bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nicotinic modulation of glutamatergic synaptic transmission in region CA3 of the hippocampus
Authors: Giocomo Lisa M. , Hasselmo Michael E. 
Published: September 2005

AbstractCholinergic modulation of synaptic transmission in the hippocampus appears to be involved in learning, memory and attentional processes. In brain slice preparations of hippocampal region CA3, we have explored the effect of nicotine on the afferent connections of stratum lacunosum moleculare (SLM) vs. the intrinsic connections of stratum radiatum (SR). Nicotine application had a lamina‐selective effect, causing changes in synaptic transmission only in SLM. The nicotinic effect in SLM was characterized by a transient decrease in synaptic potential size followed by a longer period of enhancement of synaptic transmission. The effect was blocked by γ‐aminobutyric acid (GABA)ergic antagonists, indicating the role of GABAergic interneurons in the observed nicotinic effect. The biphasic nature of the nicotinic effect could be due to a difference in receptor subtypes, as supported by the effects of the nicotinic antagonists mecamylamine and methyllycaconitine. Nicotinic modulation of glutamatergic synaptic transmission could complement muscarinic suppression of intrinsic connections, amplifying incoming information and providing a physiological mechanism for the memory‐enhancing effect of nicotine.
Frontal and parietal cortical ensembles predict single‐trial muscle activity during reaching movements in primates
Authors: Santucci David M. , Kralik Jerald D. , Lebedev Mikhail A. , Nicolelis Miguel A. L. 
Published: September 2005

AbstractPreviously we have shown that the kinematic parameters of reaching movements can be extracted from the activity of cortical ensembles. Here we used cortical ensemble activity to predict electromyographic (EMG) signals of four arm muscles in New World monkeys. The overall shape of the EMG envelope was predicted, as well as trial‐to‐trial variations in the amplitude and timing of bursts of muscle activity. Predictions of EMG patterns exhibited during reaching movements could be obtained not only from primary motor cortex, but also from dorsal premotor, primary somatosensory and posterior parietal cortices. These results suggest that these areas represent signals correlated to EMGs of arm muscles in a distributed manner, and that the larger the population sampled, the more reliable the predictions. We propose that, in the future, recordings from multiple cortical areas and the extraction of muscle patterns from these recordings will help to restore limb mobility in paralysed patients.
Differential expression and regulation of the cAMP‐selective phosphodiesterase type 4A splice variants in rat brain by chronic antidepressant administration
Authors: D'Sa Carrol , Eisch Amelia J. , Bolger Graeme B. , Duman Ronald S. 
Published: September 2005

AbstractChronic antidepressant treatment up‐regulates the cAMP cascade in limbic brain regions, suggesting that activation of this pathway contributes to the therapeutic efficacy of antidepressants. A role for cAMP signaling is supported by the finding that rolipram, a selective inhibitor of cAMP‐specific phosphodiesterases type 4 (PDE4), has antidepressant efficacy in behavioral models of depression and in clinical trials. To elucidate further the role of PDE4 isozymes, we characterized the expression and regulation of PDE4A splice variants (i.e. PDE4A1, PDE4A5, PDE4A8 and PDE4A10) in rat brain by chronic antidepressant treatment. Initial in situ hybridization studies (ISH) revealed high levels of PDE4A1 mRNA in medial septum, diagonal band, olfactory system, hippocampus and cerebellum. PDE4A5 mRNA expression was restricted to the olfactory nuclei, deep cortical layers, dentate and CA1 pyramidal layers. PDE4A10 mRNA was localized in the dentate gyrus and CA1 pyramidal layers. PDE4A8 mRNA was absent in rat brain. We determined the influence of chronic fluoxetine or electroconvulsive seizure (ECS) treatments on PDE4A splice variants expression in various brain regions. ISH analysis indicated that chronic fluoxetine or ECS treatments significantly increased PDE4A1, but not PDE4A5 or PDE4A10, mRNA levels in frontal and parietal cortices. ECS increased PDE4A5 levels in the anterior cingulate and frontoparietal cortices, CA1 and dentate gyrus, whereas chronic fluoxetine or ECS treatment increased PDE4A10 levels in the hippocampus. The differential up‐regulation of PDE4A splice variants suggests compensatory region‐specific responses to the antidepressant‐induced increase in cAMP signaling and suggests that these splice variants may be relevant as targets for antidepressant intervention.
Reduction of GnRH and infertility in the R6/2 mouse model of Huntington's disease
Authors: Papalexi Eugenia , Persson Anna , Björkqvist Maria , Petersén Åsa , Woodman Ben , Bates Gillian P. , Sundler Frank , Mulder Hindrik , Brundin Patrik , Popovic Natalija 
Published: September 2005

AbstractReductions in testosterone and luteinizing hormone levels and reduced sexual functions have been reported in Huntington's disease (HD) patients. Atrophy of the reproductive organs and loss of fertility have also been observed in the R6/2 mouse, which is currently the most studied transgenic model of HD. In an effort to define the cause of infertility we studied the expression of gonadotropin‐releasing hormone (GnRH) in the medial septum, diagonal band of Broca and hypothalamus of R6/2 male mice during sexual maturation. We found a progressive reduction in the numbers of GnRH‐immunoreactive neurons in the analysed brain areas of R6/2 mice starting at 5 weeks of age and becoming statistically significant with only 10% of the neurons remaining by 9 weeks of age. Atrophy of testes and seminal vesicles combined with a significant reduction in serum and testicular testosterone levels were detected in 12‐week‐old R6/2mice. These results suggest that infertility in the R6/2 males is due either to death of GnRH neurons or to a reduction in GnRH expression leading to a downstream impairment of the gonadotropic hormones. Gonadotropic hormone replacement did not mitigate weight loss or restore motor function in R6/2 males.
Glutamatergic neurotransmission and protein kinase C play a role in neuron–glia communication during the development of methamphetamine‐induced psychological dependence
Authors: Miyatake Mayumi , Narita Minoru , Shibasaki Masahiro , Nakamura Atsushi , Suzuki Tsutomu 
Published: September 2005

