bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stressor categorization: acute physical and psychological stressors elicit distinctive recruitment patterns in the amygdala and in medullary noradrenergic cell groups
Authors: Dayas C.V. , Buller K.M. , Crane J.W. , Xu Y. , Day T.A. 
Published: March 2003

AbstractIt has been hypothesized that the brain categorizes stressors and utilizes neural response pathways that vary in accordance with the assigned category. If this is true, stressors should elicit patterns of neuronal activation within the brain that are category‐specific. Data from previous immediate–early gene expression mapping studies have hinted that this is the case, but interstudy differences in methodology render conclusions tenuous. In the present study, immunolabelling for the expression of c‐fos was used as a marker of neuronal activity elicited in the rat brain by haemorrhage, immune challenge, noise, restraint and forced swim. All stressors elicited c‐fos expression in 25–30% of hypothalamic paraventricular nucleus corticotrophin‐releasing‐factor cells, suggesting that these stimuli were of comparable strength, at least with regard to their ability to activate the hypothalamic–pituitary–adrenal axis. In the amygdala, haemorrhage and immune challenge both elicited c‐fos expression in a large number of neurons in the central nucleus of the amygdala, whereas noise, restraint and forced swim primarily elicited recruitment of cells within the medial nucleus of the amygdala. In the medulla, all stressors recruited similar numbers of noradrenergic (A1 and A2) and adrenergic (C1 and C2) cells. However, haemorrhage and immune challenge elicited c‐fos expression in subpopulations of A1 and A2 noradrenergic cells that were significantly more rostral than those recruited by noise, restraint or forced swim. The present data support the suggestion that the brain recognizes at least two major categories of stressor, which we have referred to as ‘physical’ and ‘psychological’. Moreover, the present data suggest that the neural activation footprint that is left in the brain by stressors can be used to determine the category to which they have been assigned by the brain.
Projections from the superior temporal sulcus to the agranular frontal cortex in the macaque
Authors: Luppino Giuseppe , Calzavara Roberta , Rozzi Stefano , Matelli Massimo 
Published: March 2003

AbstractThe aim of this study was to investigate the organization of the projections from the superior temporal sulcus (STS) to the various areas forming the agranular frontal cortex. Injections of retrograde neuronal tracers were made in the various agranular areas, in nine macaque monkeys. The results showed that two rostral premotor areas, F6 (pre‐SMA) and F7, and the ventrorostral part of area F2 (F2vr) are targets of projections from the upper bank of the STS (uSTS). F6 and the dorsorostral part of F7 (supplementary eye field, SEF) are targets of projections from the rostral part of the uSTS, corresponding to the so‐called ‘superior temporal polysensory area’ (STP). In contrast, the ventral part of area F7 (not including the SEF) and F2vr are targets of afferents from the caudal part of the uSTS. Ventral F7 is the target of weak afferents from the caudalmost and dorsalmost part of the uSTS (area 7a), whilst F2vr is the target of projections from a relatively more rostral and ventral sector of the uSTS, close to the fundus of the sulcus. This sector should correspond to area MST. In conclusion, F6 and SEF receive high order information from STP, whereas ventral F7 and F2vr receive information from areas of the dorsal visual stream.
The nitric oxide system modulates the in vivo release of acetylcholine in the nucleus accumbens induced by stimulation of the hippocampal fornix/fimbria‐projection
Authors: Kraus Michaela M. , Prast Helmut 
Published: March 2003

