bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metabolic signals, hormones and neuropeptides involved in control of energy balance and reproductive success in hamsters*
Authors: Schneider J. E. , Buckley C. A. , Blum R. M. , Zhou D. , Szymanski L. , Day D. E. , Bartness T. J. 
Published: March 2003

AbstractIn the ‘postgenome era’, most research on the neuroendocrine control of energy homeostasis has focused on hormonal and neuropeptide control of food intake (i.e. the amount of food eaten) in rats and mice. The amount of food consumed is influenced by both the motivation to procure food and the consummatory act of ingestion. In some species, the rate of food intake remains relatively constant, while survival is maintained via changes in food procurement, external storage and internal expenditure. For example, in hamsters, metabolic signals, peripheral hormones and central neuropeptides influence hunger motivation, food hoarding and changes in energy expenditure without necessarily influencing the amount of food ingested. A similar suite of metabolic signals, hormones and neuropeptides is involved in optimizing reproductive success under fluctuating energetic conditions. Reproductive processes are inhibited or delayed when energy expenditure outstrips energy intake and mobilization from storage. Estrous cyclicity in Syrian hamsters is sensitive to the availability of oxidizable glucose, but the presence of central glucose alone is not sufficient for normal estrous cycles. Food deprivation‐induced anestrus does not depend upon food deprivation‐induced increases in concentrations of adrenal hormones such as glucocorticoids. If hormones such as insulin and leptin play a role, they might do so by modulating the availability of glucose detected at extra‐hypothalamic sites, instead of or in addition to direct effects on the mechanisms that control gonadotropin releasing hormone secretion. Despite our ability to measure and manipulate gene transcription, understanding of fuel homeostasis requires examination of indirect effects of hormones and neuropeptides on peripheral metabolism, attention to the motivational as well as consummatory aspects of ingestion, and the study of behaviour in a natural or seminatural context.
Multiple maps and activity‐dependent representational plasticity in the anterior Wulst of the adult barn owl (Tyto alba)
Authors: Manger Paul R. , Elston Guy N. , Pettigrew John D. 
Published: March 2003

AbstractIn the present study we addressed the issue of somatosensory representation and plasticity in a nonmammalian species, the barn owl. Multiunit mapping techniques were used to examine the representation of the specialized receptor surface of the claw in the anterior Wulst. We found dual somatotopic mirror image representations of the skin surface of the contralateral claw. In addition, we examined both representations 2 weeks after denervation of the distal skin surface of a single digit. In both representations, the denervated digital representation became responsive to stimulation of the adjacent, mutually functional, digit. The mutability and multiple representations indicates that the Wulst provides the owl with sensory processing capabilities analogous to those in mammals.
Evidence that metyrapone can act as a stressor: effect on pituitary‐adrenal hormones, plasma glucose and brain c‐fos induction
Authors: Rotllant David , Ons Sheila , Carrasco Javier , Armario Antonio 
Published: March 2003

AbstractMetyrapone, a 11‐β steroid hydroxylase inhibitor that blocks stress‐induced glucocorticoid release, is extensively used to study the physiological and behavioural roles of glucocorticoids. However, there is circumstancial evidence suggesting that metyrapone could act as a pharmacological stressor. Thus, the effects of various doses of metyrapone on two well‐characterized stress markers (ACTH and glucose) were studied in male rats. Metyrapone administration, while exerting a modest effect on plasma corticosterone levels, dose‐dependently increased plasma ACTH and glucose levels. Using the highest doses previously tested (200 mg/kg) we further observed, as evaluated by fos‐like immunoreactivity (FLI), a strong activation of a wide range of brain areas, including the parvocellular region of the hypothalamic paraventricular nucleus (PVNp), the origin of the main ACTH secretagogues. Metyrapone‐induced FLI was observed in neocortical and allocortical areas, in several limbic, thalamic and hypothalamic nuclei and, to a lesser extent, in the brainstem. In a final experiment, a dose–response study of metyrapone‐induced FLI was carried out focusing on selected brain areas. The study revealed that the paraventricular thalamic nucleus and central amygdala were the areas most sensitive to metyrapone as they responded even to the lowest dose of the drug. Most areas, among them the PVNp, only showed enhanced FLI with the two highest doses, i.e. when it was associated with ACTH and glucose responses. These data suggest that some of the effects of metyrapone could be due to its stressful properties rather than its ability to inhibit glucocorticoid synthesis. The exact mechanisms involved remain to be established.
Neither ibotenic acid nor volkensin lesions of the nucleus accumbens shell affect the expression of cocaine sensitization
Authors: Todtenkopf M. S. , Stellar J. R. , Melloni R. H. 
Published: March 2003

