bluuebunny/crossref_metadata_2025_split huggingface dataset:
Scorpion α‐like toxins, toxic to both mammals and insects, differentially interact with receptor site 3 on voltage‐gated sodium channels in mammals and insects
Authors: Cestèle Sandrine , Stankiewicz Maria , Mansuelle Pascal , De Waard Michel , Dargent Bénédicte , Gilles Nicolas , Pelhate Marcel , Rochat Hervé , Martin‐Eauclaire Marie‐France , Gordon Dalia 
Published: March 2003

Abstractα‐Like toxins, a unique group designated among the scorpion α‐toxin class that inhibit sodium channel inactivation, are highly toxic to mice but do not compete for α‐toxin binding to receptor site 3 on rat brain sodium channels. We analysed the sequence of a new α‐like toxin, which was also highly active on insects, and studied its action and binding on both mammalian and insect sodium channels. Action of the α‐like toxin on isolated cockroach axon is similar to that of an α‐toxin, and the radioactive toxin binds with a high affinity to insect sodium channels. Other sodium channel neurotoxins interact competitively or allosterically with the insect α‐like toxin receptor site, similarly to α‐toxins, suggesting that the α‐like toxin receptor site is closely related to receptor site 3. Conversely, on rat brain sodium channels, specific binding of 125I‐α‐like toxin could not be detected, although at high concentration it inhibits sodium current inactivation on rat brain sodium channels. The difficulty in measuring binding to rat brain channels may be attributed to low‐affinity binding due to the acidic properties of the α‐like toxins that also impair the interaction with receptor site 3. The results suggest that α‐like toxins bind to a distinct receptor site on sodium channels that is differentially related to receptor site 3 on mammalian and insect sodium channels.
Blockade of neurotensin receptors suppresses the dopamine D1/D2 synergism on immediate early gene expression in the rat brain
Authors: Alonso R. , Gnanadicom H. , Fréchin N. , Fournier M. , Fur G. Le , Soubrié P. 
Published: March 2003

AbstractA remarkable feature of dopamine functioning is that the concomitant activation of D1‐like and D2‐like receptors acts to intensify the expression of various dopamine‐dependent effects, in particular the expression of the immediate‐early genes, c‐fos and zif268. Using non‐peptide neurotensin receptor antagonists, including SR48692, we have determined that blockade of neurotensin receptors reduced the cooperative responses of direct acting D2‐like (quinpirole) and partial D1‐like (SKF38393) dopamine agonists on the expression of Fos‐like antigens and zif268 mRNA. Pretreatment with SR48692 (3 and 10 mg/kg) reduced the number of Fos‐like immunoreactive cells produced by the combined administration of SKF38393 (20 mg/kg) and quinpirole (1 mg/kg) in the caudate‐putamen, nucleus accumbens, globus pallidus and ventral pallidum. High‐affinity neurotensin receptors are likely to be involved in these D1‐like/D2‐like cooperative responses, as compounds structurally related to SR48692, SR48527 (3 mg/kg) and its (–)antipode, SR49711 (3 mg/kg), exerted a stereospecific antagonism in all selected brain regions. Pretreatment with SR48692 (10 mg/kg) also diminished Fos induction by the indirect dopamine agonist, cocaine (25 mg/kg), particularly at the rostral level of the caudate‐putamen. In situ hybridization experiments in the caudate‐putamen indicated that SR48692 (10 mg/kg) markedly reduced zif268 mRNA labelling produced by SKF38393 plus quinpirole in cells not expressing enkephalin mRNA, but was unable to affect the concomitant decrease of zif268 mRNA labelling in enkephalin‐positive cells. Taken together, the results of the present study indicate that neurotensin is a key element for the occurrence of cooperative responses of D2‐like and partial D1‐like agonists on immediate‐early gene expression.
X‐ray kinematic analysis of shoulder movements during target reaching and food taking in the cat
Authors: Boczek‐Funcke A. , Kuhtz‐Buschbeck J. P. , Illert M. 
Published: March 2003

