bluuebunny/crossref_metadata_2025_split huggingface dataset:
Orientation specificity of contrast adaptation in visual cortical pinwheel centres and iso‐orientation domains
Authors: Sengpiel Frank , Bonhoeffer Tobias 
Published: March 2003

AbstractExposure to a high‐contrast visual stimulus causes adaptation, a psychophysical phenomenon that is quite selective for stimulus orientation. Its mechanism is largely cortical but the underlying circuitry is still not unambiguously resolved. It has been suggested that adaptation could be the result of integration of inputs from cells within a large local pool, effectively scaling their outputs with respect to local contrast. In this case, orientation selectivity of neuronal adaptation should depend on the location of neurons within the cortical map of orientation preference. We tested this hypothesis by quantifying adaptation to optimally oriented and to orthogonal‐to‐optimum gratings among neurons recorded either from iso‐orientation domains or orientation pinwheel centres, as identified by optical imaging of cat visual cortex. We did not find a significant difference in adaptation characteristics for these two populations of cells, implying that these characteristics do not depend on the local functional architecture. Surprisingly, however, we additionally observed that under isoflurane (but not halothane) anaesthesia, most neurons exhibited adaptation by cross‐oriented gratings, regardless of their location within the orientation map. It seems likely that, under isoflurane, inputs became visible that were masked by the commonly used, deeper halothane anaesthesia. For individual cells, the presence of these inputs was independent of their location within the cortical orientation map.
Selective targeting of zebrafish olfactory receptor neurons by the endogenous OMP promoter
Authors: Çelik Arzu , Fuss Stefan H. , Korsching S. I. 
Published: March 2003

AbstractThe olfactory nervous system of fish, in particular zebrafish, has become a valid model for that of higher vertebrates. However, no genetic markers for olfactory specific cell types, e.g. the olfactory receptor neurons, have been established in this species. Olfactory marker protein (OMP) is a reliable marker for olfactory receptor neurons in several other vertebrates. We have cloned zOMP, the zebrafish homologue of olfactory marker protein. During development, zOMP is expressed exclusively in the olfactory placode, presumably in olfactory receptor neurons, as shown by in situ hybridization. In the adult nasal epithelium zOMP is found restricted to the sensory region. zOMP appears to be a single gene, without close family members. The 5′‐flanking region lacks most of the expected regulatory sequence motifs, both general and cell type‐specific ones. Nevertheless, it drives reporter gene expression strongly and specifically in olfactory receptor neurons during the whole developmental period examined. Thus the zOMP promoter constitutes a powerful tool which should be useful to selectively introduce a wide variety of genetic modifications into olfactory receptor neurons.
Periwound dopaminergic sprouting is dependent on numbers of wound macrophages
Authors: Batchelor P. E. , Porritt M. J. , Nilsson S. K. , Bertoncello I. , Donnan G. A. , Howells D. W. 
Published: March 2003

AbstractInjury to many regions of the central nervous system, including the striatum, results in a periwound or ‘abortive’ sprouting response. In order to directly evaluate whether macrophages play an important role in stimulating periwound sprouting, osteopetrotic (op/op) mice, which when young are deficient in a variety of macrophage subtypes, were given striatal wounds and the degree of dopaminergic sprouting subsequently assessed. Two weeks postinjury, significantly fewer wound macrophages were present in the striata of op/op mice compared with controls (144 ± 30.1 in op/op mice vs. 416.6 ± 82.3 in controls, P < 0.005, analysis performed on a section transecting the middle of the wound). Dopamine transporter immunohistochemistry revealed a marked decrease in the intensity of periwound sprouting in the op/op group of animals. Quantification of this effect using [H3]‐mazindol autoradiography confirmed that periwound sprouting was reduced significantly in the op/op mice compared with controls (71.4 ± 21.7 fmol/mg protein in op/op mice vs. 210.7 ± 27.1 fmol/mg protein in controls, P < 0.0005). In the two groups of animals the magnitude of the sprouting response in individuals was closely correlated with the number of wound macrophages (R = 0.83, R2 = 0.69). Our findings provide strong support for the crucial involvement of macrophages in inducing dopaminergic sprouting after striatal injury.
µ/δ Cooperativity and opposing κ‐opioid effects in nucleus accumbens‐mediated antinociception in the rat
Authors: Schmidt Brian L. , Tambeli Claudia H. , Levine Jon D. , Gear Robert W. 
Published: March 2003