AbstractNerve signals from the hippocampus to the nucleus accumbens (NAc) are transmitted through a glutamatergic pathway via the fornix/fimbria fibres. The aim of the present study was to investigate whether cholinergic neurons are activated by this projection and whether the nitric oxide (NO) system is also involved in the signal transduction within this nucleus. For this purpose, the NAc of urethane‐anaesthetized rats was superfused, by the push‐pull technique, with compounds that influence the NO system while the fornix/fimbria was electrically stimulated for short periods. The amount of acetylcholine (ACh) released in the superfusate was then determined. Electrical stimulation of the fornix/fimbria increased the ACh output in the NAc. This effect was abolished by superfusion with tetrodotoxin and decreased by superfusion with the glutamate receptor antagonists AP‐5 and DNQX indicating the involvement of action potentials and glutamate. Superfusion with the inhibitor of neuronal NO synthase, NS 2028 also diminished stimulation‐evoked ACh release. The NO donor PAPA/NO increased basal release. Simultaneous application of PAPA/NO and electrical stimulation led to an over‐additive increase of ACh release. The effect of PAPA/NO on stimulation‐evoked release was also abolished by NS 2028. The selective inhibitor of phosphodiesterase type 5 (PDE 5), 5‐[2‐ethoxy‐5‐(morpholinylacetyl)phenyl]‐1,6‐dihydro‐1‐methyl‐3‐propyl‐7H‐pyrazolo[4,3‐d]pyrimidin‐7‐one methanesulphanate monohydrate also enhanced stimulation‐induced release of ACh. Our findings indicate, that action potentials propagated by the fornix/fimbria to the NAc release glutamate which increases ACh release predominantly via NMDA receptors. In addition, nitrergic neurons are activated to enhance NO synthesis. The released NO seems to exert, via cGMP, a potent facilitatory role in the transduction and processing of signals from the hippocampus within the NAc, while the PDE 5 decreases the effects of NO.
Capsaicin‐evoked CGRP release from rat buccal mucosa: development of a model system for studying trigeminal mechanisms of neurogenic inflammation
Authors: Flores Christopher M. , Leong Anthony S. , O. Dussor Gregory ,   Catherine Harding‐Rose,, Hargreaves Kenneth M. , Kilo Sonja 
Published: March 2003

AbstractMany of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin‐sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene‐related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague–Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10–300 µm), to the superfusion buffer resulted in a significant, concentration‐dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mm) or by the calcium ionophore A23187 (1 µm). The specific, capsaicin receptor antagonist, capsazepine (300 µm), completely abolished the capsaicin‐evoked release of iCGRP while having no effect whatsoever on the potassium‐evoked release. Moreover, capsaicin‐evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor‐mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation.
Selective activation of the ventrolateral prefrontal cortex in the human brain during active retrieval processing
Authors: Cadoret Geneviève , Pike G. Bruce , Petrides Michael 
Published: March 2003

AbstractThe present study examined the role of the prefrontal cortex in retrieval processing using functional magnetic resonance imaging in human subjects. Ten healthy subjects were scanned while they performed a task that required retrieval of specific aspects of visual information. In order to examine brain activity specifically associated with retrieval, we designed a task that had retrieval and control conditions that were perfectly matched in terms of depth of encoding, decision making and postretrieval monitoring and differed only in terms of whether retrieval was required. In the retrieval condition, based on an instructional cue, the subjects had to retrieve either the particular stimulus that was previously presented or its location. In the control condition, the cue did not instruct retrieval but shared with the instructional cues the function of alerting the subjects of the impending test phase. The comparison of activity between the retrieval and control conditions demonstrated a significant and selective increase in activity related to retrieval processes within the ventrolateral prefrontal cortical region, more specifically within area 47/12. These activity increases were bilateral but stronger in the right hemisphere. The present study by strictly controlling the level of encoding, postretrieval monitoring, and decision making has demonstrated a specific increase in the ventrolateral prefrontal region that could be clearly related to active retrieval processing, i.e. the active selection of particular stored visual representations.
Characterization of serial order encoding in the monkey anterior cingulate sulcus
Authors: Procyk E. , Joseph J. P. 
Published: March 2003