AbstractStudies have shown that the nucleus accumbens shell plays an integral role in the expression of psychostimulant‐induced behavioural sensitization. Dopaminergic regulation of excitatory amino acid inputs in this region of the brain could be a key factor in the neural influence of this phenomenon. Alterations in the dopaminergic innervation patterns in the shell have been demonstrated in rats that received repeated cocaine injections. Furthermore, lesions of brain regions that send projections to the shell alter psychostimulant‐induced locomotion, both acutely and in sensitization paradigms. A previous study from our laboratory demonstrated that lesions of the shell before repeated cocaine treatment decrease the locomotor response to cocaine during the induction phase of behavioural sensitization. To better understand the role of this brain region during the expression phase of behavioural sensitization, the present study examined the effects of two forms of cytotoxic lesions of the shell. Rats received a sensitization‐inducing regimen of cocaine (bi‐daily injections of 15 mg/kg i.p. for 5 consecutive days). Two days after the last injection, rats demonstrating behavioural sensitization received one of three bilateral microinjections into the shell: (i) 0.5 µL 0.9% saline; (ii) 2.5 µg/0.5 µL ibotenic acid (which lesions the cell bodies at the injection site); or (iii), 0.5 ng/0.2 µL of volkensin (a retrograde suicide transport lectin). Upon challenge with cocaine (15 mg/kg) 12 days after surgery, neither ibotenic acid‐ nor volkensin‐lesioned rats showed any difference in their locomotor response compared with sham controls. These data indicate that bilateral shell lesions do not affect the long‐term expression of behavioural sensitization in cocaine‐sensitized rats.
Mice lacking the adenosine A1 receptor are anxious and aggressive, but are normal learners with reduced muscle strength and survival rate
Authors: Giménez‐Llort Lydia , Fernández‐Teruel Alberto , Escorihuela Rosa Maria , Fredholm Bertil B. , Tobeña Adolf , Pekny Milos , Johansson Björn 
Published: March 2003

AbstractBehavioural assessment of mice lacking adenosine A1 receptors (A1Rs) showed reduced activity in some phases of the light–dark cycle, reduced exploratory behaviour in the open‐field and in the hole‐board, increased anxiety in the plus maze and dark‐light box and increased aggressiveness in the resident‐intruder test. No differences were found in spatial reference and working memory in several Morris water maze tasks. Both mutant mice had reduced muscle strength and survival rate. These results confirm the involvement of adenosine in motor activity, exploratory behaviour, anxiety and aggressiveness. A1Rs also appear to play a critical role in ageing‐related deterioration.
Differential effects of laminar stimulation of V1 cortex on target selection by macaque monkeys
Authors: Tehovnik Edward J. , Slocum Warren M. , Schiller Peter H. 
Published: March 2003

AbstractWe explored the effects of microstimulation on target selection by delivering stimulation at different depths within V1 (striate cortex) of the rhesus monkey (Macaca mulatta). Stimulation evoked saccadic eye movements that terminated in the receptive‐field location of the activated neurons. The current thresholds for saccade evocation were highest (≥ 30 µA) in the superficial layers and lowest (≤ 10 µA) in the deep layers. To study target selection, one visual target was presented in the receptive‐field location of the stimulated neurons and a second visual target was presented outside this location. Microstimulation delivered in concert with the appearance of the two targets decreased the probability that a monkey would select the target placed in the receptive‐field location when the upper layers of V1 were stimulated, and it increased this probability when the lower layers were stimulated. We suggest that microstimulation of the upper layers of V1 disrupts visual signals from retina en route to higher cortical areas, whereas microstimulation of the lower layers activates V1 efferents that innervate the oculomotor system.
Akt mediates the anti‐apoptotic effect of NMDA but not that induced by potassium depolarization in cultured cerebellar granule cells
Authors: Lafon‐Cazal Mireille , Perez Virgili , Bockaert Joël , Marin Philippe 
Published: March 2003