AbstractWe previously demonstrated that noxious peripheral stimulation (e.g. subdermal capsaicin injection in the hind paw) produces antinociception that is mediated by opioid receptors in nucleus accumbens. The current study used the trigeminal jaw‐opening nociceptive reflex responses in the rat to assess the role of intra‐accumbens µ‐, δ‐ and κ‐opioid receptors in the antinociceptive effect of noxious stimulation and intra‐accumbens opioid agonism. Whilst intra‐accumbens injection of either the µ‐receptor‐selective antagonist Cys2,Tyr3,Orn5,Pen7amide (CTOP) or the δ‐receptor‐selective antagonist naltrindole blocked capsaicin‐induced antinociception, neither the selective µ‐agonist [D‐Ala2,N‐Me‐Phe4,Gly5‐ol]‐enkephalin (DAMGO; 150 or 300 ng) nor the selective δ‐agonist D‐Pen2,5‐enkephalin (DPDPE; 150 or 300 ng) alone induced antinociception. Simultaneous injection of DAMGO and DPDPE (150 ng each), however, produced significant antinociception. Capsaicin‐induced antinociception was not blocked by the selective κ‐receptor antagonist nor‐binaltorphimine, but was blocked by the κ‐agonist U69,593. U69,593 also antagonized the antinociceptive effect of the DAMGO/DPDPE combination. Thus, in nucleus accumbens, µ‐ and δ‐ but not κ‐opioid receptors contributed to capsaicin‐induced antinociception; selective activation of individual receptor subtypes was insufficient, but coactivation of µ‐ and δ‐opioid receptors induced antinociception, and κ‐receptors appeared to play an antianalgesic role in nucleus accumbens.
Spinal cord injury induces expression of RGS7 in microglia/macrophages in rats
Authors: Hausmann Oliver N. , Hu Wen‐Hui , Keren‐Raifman Tal , Witherow D. Scott , Wang Qiang , Levay Konstantin , Frydel Beata , Z. Slepak Vladlen , R. Bethea John 
Published: March 2003

AbstractRGS proteins regulate G protein‐mediated signalling pathways through direct interaction with the Gα subunits and facilitation of GTP hydrolysis. An RGS subfamily consisting of RGS 6, 7, 9, and 11 also interacts with the G protein β subunit Gβ5 via a characteristic Gγ‐like domain. Thus far, these complexes were found only in neurons, with RGS7 being the most widely distributed in the brain. Here we confirm the expression of RGS7 in spinal neurons and show as a novel finding that following an experimental spinal cord injury in rats, expression of RGS7 is induced in a subpopulation of other cells. Immunofluorescent confocal microscopy using a series of cell specific antibodies identified these RGS7 positive cells as activated microglia and/or invading peripheral macrophages. To rule out interference from the adjacent neurons and confirm the presence of RGS7‐Gβ5 complex in inflammatory cells, we performed immunocytochemistry, RT‐PCR, Western blot, and immunoprecipitation using microglial (BV2) and peripheral macrophage (RAW) cell lines. Expression of RGS7 mRNA and protein are nearly undetectable in non‐stimulated BV2 and RAW cells, but remarkably increased after stimulation with LPS or TNF‐α In addition, RGS7‐positive cells were also found in the perinodular rim in the rat spleen. Our findings show that RGS7‐Gβ5 complex is expressed in immunocompetent cells such as resident microglia and peripheral macrophages following spinal cord injury. This expression might contribute to the post‐traumatic inflammatory responses in the central nervous system.
Altered regulation of the 5‐HT system in the brain of MAO‐A knock‐out mice
Authors: Evrard A. , Malagié I. , Laporte A.‐M. , Boni C. , Hanoun N. , Trillat A.‐C. , Seif I. , De Maeyer E. , Gardier A. , Hamon M. , Adrien J. 
Published: March 2003