AbstractIn a previous report we showed that neurons in the anterior cingulate cortex might encode the serial order of the three components (first, second and third) of motor sequences, irrespective of which component is performed, and irrespective of the component that precedes or follows. Here we further explore these data by comparing the magnitude of cell activity at the different ranks. We also compare the activity recorded in the motor sequences and in tasks with only one motor component. We finally discuss functional hypotheses, which may account for the serial order encoding.
Gaze shifts evoked by electrical stimulation of the superior colliculus in the head‐unrestrained cat. II. Effect of muscimol inactivation of the caudal fastigial nucleus
Authors: Guillaume Alain , Pélisson Denis 
Published: March 2003

AbstractThe medioposterior cerebellum [vermian lobules VI and VII and caudal fastigial nucleus (cFN)] is known to play a major role in the control of saccadic gaze shifts toward a visual target. To determine the relative contribution of the cFN efferent pathways to the brainstem reticular formation and to the superior colliculus (SC), we recorded in the head‐unrestrained cat the effects of cFN unilateral inactivation on gaze shifts evoked by electrical microstimulation of the deeper SC layers. Gaze shifts evoked after muscimol injection still exhibited the typical qualitative features of normal saccadic gaze shifts. Nevertheless, consistent modifications in amplitude and latency were observed. For ipsiversive movements (evoked by the SC contralateral to the inactivated cFN), these changes depended on the locus of stimulation on the motor map: for the anterior 2/3 of the SC, amplitude increased and latency tended to decrease; for the posterior 1/3 of the SC, amplitude decreased and latency increased. For the contraversive direction, amplitude moderately decreased and latency tended to increase for all but the caudal‐most stimulated SC site. These modifications of SC‐evoked gaze shifts during cFN inactivation differed from the ipsiversive hypermetria/contraversive hypometria pattern observed for visually triggered gaze shifts recorded during the same recording sessions. We conclude that (i) the topographical organization of gaze shift amplitude in the deeper SC layers is influenced by the cerebellum and is either severely distorted or demonstrates an amplitude reduction during inactivation of the contralateral or ipsilateral cFN, respectively; (ii) gaze shifts evoked by SC microstimulation and visually triggered gaze shifts either rely on distinct cerebellar‐dependent control processes or differ by the location of the caudal‐most active SC population. We present a functional scheme providing several predictions regarding the modulatory influence of the cerebellum on SC neuronal activities and on the topographical organization of fastigial–SC projections.
Insulin promotes functional induction of silent synapses in differentiating rat neocortical neurons
Authors: Plitzko Daniela , Rumpel Simon , Gottmann Kurt 
Published: March 2003

AbstractLong‐term synaptic plasticity is thought to underlie synaptic reorganization phenomena that occur during neocortical development. Recently, it has been proposed, that the functional induction of AMPA receptors at silent glutamatergic synapses is of major importance in activity‐dependent, developmental plasticity. To investigate the mechanisms involved in the developmental regulation of silent synapses, we analysed the functional maturation of the thalamocortical projection in culture. A large proportion of the thalamocortical synapses were functionally silent at an early stage in vitro. During further differentiation, the incidence of silent synapses decreased drastically, indicating a conversion of silent into functional synapses. Chronic blockade of spontaneous network activity by addition of tetrodotoxin to the culture medium strongly impaired this developmental maturation. Moreover, the developmental decline in the proportion of silent synapses was dramatically accelerated by chronic addition of the neurotrophic factor, insulin. This effect of insulin was partly dependent on spontaneous activity. Thus, insulin appears to be involved in the modulation of long‐term developmental plasticity at immature glutamatergic synapses.
Noxious heat‐induced CGRP release from rat sciatic nerve axons in vitro
Authors: Sauer S. K. , Reeh P. W. , Bove G. M. 
Published: March 2003