AbstractApoptosis of cultured cerebellar granule neurons (CGNs) deprived of serum is prevented by K+ depolarization or moderate concentrations of N‐methyl‐d‐aspartate (NMDA). Here, we have examined the role of the serine/threonine kinase Akt in these protective effects. The exposure of mouse CGNs to NMDA or K+ depolarization increased the phosphorylation of Akt, compared with that measured in cells incubated in a physiological K+ concentration. Only the NMDA‐evoked response was reduced by inhibitors of phosphatidylinositol 3‐kinase (wortmannin and LY294002) and mitogen‐activated protein kinase (PD98059 and U0126). Similarly, the capacity of NMDA to inhibit apoptosis of CGNs deprived of serum was greatly reduced by these inhibitors as well as by the transfection of neurons with a catalytically inactive mutant of Akt, whereas the protective effect of K+ depolarization remained unaffected. These findings indicate that K+ depolarization and NMDA activate Akt through different signalling pathways in CGNs. Moreover, Akt mediates the anti‐apoptotic effect of NMDA, but not that evoked by K+ depolarization.
Erythropoietin exerts anti‐apoptotic effects on rat microglial cells in vitro
Authors: Vairano Mauro , Russo Cinzia Dello , Pozzoli Giacomo , Battaglia Alessandra , Scambia Giovanni , Tringali Giuseppe , Aloe‐Spiriti Maria Antonietta , Preziosi Paolo , Navarra Pierluigi 
Published: March 2003

AbstractErythropoietin (EPO), a renal cytokine regulating haematopoiesis, is also produced by different cell types within the central nervous system, where it acts via the activation of specific receptors. Current evidence shows that EPO exerts neurotrophic and neuroprotective activities in different in vivo and in vitro models of brain damage. In the present study we investigated the effects of EPO on primary cultures of rat cortical microglia and astrocytes. We found that: (i) EPO exerted a marked stimulatory effect on microglial cell viability, assessed through the MTS assay, whereas astrocytes were almost unaffected; (ii) the cytokine increased microglial cell population size in a concentration‐dependent manner; however, as microglia cultures undergo spontaneous apoptosis after separation from astrocytes, the apparent effect on cell proliferation could be attributed to EPO antagonism of normal apoptosis; (iii) subsequent flow cytometry analysis on microglial cells demonstrated both the trophic role of factor(s) released by astrocytes in mixed cultures, and the putative anti‐apoptotic action of EPO; (iv) the latter was further confirmed through the assessment of gene expression of anti‐ and pro‐apoptotic factors, which showed that EPO is able to shift the Bcl : Bax ratio towards a net anti‐apoptotic effect; (v) EPO did not affect the pro‐inflammatory function of microglial cells.
Phosphorylated MAP1B is induced in central sprouting of primary afferents in response to peripheral injury but not in response to rhizotomy
Authors: Soares Sylvia , Von Boxberg Ysander , Lombard Marie‐Christine , Ravaille‐Veron Michèle , Fischer Itzhak , Eyer Joel , Nothias Fatiha 
Published: March 2003

AbstractA peripheral nerve lesion induces sprouting of primary afferents from dorsal root ganglion (DRG) neurons into lamina II of the dorsal horn. Modifications of the environment in consequence to the axotomy provide an extrinsic stimulus. A potential neuron‐intrinsic factor that may permit axonal sprouting is microtubule‐associated protein 1B (MAP1B) in a specific phosphorylated form (MAP1B‐P), restricted to growing or regenerating axons. We show here that both in rat and mouse, a sciatic nerve cut is rapidly followed by the appearance of MAP1B‐P expression in lamina II, increasing to a maximum between 8 and 15 days, and diminishing after three months. Evidence is provided that sprouting and induction of MAP1B‐P expression after peripheral injury are phenomena concerning essentially myelinated axons. This is in accordance with in situ hybridization data showing especially high MAP1B‐mRNA levels in large size DRG neurons that give rise to myelinated fibers. We then employed a second lesion model, multiple rhizotomy with one spared root. In this case, unmyelinated CGRP expressing fibers do indeed sprout, but coexpression of MAP1B‐P and CGRP is never observed in lamina II. Finally, because a characteristic of myelinated fibers is their high content in neurofilament protein heavy subunit (NF‐H), we used NF‐H‐LacZ transgenic mice to verify that MAP1B‐P induction and central sprouting were not affected by perturbing the axonal organization of neurofilaments. We conclude that MAP1B‐P is well suited as a rapidly expressed, axon‐intrinsic marker associated with plasticity of myelinated fibers.
Hormonal enhancement of neuronal firing is linked to structural remodelling of excitatory and inhibitory synapses
Authors: Parducz A. , Hoyk Z. , Kis Z. , Garcia‐Segura L. M. 
Published: March 2003