AbstractCo‐ordinate movements around the shoulder are essential during reaching movements. We performed a quantitative kinematic analysis of movements of the shoulder girdle: three‐dimensional X‐ray frames (time resolution 20 ms) were recorded during the target‐reaching and food‐taking paradigm in five cats either sitting (n = 4) or standing (n = 1) in front of a food well. Movements of the scapula consisted of a flexion of the scapula (anteversion of the glenoid) followed by flexion of the gleno‐humeral joint (decrease in the angle between the scapular spine and humerus). In the sitting animals, the gleno‐humeral flexion reversed to extension some 120 ms before object contact, while in the standing animal flexion continued during the ongoing scapular flexion. In both cases, the scapula was nearly horizontal at the end of target reaching. The fulcrum for scapular movements was located near the vertebral border of the scapula at the medial elongation of the scapular spine. No major translational components of the fulcrum with respect to the trunk were found during reaching. Together with full flexion of the scapula, this reduces the number of degrees of freedom considerably and thereby probably simplifying the specification of the end‐point of the limb chain. End‐point specification is further supported by rotational movements of the scapula. In the sitting animal, the amplitude of inward rotation along the long axis of the scapula was around 20 °, while it was much more variable in the standing animal, reflecting more variable starting positions. We hypothesize that the glenoid is used to ‘foveate’ the target object.
Vasopressin released within the septal brain area during swim stress modulates the behavioural stress response in rats
Authors: Ebner Karl , Wotjak Carsten T. , Holsboer Florian , Landgraf Rainer , Engelmann Mario 
Published: March 2003

AbstractThe aim of the present study was to investigate the physiological significance of the neuropeptide arginine vasopressin (AVP) released within the septum, in the behavioural response of rats to stress. In the first experiment, rats were chronically implanted with a microdialysis probe aimed at the mediolateral or ventral septum to monitor the local release of AVP in response to 10 min of forced swimming in 20 °C warm water. Exposure to this stressor caused a significant increase in AVP release in both the mediolateral (174 ± 21%, P < 0.01) and ventral septum (220 ± 33%, P < 0.01). In contrast, microdialysates collected outside the mediolateral septum or in the lateral ventricle remained at prestress levels throughout the dialysis period. Furthermore, unstressed control animals failed to show significant alterations in vasopressin release in the mediolateral septum. In a second experiment, the introduction of the V1 receptor antagonist d(CH2)5Tyr(Me)AVP into the mediolateral septum via inverse microdialysis concomitant with stressor exposure caused the rats to spend an increased time floating and a reduced time swimming compared to vehicle‐treated rats. This effect was acute and also detected 24 h after antagonist administration. Taken together, these findings demonstrate a significant activation of the septal vasopressinergic system in response to swim stress. Furthermore, our data support the view that AVP released within this brain area is involved in the generation of active behavioural strategies aimed at coping with new and challenging situations.
Reaction time performance following unilateral striatal dopamine depletion and lesions of the subthalamic nucleus in the rat
Authors: Phillips Janice M. , Brown Verity J. 
Published: March 2003

AbstractThe akinesia resulting from Parkinson's disease or striatal dopamine depletion in experimental animals can be ameliorated or reversed by inactivation of the subthalamic nucleus. This inactivation might be effective by restoring balance to the basal ganglia motor circuits. Alternatively, new movement‐related deficits might be introduced which mask the original impairments (e.g. hyperkinesia might replace hypokinesia). In the present study, striatal dopamine depletion was effected unilaterally, in order to dissociate generalized effects, e.g. hyperkinesia, from response‐specific initiation effects. Rats were trained in a lateralized visual reaction time task and then assigned to one of four groups: striatal dopamine depletion; cell body lesion of the subthalamic nucleus; combined striatal dopamine depletion and subthalamic nucleus lesion; or control.As expected, rats with striatal dopamine depletion exhibited slower reaction time and a bias to respond to the ipsilateral side. The subthalamic nucleus lesion resulted in no reaction time change (in particular, there was no evidence of faster reaction times), but there was an increase in anticipatory responding. The group with the combined striatal dopamine depletion and subthalamic nucleus lesion had no reaction time impairment. This group showed an increase in anticipatory errors and a contralateral response bias. These data demonstrate that lesions of the subthalamic nucleus do not merely cancel the akinesia which follows striatal dopamine depletion by the addition of a hyperkinetic impairment. Rather, there appears to be a change in the balance of the motor system.
Acetylcholinesterase and inhibitors: effects upon normal and regenerating nerves of the rat
Authors: Keymer Juan Eduardo , Gaete Jorge , Kameid Gonzalo , Alvarez Jaime 
Published: March 2003