AbstractNoxious heat may act as an endogenous activator of the ionotropic capsaicin receptor (VR1) and of its recently found homologue VRL1, expressed in rat dorsal root ganglion cells and present along their nerve fibres. We have previously reported that capsaicin induces receptor‐mediated and Ca++‐dependent calcitonin gene‐related peptide (CGRP) release from axons of the isolated rat sciatic nerve. Here we extended the investigation to noxious heat stimulation and the transduction mechanisms involved. Heat stimulation augmented the CGRP release from desheathed sciatic nerves in a log–linear manner with a Q10 of ≈ 15 and a threshold between 40 and 42 °C. The increases were 1.75‐fold at 42 °C, 3.8‐fold at 45 °C and 29.1‐fold at 52 °C; in Ca++‐free solution these heat responses were abolished or reduced by 71 and 92%, respectively. Capsazepine (10 µm) and Ruthenium Red (1 µm) used as capsaicin receptor/channel antagonists did not significantly inhibit the heat‐induced release. Pretreatment of the nerves with capsaicin (100 µm for 30 min) caused complete desensitization to 1 µm capsaicin, but a significant heat response remained, indicating that heat sensitivity is not restricted to capsaicin‐sensitive fibres. The sciatic nerve axons responded to heat, potassium and capsaicin stimulation with a Ca++‐dependent CGRP release. Blockade of the capsaicin receptor/channels had little effect on the heat‐induced neuropeptide release. We conclude therefore that other heat‐activated ion channels than VR1 and VRL1 in capsaicin‐sensitive and ‐insensitive nerve fibres may cause excitation, axonal Ca++ influx and subsequent CGRP release.
Stimulation of α1‐adrenoceptors inhibits memory consolidation in the chick
Authors: Gibbs Marie E. , Summers Roger J. 
Published: March 2003

AbstractInvestigation of the effects of the different adrenoceptor (AR) subtypes in memory formation may reveal discrete actions of noradrenaline in memory modulation and storage mediated through particular AR subtypes. Noradrenaline injected intracerebrally in the chick produced biphasic effects on memory consolidation with enhancement at low doses and inhibition at high doses. We have previously shown that the enhancement by the lower doses of noradrenaline is attributable to actions at β2‐ and β3‐adrenoceptors, whereas the inhibitory effect of higher doses is attributable to α1‐adrenoceptors. The present studies show that the inhibition of memory by high doses of noradrenaline is mimicked by the α1‐AR agonist methoxamine, and the dose–response curve is shifted to the right by pretreatment with the α1‐AR antagonist prazosin. α1‐ARs may play a critical role in memory formation in highly stressful situations, when noradrenaline levels are high in particular brain regions. It is not known where the α1‐ARs responsible for the effect on memory are localized. α1‐ARs are found on neurons and astrocytes and in the cerebral vasculature and therefore the action of high doses of noradrenaline via α1‐AR agonists could be via an action at any of these sites. Activation of α1‐adrenoceptors in the intermediate hyperstriatum ventrale in the chick forebrain by the α1 adrenoceptor agonist methoxamine inhibits the consolidation of memory. Because the same effect is produced by high levels of noradrenaline, it is likely that stimulation of α1‐ARs is the mechanism underlying this effect.
Persistent changes in striatal gene expression induced by long‐term l‐DOPA treatment in a rat model of Parkinson's disease
Authors: Westin J. E. , Andersson M. , Lundblad M. , Cenci M. A. 
Published: March 2003