AbstractGenetic deficiency of monoamine oxidase‐A (MAO‐A) induces major alterations of mood and behaviour in human. Because serotonin (5‐HT) is involved in mood regulation, and MAO‐A is responsible for the catabolism of 5‐HT, we investigated 5‐HT mechanisms in knock‐out mice (2‐month‐old) lacking MAO‐A, using microdialysis, electrophysiological, autoradiographic and molecular biology approaches. Compared to paired wild‐type mice, basal extracellular 5‐HT levels were increased in ventral hippocampus (+202%), frontal cortex (+96%) and dorsal raphe nucleus (DRN, +147%) of MAO‐A mutant mice. Conversely, spontaneous firing rate of 5‐HT neurons in the DRN (recorded under chloral hydrate anaesthesia) was ∼40% lower in mutants. Acute 5‐HT reuptake blockade by citalopram (0.2 and 0.8 mg/kg i.v.) produced a much larger increase in extracellular 5‐HT levels (by ∼4 fold) and decrease in DRN neuronal firing (with a ∼4.5 fold decrease in the drug's ED50) in MAO‐A knock‐out mice, which expressed lower levels of the 5‐HT transporter throughout the brain (−13 to −34% compared to wild‐type levels). The potency of the 5‐HT1Aagonist 8‐OH‐DPAT to produce hypothermia and to reduce the firing of DRN serotoninergic neurons was significantly less in the mutants, indicating a desensitization of 5‐HT1Aautoreceptors. This was associated with a decreased autoradiographic labelling of these receptors (−27%) in the DRN. Altogether, these data indicate that, in MAO‐A knock‐out mice, the enhancement of extracellular 5‐HT levels induces a down‐regulation of the 5‐HT transporter, and a desensitization of 5‐HT1Aautoreceptors which allows the maintenance of tonic activity of 5‐HT neurons in the DRN.
D2‐mediated modulation of N‐type calcium currents in rat globus pallidus neurons following dopamine denervation
Authors: Stefani Alessandro , Spadoni Francesca , Martorana Alessandro , Lavaroni Franco , Martella Giuseppina , Sancesario Giuseppe , Bernardi Giorgio 
Published: March 2003

AbstractWe have studied the effects of dopamine and the D2‐like agonist quinpirole on calcium currents of neurons isolated from the striatum and the globus pallidus (GP). Experiments were performed in young adult rats, either in control conditions or following lesion of the nigrostriatal pathway by the unilateral injection of 6‐hydroxydopamine (6‐OHDA) in the substantia nigra. Apomorphine‐driven contralateral turning, 15 days after lesioning, assessed the severity of the dopamine denervation. In addition, the loss of tyrosine hydroxylase immunohistochemistry confirmed the extent of the toxin‐induced damage. In both striatal medium spiny (MS) and GP neurons of control animals dopamine and quinpirole promoted a very modest inhibition of calcium conductance. Following 6‐OHDA, the inhibition was unaltered in MS (from 10 to 12%), but significantly augmented in GP neurons (21% vs. 9%). Interestingly, analogous inhibition was observed in GP neurons dissociated 20 h after reserpine treatment. Further features of the D2 response were thus studied only in neurons isolated from 6‐OHDA‐lesioned GP. The D2 modulation was G‐protein‐mediated but not strictly voltage‐dependent. ω‐Conotoxin‐GVIA occluded the response implying the involvement of N‐type calcium channels. The effect of quinpirole developed fast and was insensitive to alterations of cytosolic cAMP. The incubation in phorbol esters or OAG blocked the D2 effect, supporting the involvement of PKC. These findings suggest that postsynaptic D2‐like receptors are functionally expressed on GP cell bodies and may supersensitize following dopamine‐denervation. A direct D2 modulation of calcium conductance in GP may alter GP firing properties and GABA release onto pallidofugal targets.
Group III metabotropic glutamate receptors and D1‐like and D2‐like dopamine receptors interact in the rat nucleus accumbens to influence locomotor activity
Authors: David Hélène N. , Abraini Jacques H. 
Published: March 2003

AbstractEvidence for functional interactions between metabotropic glutamate (mGlu) receptors and dopamine (DA) neurotransmission is now clearly established. In the present study, we investigated interactions between group III mGlu receptors and D1‐ and D2‐like receptors in the nucleus accumbens (NAcc). Administration, into the NAcc, of the selective group III mGlu receptor agonist, AP4, resulted in an increase in locomotor activity, which was blocked by pretreatment with the group III mGlu receptor antagonist, MPPG. In addition, pretreatment with AP4 further blocked the increase in motor activity induced by the D1‐like receptor agonist, SKF 38393, but potentiated the locomotor responses induced by either the D2‐like receptor agonist, quinpirole, or coinfusion of SKF 38393 and quinpirole. MPPG reversed the effects of AP4 on the motor responses induced by D1‐like and/or D2‐like receptor activation. These results confirm that glutamate transmission may control DA‐dependent locomotor function through mGlu receptors and further indicate that group III mGlu receptors oppose the behavioural response produced by D1‐like receptor activation and favour those produced by D2‐like receptor activation.
Comparison of neuronal activity in the rostral supplementary and cingulate motor areas during a task with cognitive and motor demands
Authors: Akkal D. , Bioulac B. , Audin J. , Burbaud P. 
Published: March 2003