AbstractIn peripheral nerves, the function of acetylcholinesterase (AChE) is not related to hydrolysis of acetylcholine. To test for a trophic role, AChE or its inhibitors were administered locally to normal and regenerating nerves of rats. In the normal nerve, neither AChE nor serum albumin affected the cytological pattern of the nerve. BW284c51, a specific inhibitor of AChE, resulted in demyelination, proliferation of Schwann cells and sprouting of axons after 5–7 days. Edrophonium or propidium, other specific inhibitors of AChE, did so to a much lesser extent. Vehicle, and iso‐OMPA (inhibitor of pseudocholinesterases) did not affect the cytology of the nerve. Elongation of regenerating axons was evaluated at day 3 post‐crush. Native AChE applied distal to the crush reduced the elongation of regenerating axons (– 36%), while serum albumin, heated AChE and filtered AChE did not. BW284c51, edrophonium or propidium enhanced the axonal elongation (33%) when they were administered for 2 days before, but not after, the crush. Iso‐OMPA or vehicle administered before or after the crush were not effective. Thus, AChE reduces elongation of regenerating axons, while inhibition of AChE enhances elongation and affects the cytology of the normal nerve as well. We propose that AChE has a trophic role in mammalian peripheral nerves.
Origins of the glycinergic inputs to the rat locus coeruleus and dorsal raphe nuclei: a study combining retrograde tracing with glycine immunohistochemistry
Authors: Rampon Claire , Peyron Christelle , Gervasoni Damien , Pow David V. , Luppi Pierre‐Hervé , Fort Patrice 
Published: March 2003

AbstractThe amino acid glycine is a major inhibitory neurotransmitter in the brainstem and is likely involved in the tonic inhibition of the monoaminergic neurons during all sleep‐waking stages. In order to determine the neurons at the origin of the glycinergic innervation of the two principal monoaminergic nuclei, the locus coeruleus and the dorsal raphe of the rat, we applied a double‐labelling technique, combining retrograde transport of cholera‐toxin B subunit with glycine immunohistochemistry. Using this technique, we found that the locus coeruleus and dorsal raphe nuclei receive a common glycinergic innervation from the ventral and ventrolateral periaqueductal grey, including the adjacent deep mesencephalic reticular nucleus. Small additional glycinergic inputs to these nuclei originated from the lateral paragigantocellular nucleus and the rostral ventromedial medullary reticular formation. The potential role of these glycinergic inputs in the control of the excitability of the monoaminergic neurons of the locus coeruleus and dorsal raphe nuclei is discussed.
Cytochrome c release and caspase‐3 activation during colchicine‐induced apoptosis of cerebellar granule cells
Authors: Gorman A. M. , Bonfoco E. , Zhivotovsky B. , Orrenius S. , Ceccatelli S. 
Published: March 2003

AbstractThe microtubule‐disrupting agent colchicine is known to be neurotoxic toward certain neuronal populations including cerebellar granule cells (CGCs). In this study we investigated the involvement of cytochrome c release and caspase‐3 activation during colchicine‐induced CGC apoptosis. Treatment of rat CGCs with 1 μm colchicine (for up to 24 h) caused high molecular weight DNA fragmentation and nuclear condensation. An involvement of group II caspases (which includes caspase‐3) was demonstrated by the proteolytic degradation of poly(ADP‐ribose) polymerase (PARP) after 18 h exposure to colchicine. Colchicine induced a time‐dependent increase in Ac‐Asp‐Glu‐Val‐Asp‐α‐(4‐methyl‐coumaryl‐7‐amide) (DEVD‐MCA) cleavage activity in CGCs, which was blocked with a specific, peptide‐based, aldehyde inhibitor of group II caspases, i.e. DEVD‐CHO. We also observed a time‐dependent proteolysis of caspase‐3 as judged by the appearance of p17 which is one of the subunits of active caspase‐3. Activation of caspase‐3 during colchicine‐induced apoptosis may be mediated by cytochrome c since there was a close correlation between the time courses of cytochrome c release from the mitochondria and of caspase‐3 activation. Furthermore, colchicine‐induced apoptosis, as assessed by propidium iodide visualization of the nuclei, could be blocked by the caspase inhibitor benzyloxycarbonyl‐Val‐Ala‐Asp (O‐methyl) fluoromethyl ketone.
GDNF family ligands and receptors are differentially regulated after brain insults in the rat
Authors: Kokaia Zaal , Airaksinen Matti S. , Nanobashvili Avtandil , Larsson Elin , Kujamäki Eila , Lindvall Olle , Saarma Mart 
Published: March 2003