AbstractThe ovarian hormone estradiol induces morphological changes in the number of synaptic inputs in specific neuronal populations. However, the functional significance of these changes is still unclear. In this study, the effect of estradiol on the number of anatomically identified synaptic inputs has been assessed in the hypothalamic arcuate nucleus. The number of axo‐somatic, axodendritic and spine synapses was evaluted using unbiased stereological methods and a parallel electrophysiological study was performed to assess whether synaptic anatomical remodelling has a functional consequence on the activity of the affected neurons. Estradiol administration to ovariectomized rats induced a decrease in the number of inhibitory synaptic inputs, an increase in the number of excitatory synapses and an enhancement of the frequency of neuronal firing. These results indicate that oestrogen modifications in firing frequency in arcuate neurons are temporally linked to anatomical modifications in the numerical balance of inhibitory and excitatory synaptic inputs.
Early behavioural changes in mice infected with BSE and scrapie: automated home cage monitoring reveals prion strain differences
Authors: Dell'Omo Giacomo , Vannoni Elisabetta , Vyssotski Alexei L. , Di Bari Michele Angelo , Nonno Romolo , Agrimi Umberto , Lipp Hans‐Peter 
Published: March 2003

AbstractMice inoculated with transmissible spongiform encephalopathies (TSE) show behavioural abnormalities well before the appearance of clinical signs. TSE strains are obtained by serial re‐infection of infectious brain homogenates in laboratory rodents. They are characterized by strain‐typical brain lesion profiles, which implies that they might be differentiated behaviourally as well. Seventy female C57BL/6 mice were tested, 14 per group. Controls received no or sham inocula, two other groups received scrapie strains adapted to mice (139A, ME7) and one group a mouse‐adapted BSE strain (301C). From week 7 until the end of the incubation period, 8 mice per group were subjected once every 2 weeks to open‐field and hot‐plate tests. Assessment of clinical signs, and measuring of body weight, food and water consumption were carried out weekly on the remaining animals kept in single cages. In addition, locomotor activity was recorded continuously in these mice by means of infrared detectors. Monitoring of circadian activity revealed early significant TSE strain differences, most pronounced during the nocturnal active phase. Behavioural changes in open‐field tests also occurred before the appearance of clinical signs, and differences in rearing, wall rearing and sniffing were strain‐specific, however, such differences varied according to the period of testing. Hind paw lick latencies increased equally in all groups after week 19, jump latencies also increased in the two scrapie groups but not in the BSE group. It was at this time that clinical signs first appeared consisting of ataxia, lack of balance, motor dyscoordination, and lordosis. These data imply that automated assessment of circadian activity in mice is a powerful and economical tool for early behavioural typing of TSE strains.
Met‐enkephalin immunoreactive neurons recruited by acute stress are innervated by axon terminals immunopositive for tyrosine hydroxylase and dopamine‐α‐hydroxylase in the anterolateral division of bed nuclei of the stria terminalis in the rat
Authors: Kozicz Tamás 
Published: March 2003

AbstractThe bed nuclei of the stria terminalis (BST) are highly heterogeneous forebrain structures, which play a central role in the regulation/modulation of stress responses. Studies using the inducible immediate early gene c‐fos as a marker of activated neurons have demonstrated significant stress‐induced neuronal activation in this limbic region. The BST also exhibit a dense network of dopamine and noradrenaline immunoreactive (ir) axon terminals. These catecholaminergic projections from various brainstem sources to the BST play an important role in a neurochemically mediated coordination of stress responses. In the anterolateral division of bed nuclei of the stria terminalis, the distribution of several Met‐enkephalin immunopositive perikarya overlaps with that of catecholaminergic axon terminals. Both monoaminergic and enkephalinergic structures have been postulated to play a role in the regulation/modulation of the central regulatory pathways of endocrine, behavioural and physiological responses during stress. Therefore the aims of this study were: (i) to study the possible involvement of dopaminergic fibre terminals in stress‐induced activation of BST perikarya; (ii) to investigate whether Met‐enkephalin‐immunoreactive neurons are recruited by acute volumen/osmotic challenge; and (iii), to demonstrate synaptic interactions between Met‐enkephalin‐ir neurons and fibre terminals immunopositive for dopamine or noradrenaline in the anterolateral division of the BST. From the results of this study we can conclude that depletion of dopamine in fibre terminals completely abolished stress‐induced activation of perikarya in the anterolateral division of BST. Furthermore, the innervation of stress‐induced Met‐enkephalin‐ir perikarya by dopaminergic fibre terminals in the oval nucleus of BST was demonstrated, whereas noradrenergic axons contacted enkephalinergic structures in the fusiform and subcomissural nuclei of BST. These interactions can be central in the modulatory control of the major stress regulatory pathway, the limbic hypothalamo–pituitary–adrenal axis.
CNS region‐specific regulation of glial glutamate transporter expression
Authors: Schlüter Karen , Figiel Maciej , Rozyczka Joanna , Engele Jürgen 
Published: March 2003