AbstractA number of cortical motor areas have been identified on the medial wall of the hemisphere in monkeys. However, their specific role in motor control remains unclear. In this study, we sought to describe and compare the functional properties of the presupplementary (pre‐SMA) and rostral cingulate (CMAr) motor areas in two monkeys performing a visually instructed, delayed, sequential movement. We recorded 134 task‐related neurons in the pre‐SMA and 149 in the CMAr. The main difference between the two areas was the abundance of responses to targets (46%) in the pre‐SMA, while CMAr activity was more related to reward (28%). Neuronal responses to targets were more phasic and higher in frequency in the pre‐SMA than in the CMAr. During the delay, the percentage of neuronal responses was similar in the two areas. The discharge pattern was different depending upon whether the delay duration was fixed or variable but in most neurons was the same regardless of the sequence performed. Movement‐related changes were common in the pre‐SMA (75%) and in the CMAr (81%) but they occurred earlier in the former. Neurons activated exclusively during movement were more numerous in the CMAr. Finally, neuronal activity in the pre‐SMA was more related to the sequential aspect of the task compared to the CMAr. Our results suggest that although the two areas share functional properties, they also participate in different aspects of motor behaviour. Their functional properties reflect their anatomical positions, which give them the potential to integrate external stimuli (pre‐SMA) and internal states (CMAr) during motor planning.
EEG theta synchronization conjoined with alpha desynchronization indicate intentional encoding
Authors: Mölle Matthias , Marshall Lisa , Fehm Horst L. , Born Jan 
Published: March 2003

AbstractThe involvement of different oscillating neuronal systems activated during intentional learning was investigated by measuring ongoing EEG activity. In 17 subjects, the EEG was recorded while learning pairs of words and faces. Subjective task difficulty was rated and a control condition of mental relaxation was also run. Spontaneous EEG activity during epochs which subsequently resulted in efficient encoding was associated with upper alpha desynchronization (10–12 Hz) and theta synchronization (4–8 Hz) when compared with spontaneous EEG activity during epochs of poor recall performance. The combined measure of theta synchronization plus upper alpha desynchronization was enhanced selectively over left frontotemporal cortical regions during efficient learning of words and over right parietal cortical regions during efficient learning of faces (P < 0.001). This striking topographical dissociation between learning materials for the combined measure of theta and upper alpha EEG activity suggests that the mode of intentional learning relies essentially on an interdependent regulation of two neuronal circuits: the thalamo‐cortical circuit and the hippocampo‐cortical circuit.
Reduction of drug‐induced yawning and penile erection and of noncontact erections in male rats by the activation of GABAAreceptors in the paraventricular nucleus: involvement of nitric oxide
Authors: Melis Maria Rosaria , Argiolas Antonio 
Published: March 2003

AbstractThe effect of muscimol, a GABAAreceptor agonist, injected into the paraventricular nucleus (PVN) of the hypothalamus on drug‐induced (apomorphine, oxytocin and NMDA) yawning and penile erection, and on the increase in the concentration of NO2–and NO3–occurring in the paraventricular dialysate in these experimental conditions, was studied in male rats. Muscimol (50, 100 and 200 ng) reduced, in a dose‐dependent manner, penile erection and yawning induced by apomorphine (50 ng), oxytocin (30 ng) and NMDA (50 ng) delivered into the PVN. The reduction of penile erection and yawning was parallel to a reduction of the concomitant NO2–and NO3–increase that occurs in the paraventricular dialysate in this experimental condition. In contrast, baclofen (200 ng), a GABABreceptor agonist, was ineffective. The muscimol effects on drug‐induced penile erection, yawning and NO2–increase were prevented by the prior administration of bicuculline (250 ng into the paraventricular nucleus). Muscimol (200 ng) but not baclofen (200 ng), injected into the PVN, reduced both noncontact erections in male rats placed in the presence of an inaccessible receptive female, and also the NO2–increase that occurs in the paraventricular dialysate in this experimental condition. As found with drug‐induced penile erection, the muscimol reduction of noncontact erections and of NO2–increase was prevented by bicuculline. The present results show that the activation of GABAAreceptors in the PVN reduces yawning and penile erection induced by drugs or physiological stimuli by reducing the increase in NO activity that occurs in this hypothalamic nucleus in these experimental conditions.
Oestrogen‐dependent tracing in the rat CNS after pseudorabies virus infection
Authors: Horváth Szatmár , Kis Zsolt , Boldogköi Zsolt , Nógrádi Antal , Toldi József 
Published: March 2003