AbstractExpression of mRNAs for glial cell line‐derived neurotrophic factor (GDNF), neurturin (NTN) and their receptors was studied in adult rat brain using in situ hybridization after 40 kindling‐evoked, rapidly recurring seizures or 10 min of global forebrain ischaemia. Following seizures, GDNF and NTN mRNAs were elevated in dentate granule cells, and c‐Ret mRNA in hilar neurons and non‐pyramidal cells in CA1 and CA3 regions. GFRα‐1 mRNA levels showed more widespread increases in the dentate granule cell layer and hilus, CA1 and CA3 pyramidal layers, basolateral amygdala and parietal cortex. The expression of GFRα‐2 mRNA increased in the piriform cortex and decreased in the CA1 region and basolateral amygdala. Forebrain ischaemia induced elevated expression of GDNF mRNA in dentate granule cells, GFRα‐1 mRNA in the dentate granule cell layer, hilus and CA3 pyramidal layer, and GFRα‐2 mRNA in the parietal cortex. The gene expression patterns observed here suggest that GDNF and NTN may act as target‐derived factors, but also in an autocrine or paracrine manner. GFRα‐1 can be coexpressed with GFRα‐2 and c‐Ret mRNAs in the same hippocampal or thalamic neurons, but other neurons contain GFRα‐1 alone or together with c‐Ret mRNA. The gene expression changes for the ligands, and the receptor components are region‐, cell‐ and insult‐specific, and occur independently of each other, mainly within 24 h after seizures or ischaemia. This dynamic regulation of GDNF and NTN circuits primarily at the receptor level may be important for the effectiveness of neuroprotective responses but could also trigger plastic changes, e.g. those underlying the development of epileptic syndromes.
AMPA‐preferring receptors with high Ca2+ permeability mediate dendritic plasticity of retinal horizontal cells
Authors: Okada Takashi , Schultz Konrad , Geurtz Wiltrud , Hatt Hanns , Weiler Reto 
Published: March 2003

AbstractThe synaptic complex formed by the cone photoreceptor pedicles and the dendrites of horizontal cells in the teleost retina undergoes structural changes during light adaptation. Numerous spinules are formed by the terminal dendrites, and they are subsequently retracted during dark adaptation. In a retina kept under continuous illumination, the retraction process can be initiated by analogues of the neurotransmitter glutamate acting at AMPA/kainate receptors. On the other hand, the retraction process depends on calcium influx and the subsequent activation of CaMkII. We show here that the retraction of spinules induced by AMPA or kainate is not impaired in the presence of cobalt, making an involvement of voltage‐gated calcium channels unlikely. Using calcium imaging techniques with isolated horizontal cells, we demonstrate that AMPA and kainate, but not NMDA, increase [Ca2+]i in the presence of nicardipine, caffeine and thapsigargin. The increase of [Ca2+]i under these conditions depends on [Ca2+]o and on the agonist in a dose‐dependent manner, suggesting that the increase of [Ca2+]i is largely due to calcium influx through the agonist‐gated channel. Pharmacological studies were performed to determine whether AMPA‐ and/or kainate‐preferring receptors mediate the calcium influx. The AMPA‐preferring receptor antagonist LY303070 blocked glutamate‐ and kainate‐evoked increases of [Ca2+]i in a concentration‐dependent manner, indicating that kainate‐preferring receptors contributed little or nothing to the observed [Ca2+]i increase. This was supported by experiments where cyclothiazide (which blocks the desensitization of AMPA receptors) and concanavalin A (which potentiates responses mediated by kainate receptors) were applied. In all cases, LY303070 blocked the agonist‐evoked increase of [Ca2+]i. The presence of AMPA‐preferring receptors with high Ca2+ permeability on horizontal cells was also supported by measuring agonist‐induced currents using whole‐cell recording techniques. Furthermore, LY303070 was able to impair the retraction of spinules during dark adaption in the in vivo situation.
Semaphorin D acts as a repulsive factor for entorhinal and hippocampal neurons
Authors: Steup Andreas , Ninnemann Olaf , Savaskan Nicolai E. , Püschel Robert Nitsch andreas W. , Skutella Thomas 
Published: March 2003