AbstractThe neuronal cell death associated with certain neurodegenerative disorders as well as acute brain injuries is in part due to the reduced expression of glial glutamate transporters and the subsequent accumulation of toxic extracellular glutamate concentrations. Extracellular factors previously found to potently stimulate the expression of the glial glutamate transporters, GLT‐1/EAAT2 and GLAST/EAAT1, in astroglial cultures of rat cerebral hemispheres are PACAP, TGFα, and EGF. In the present study, we sought to determine whether similar stimulatory influences apply for astroglia from other areas of the central nervous system (CNS). Immunoblot and real‐time RT‐PCR analysis of striatal astroglial cultures maintained for 72 h with PACAP, TGFα, or EGF revealed a prominent increase in GLT‐1 and GLAST expression. In apparent contrast, all factors completely failed to affect GLT‐1 and GLAST expression in astroglial cultures from the cerebellum, mesencephalon, and spinal cord between 36 h and 7 days. This failure was not due to the absence of functional recognition or transduction machineries for the extracellular factors as suggested by the additional observations that cerebellar, mesencephalic and spinal cord glia were capable of responding to stimulation with PACAP, TGFα, or EGF for 10 min with activation of CREB. Moreover, dibutyryl cyclic AMP (dbcAMP) potently promoted GLT‐1 and/or GLAST expression in mesencephalic, cerebellar and spinal cord glia, further indicating that extracellular factors regulate glial glutamate transporter expression throughout the CNS. Together these findings identify PACAP, TGFα and EGF as potent regulators of glutamate transporter expression in striatal glia. In addition, these findings provide evidence for a CNS region‐specific regulation of glial glutamate transport.
Somatic nociception activates NK1receptors in the nucleus tractus solitarii to attenuate the baroreceptor cardiac reflex
Authors: Boscan Pedro , Kasparov Sergey , Paton Julian F. R. 
Published: March 2003

AbstractThere is limited information regarding the integration of visceral and somatic afferents within the nucleus of the solitary tract (NTS). We studied the interaction of nociceptive and baroreceptive inputs in this nucleus in anin situarterially perfused, un‐anaesthetized decerebrate preparation of rat. At the systemic level, the gain of the cardiac component of the baroreceptor reflex was attenuated significantly by noxious mechanical stimulation of a forepaw. This baroreceptor reflex depression was mimicked by NTS microinjection of substance P and antagonized by microinjection of either bicuculline (a GABAAreceptor antagonist) or a neurokinin type 1 (NK1) receptor antagonist (CP‐99,994). The substance P effect was also blocked by a bilateral microinjection of bicuculline, at a dose that was without effect on basal baroreceptor reflex gain. Baroreceptive NTS neurons were defined by their excitatory response following increases in pressure within the ipsilateral carotid sinus. In 27 of 34 neurons the number of evoked spikes from baroreceptor stimulation was reduced significantly by concomitant electrical stimulation of the brachial nerve (P < 0.01). Furthermore, the attenuation of baroreceptor inputs to NTS neurons by brachial nerve stimulation was prevented by pressure‐ejection of bicuculline from a multi‐barrelled microelectrode (n = 8). In a separate population of 17 of 45 cells tested, brachial nerve stimulation evoked an excitatory response that was antagonized by blockade of NK1receptors. We conclude that nociceptive afferents activate NK1receptors, which in turn excite GABAergic interneurons impinging on cells mediating the cardiac component of the baroreceptor reflex.