Authors: Solà C. , Mengod G. , Low W. C. , Norton J. , Ghetti B. , Palacios J. M. , Triarhou L. C. 
Published: April 2006

AbstractUsing in situ hybridization histochemistry with [32P]oligonucleotide probes, we studied the cellular localization of RNA transcripts for amyloid β‐protein precursor (βAPP), growth‐associated phosphoprotein‐43 (GAP‐43) and microtubule‐associated protein 2 (MAP2) in the mesostriatal system of normal (+/+) and weaver (wv/wv) mutant mice, which lose mesencephalic dopamine neurons. In addition, expression of the same messages was studied in ventral mesencephalic cell suspensions transplanted to the weaver striatum. Transcripts encoding GAP‐43, MAP2 and isoforms βAPP695, βAPP714 and βAPP751 were present in normal substantia nigra and progressively reduced in weaver substantia nigra; such a reduction was correlated with dopamine neuron loss. The survival of dopamine neurons in unilateral intrastriatal grafts was documented by methamphetamine‐induced rotational asymmetry tests and by tyrosine hydroxylase immunocytochemistry. High hybridization signals were obtained for GAP‐43, MAP2, βAPP695, βAPP714 and βAPP751 RNA transcripts in the grafted tissue; the βAPP770 species‐normally seen in striatum and not substantia nigra‐was not expressed in the grafts, but it was present in the recipient striatum. Following immunocytochemical labelling with antibodies, GAP‐43 and MAP2 immunoreactivities were seen in cell processes in the grafts and surrounding tissue, whereas βAPP immunoreactivity was mainly found in grafted cell bodies. These results suggest that the transplanted mesencephalic cells mature very similarly to those in the normal substantia nigra, expressing different mRNAs that are normally present in the ventral midbrain and which are reduced in the weaver mutant as a consequence of dopamine neuron loss.
Temporal Integration in Visual Cortex of Cats with Surgically Induced Strabismus
Authors: Eschweiler G. W. , Rauschecker J. P. 
Published: April 2006

AbstractSingle unit response latencies in striate cortex after visual stimulation with stationary flashed bars were measured and interocularly compared in anaesthetized cats with surgically induced strabismus, in order to elucidate the neural basis of strabismic amblyopia. Four unilateral esotropic and two exotropic cats were studied. The visual onset latencies of cortical neurons ranged from 30 to 170 ms after stimulation of the non‐deviating eye at a contrast of 82%. Responses after visual stimulation of the deviating eye were consistently delayed by ∼10 ms. The latency increase was independent of the direction and absolute angle of squint in the different animals. Peak latencies of cortical neurons ranged from 43 to 245 ms. Median peak latency was 85 ms for the non‐deviating and 95 ms for the deviating eye. The rise time of cortical flash responses, as determined from onset ‐ peak differences, ranged between 2 and 170 ms. Direct interocular comparison of response latencies in the remaining binocular neurons revealed an invariable advantage for the non‐deviating eye. Supragranular neurons showed a greater interocular latency difference than neurons in layer IV. Visual latencies were contrast‐dependent. However, the latency reduction with increasing contrast was less pronounced for the deviating eye. We discuss the possibility that central integration times, especially within cortex, are prolonged in strabismic cats, affecting temporal coincidence of signal processing in the visual cortex. The resulting disturbance of spatio‐temporal integration, as caused by a scrambling of geniculo‐striate and intracortical connections, may be the substrate of binocular suppression and strabismic amblyopia.