AbstractThis study examines the hypothesis that neuronal infectivity and the spreading of the pseudorabies virus (PRV) through the synapses in the central nervous system (CNS) are influenced by the oestrogen levels. The arcuate nucleus (ARC) and the subfornical organ (SFO) were chosen as models for analysis; the neurons in both structures possess oestrogen receptors and are mutually connected. A genetically engineered pseudorabies virus (Ba‐DupLac) was used as a transneuronal tract tracer. This virus is taken up preferably by axon terminals, and transported very specifically through the synapses in a retrograde manner. Ba‐DupLac was injected into the ARC of rats, followed by monitoring of the PRV‐immunoreactivity (PRV‐IR) in the SFO 72 h following inoculation. We found no PRV immunolabelling in the SFO of ovariectomized (OVX) rats, or in those OVX animals that received oestrogen shortly (4 h) before PRV infection (OVX + E 4 h). In contrast, in those OVX animals that received oestrogen 12 h before PRV infection (OVX + E 12 h), and also in intact control animals, PRV‐IR was demonstrated in the SFO in all cases. Surprisingly, a reverse labelling was observed in the OVX rats; PRV‐IR appeared in the pyriform cortex, whereas PRV‐IR could not be detected in the control and OVX + E 12 h animals. As far as we are aware, this is the first study to demonstrate that transneuronal PRV labelling depends on the effects of oestrogen on certain CNS structures and connections.
Basolateral amygdala lesions block the memory‐enhancing effect of 8‐Br‐cAMP infused into the entorhinal cortex of rats after training
Authors: Roesler Rafael , Roozendaal Benno , McGaugh James L. 
Published: March 2003

AbstractThere is extensive evidence suggesting that the basolateral nucleus of the amygdala plays a critical role in modulating memory consolidation processes in other brain regions. The present experiments examined interactions between the basolateral amygdala and the entorhinal cortex in modulating memory consolidation for inhibitory avoidance training. Several studies have reported that activation of the second messenger system adenosine 3′,5′‐cyclic monophosphate (cAMP) in several brain regions enhances memory and induces long‐term plasticity. In the present experiments, a unilateral infusion of the cAMP analogue, 8‐Br‐cAMP (0.25 or 1.25 µg in 0.5 µL), administered into the entorhinal cortex of male Sprague–Dawley rats immediately after training, enhanced 48‐h retention. An N‐methyl‐d‐aspartate‐induced lesion of the ipsilateral basolateral amygdala did not impair retention, but blocked the memory‐enhancing effect of 8‐Br‐cAMP (infused into the entorhinal cortex) post‐training. A lesion of the contralateral basolateral amygdala did not block the 8‐Br‐cAMP‐induced retention enhancement. These findings indicate that an intact basolateral amygdala is essential for modulation of memory consolidation involving the entorhinal cortex, and are consistent with evidence that the basolateral amygdala regulates memory consolidation mediated by other brain regions.
Expression of RGS2, RGS4 and RGS7 in the developing postnatal brain
Authors: Ingi Tatsuya , Aoki Yaeko 
Published: March 2003

AbstractThe abundant expression of RGS (regulator of G‐protein signalling) proteins in neurons, together with their modulatory function on G‐protein‐dependent neurotransmission, provides the basis for cellular adaptation to sensory inputs. To identify the molecular mechanism involved in the sensory experience‐induced neural development, we performed a systematic survey of the localization of mRNAs encoding three subtypes of the RGSs (RGS2, RGS4 and RGS7) in developing rat brains by in situ hybridization through postnatal day 2 (P2), P10 and P18 to adult. The most dramatic changes of expression patterns were observed in the discrete neuronal cell layers of the cerebral neocortex (for RGS2 and 4), the hippocampus (for RGS2, 4 and 7), the thalamus (for RGS4) and the cerebellum (for RGS2 and 7). In the neocortex, RGS2 mRNA was enriched in the superficial cortical plate at P2, in contrast to RGS4, which was enriched in more mature neurons of the deeper layer V and VI. In the hippocampus, the neuronal cell layer‐specific expression pattern of RGS2 developed from P2 to P18. RGS4 expression was temporarily confined to the CA pyramidal cell layer and not detectable in the dentate gyrus at P10 and P18. Similarly, a high level of expression of RGS7 was observed in the CA area, but not in the dentate gyrus at P2 and P10. In the cerebellum, the maturation of laminar expression patterns for the three RGSs correlated with neuronal maturation and synaptogenesis at P18. The most characteristic temporal pattern among the three RGSs was observed for RGS4 mRNA, which was highly enriched in the thalamocortical regions. The peaks of RGS4 expression were seen in the following regions with distinct onset and duration: the neocortex (from P2 onward), the hippocampus (P10 and P18) and the thalamus (from P18 onward). The divergent temporal and spatial expression of RGS subtypes and their dynamic control in the cortex, the hippocampus and the thalamus suggest that the RGS family could play multiple distinct roles in experience‐dependent brain development.