AbstractWe analysed the effects of semaphorin D on axons from the developing rat entorhinal–hippocampal formation. Explants from superficial layers of the entorhinal cortex and of the hippocampus anlage were obtained from various developmental stages and co‐cultured with cell aggregates expressing semaphorin D. Neurites extending from entorhinal explants that had been isolated from early embryonic stages (E16 and E17) were not affected by semaphorin D, but were repelled at later stages (E20 and E21). Axons from hippocampal neurons explanted at E21 were also repelled by semaphorin D. In situ hybridization studies revealed expression of the semaphorin D receptor neuropilin‐1 in the entorhinal cortex from stage E17 to stage P7, and in the dentate gyrus and CA1–3 regions between E17 and adulthood. These data suggest that semaphorin D is involved in the formation of the perforant pathway and acts, via the neuropilin‐1 receptor, as a repulsive signal that prevents entorhinal fibres from growing into the granular layer of the dentate gyrus. These data also suggest a role for semaphorin D in the development of intrahippocampal connections.
Dorsolateral prefrontal cortex: comparative cytoarchitectonic analysis in the human and the macaque brain and corticocortical connection patterns
Authors: Petrides M. , Pandya D. N. 
Published: March 2003

AbstractThe cytoarchitecture of the human and the macaque monkey dorsolateral prefrontal cortex has been examined in a strictly comparative manner in order to resolve major discrepancies between the available segmentations of this cortical region in the human and the monkey brain. In addition, the connections of the dorsolateral prefrontal cortical areas were re‐examined in the monkey. The present analysis showed that only a restricted portion of what had previously been labelled as area 46 in the monkey has the same characteristics as area 46 of the human brain; the remaining part of this monkey region has the characteristics of a portion of the middle frontal gyrus in the human brain that had previously been included as part of area 9. We have labelled this cortical area as 9/46 in both species. These two areas (i.e. 46 and 9/46), which constitute the lower half of the mid‐dorsolateral frontal cortex, have a well‐developed granular layer IV, and can easily be distinguished from area 9, on the upper part of the mid‐dorsolateral region, which does not have a well‐developed granular layer IV. Area 9 has the same basic pattern of connections as areas 46 and 9/46, but, unlike the latter areas, it does not receive input from the lateral parietal cortex. Caudal to area 9, on the dorsomedial portion of the frontal cortex, there is a distinct strip of cortex (area 8B) which, unlike area 9, receives significant input from the prestriate cortex and the medial parietal cortex. The present results provide a basis for a closer integration of findings from functional neuroimaging studies in human subjects with experimental work in the monkey.
GABAB‐receptor‐mediated control of GABAergic inhibition in rat histaminergic neurons in vitro
Authors: Stevens David R. , Kuramasu Atsuo , Haas Helmut L. 
Published: March 2003

AbstractThe onset of slow wave sleep may require an inhibition of histaminergic neurons by GABAergic afferents from the ventrolateral preoptic area. We have utilized electrophysiological methods in an in vitro brain slice preparation to examine the role of GABAB receptor activation in GABAergic synaptic inhibition in histaminergic neurons of the tuberomammillary nucleus. Tetrodotoxin blocked evoked GABAergic IPSPs but not miniature IPSPs or IPSCs. Evoked IPSPs varied in amplitude and exhibited failures of transmission. Baclofen reduced the amplitude of evoked IPSPs in all experiments and often caused an increase in failures of transmission. Responses elicited by application of exogenous GABA were insensitive to baclofen treatment. The action of baclofen was blocked by CGP‐35348 (100 μm), a GABAB receptor antagonist, which also enhanced the amplitude of evoked IPSPs. The frequency of spontaneous and miniature IPSPs and IPSCs was reduced by baclofen. However, the amplitude distribution of mIPSCs was not altered. We conclude that GABA release onto TM neurons is under presynaptic control via GABAB receptors. This presynaptic control of transmission to tuberomammillary neurons may reduce inhibition, increasing histamine release and enhancing wakefulness.