AbstractCurrent knowledge of the molecular changes induced by dopamine denervation and subsequent treatment with l‐DOPA is based on studies performed on relatively acute and young animal models of parkinsonism. It is highly warranted to ask how well these models simulate the state of chronic denervation and sustained l‐DOPA pharmacotherapy which are typical of advanced Parkinson's disease. This study investigates the effects of time postdenervation and l‐dopa treatment duration on the striatal expression of opioid precursor mRNAs and FosB/ΔFosB‐related proteins. Unilaterally 6‐hydroxydopamine‐lesioned rats were treated with therapeutical doses of l‐DOPA for one year (long‐term group) or a few weeks (short‐term group). Age‐matched lesioned rats received injections of vehicle or bromocriptine, an antiparkinsonian compound which does not produce dyskinesia when administered de novo. The lesion‐induced up‐regulation of preproenkephalin mRNA expression persisted at more than one year postlesion, and was unaffected by the pharmacological treatments applied. l‐DOPA, but not bromocriptine, induced high striatal levels of FosB/ΔFosB immunoreactivity and prodynorphin mRNA, and these did not differ between short‐term and long‐term l‐DOPA‐treated rats. The present data provide the first demonstration that l‐DOPA maintains high striatal levels of fosB and prodynorphin gene expression during a prolonged course of treatment, which simulates the clinical practice in Parkinson's disease more closely than the short‐treatment paradigms studied thus far.
Gaze shifts evoked by electrical stimulation of the superior colliculus in the head‐unrestrained cat. I. Effect of the locus and of the parameters of stimulation
Authors: Guillaume Alain , Pélisson Denis 
Published: March 2003

AbstractSeveral studies have suggested that the pattern of neuronal activity in the superior colliculus (SC) interacts with the well‐known topographical coding of saccades (motor map). To further describe this interaction, we recorded gaze saccades evoked by electrical microstimulation of SC deeper layers in the head‐unrestrained cat and systematically varied the collicular locus (25 sites) and parameters (intensity, frequency) of the stimulation. Long stimulation trains were used to avoid saccade truncation. We found that the direction and amplitude of evoked gaze shifts were related to the stimulation locus, describing a gaze shift map. For 18 out of 20 sites the amplitude, but not the direction, also strongly depended on stimulation strength. Indeed, gaze amplitude continuously increased when raising current intensity up to several times the threshold value T (the largest intensity tested was 6 × T), whereas varying pulse frequency from 150 to 750 pulses per second (p.p.s.) revealed an optimal frequency range (300 and 500 p.p.s.) eliciting the largest gaze shifts. Moreover, the intensity effect on amplitude increased in an orderly fashion with the rostro‐caudal stimulation locus. Gaze shift amplitude was not related to the number of delivered stimulation pulses. Concerning movement initiation, increasing either intensity or frequency led to an exponential decrease in gaze latency until minimal values near 30 ms were reached, but the number of pulses delivered during the corresponding latency period remained constant within a 300–500 p.p.s. frequency range. These findings indicate that the pattern of collicular discharge evoked by electrical stimulation strongly interacts with the gaze shift map and provide evidence for a summation of collicular activities by downstream premotor neurons.
Thyroid hormone regulates TAG‐1 expression in the developing rat brain
Authors: Alvarez‐Dolado Manuel , Figueroa Angélica , Kozlov Serguei , Sonderegger Peter , Furley Andrew J. , Muñoz Alberto 
Published: March 2003

AbstractTAG‐1 is a member of the immunoglobulin superfamily of cell adhesion molecules thought to play important roles in neuronal differentiation and the establishment of connectivity during brain development. Because these are processes also affected by hypothyroidism, we studied the effects of thyroid hormone deprivation and administration on TAG‐1 expression in the developing rat brain. By in situ hybridization, immunohistochemistry and Western blotting we found that TAG‐1 RNA and protein levels are upregulated in the hypothyroid brain. From embryonic day 20 to postnatal day (P) 15, elevated TAG‐1 RNA was found in several areas including the cerebral cortex, hippocampus and olfactory bulb. In agreement with this, TAG‐1 protein was overexpressed in the major fibre tracts arising from these structures, including the corpus callosum, anterior and hippocampal commissures and lateral olfactory tract. A similar overexpression of TAG‐1 by hypothyroidism was detected in the cerebellum, but starting only at P15. In all cases, elevation of TAG‐1 RNA and protein expression could be reversed by thyroid hormone treatment. These results show that the deregulation of TAG‐1 might contribute to the alterations caused by the lack of thyroid hormone during brain development.