AbstractMethamphetamine (METH) is a strongly addictive psychostimulant that dramatically affects the central nervous system (CNS). On the other hand, protein kinase C (PKC) plays a major role in cellular regulatory and signalling processes that involve protein phosphorylation. The purpose of this study was to investigate the role of neuronal and astrocytic PKC in changes in the central glutamatergic system induced by METH. We show here thatin vitrotreatment with METH caused the phosphorylation of both neuronal and astrocytic PKC and the activation of astrocytes in cortical neuron/glia co‐cultures. Treatment of cortical neuron/glia co‐cultures with either the PKC activator phorbol 12,13‐dibutyrate (PDBu) or glutamate also caused the PKC‐dependent activation of astrocytes. The PKC inhibitor chelerythrine suppressed the Ca2+responses to glutamate in both cortical neurons and astrocytes. Moreover, a low concentration of PDBu significantly enhanced the Ca2+responses to glutamate, but not to dopamine, in both cortical neurons and astrocytes. Notably, treatment with METH also enhanced the Ca2+responses to glutamate in cortical neurons. The activation of astrocytes induced by METH was also reversed by co‐treatment with glutamate receptor antagonists (ifenprodil, DNQX or MPEP) in cortical neuron/glia co‐cultures. In the conditioned place preference paradigm, intracerebroventricular administration of glutamate receptor antagonists (ifenprodil, DNQX or MPEP) attenuated the METH‐induced rewarding effect. These findings provide evidence that the changes in PKC‐dependent neuronal and astrocytic glutamatergic transmission induced by METH may, at least in part, contribute to the development of psychological dependence on METH.
Distribution of D2 dopamine receptor in the olfactory glomeruli of the rat olfactory bulb
Authors: Gutièrrez‐Mecinas María , Crespo Carlos , Blasco‐Ibáñez José Miguel , Gracia‐Llanes Francisco Javier , Marqués‐Marí Ana Isabel , Nácher Juan , Varea Emilio , Martínez‐Guijarro Francisco José 
Published: September 2005

AbstractDopamine plays key roles in the processing of the olfactory information that takes place in the olfactory glomeruli. Previous studies using autoradiography demonstrate that, at the glomerular level, these actions are mainly mediated via activation of D2 dopamine receptors. Moreover, it has been suggested that D2 receptors could be present in the olfactory nerve, where they might modulate the entrance of olfactory input into the brain. Nevertheless, the precise subcellular localization of D2 receptors in the glomerular neuropil has not been investigated. In this report, we show the subcellular distribution of D2 receptors in the glomerular circuits of Wistar rats, using pre‐embedding immunogold‐silver labelling and electron microscopy. Present results demonstrate for the first time the presence of D2 dopamine receptors into the terminals of the olfactory axons. In addition, we demonstrate that D2 receptors are located into presynaptic elements of the glomerular neuropil other than the olfactory axons. These elements include the dendrites of the mitral/tufted cells and the dendrites of a subset of periglomerular cells that are GABAergic and dopaminergic. This distribution pattern provides anatomical support for a wide range of actions of dopamine in the glomerular circuits through presynaptic mechanisms mediated by D2 receptors. These actions would include: (i) modulation of the glutamate release from the olfactory axons to the dendrites of mitral/tufted cells and periglomerular cells; (ii) modulation of glutamatergic synapses from the dendrites of mitral/tufted cells to the dendrites of periglomerular cells and (iii) modulation of the neurotransmission from a subset of GABAergic/dopaminergic periglomerular cells to mitral/tufted cells.
Contribution of the vagus nerve and lamina terminalis to brain activation induced by refeeding
Authors: Timofeeva Elena , Baraboi Elena Dana , Richard Denis 
Published: September 2005

AbstractFollowing refeeding, c‐fos expression is induced in a particular set of brain regions that include the nucleus of the solitary tract (NTS), parabrachial nucleus (PB), central amygdala (CeA), paraventricular hypothalamic nucleus (PVH), supraoptic nucleus (SON) and the circumventricular organs. Within the PVH, the expression is particularly intense in the magnocellular division of the nucleus and it is as yet not clear how this activation occurs. The respective contribution of the vagus afferents and lamina terminalis, which conveys signals entering the brain through the forebrain circumventricular organs, has been investigated in rats subjected to a unilateral cervical vagotomy (UCV) or a unilateral lesion of the fibres running within the lamina terminalis (ULT) and projecting to the neuroendocrine hypothalamus. UCV significantly decreased postprandial c‐fos expression in the NTS, PB, CeA and parvocellular division of the PVH. In contrast, ULT impaired postprandial activation of the magnocellular neurons in the PVH and SON. The present study also characterized the types of neurons activated in the PVH and SON during refeeding. In the magnocellular regions, arginine‐vasopressin (AVP) neurons were activated upon refeeding whereas there was no apparent induction of Fos expression in oxytocin cells. In the parvocellular PVH, postprandial Fos was induced only in 30% of the corticotrophin‐releasing factor (CRF) and AVP neurons. The results of the present study suggest that the postprandial activation of the brain requires the integrity of both the vagal‐ and lamina terminalis‐associated pathways.
Post‐ischaemic mild hypothermia inhibits apoptosis in the penumbral region by reducing neuronal nitric oxide synthase activity and thereby preventing endothelin‐1‐induced hydroxyl radical formation
Authors: Van Hemelrijck An , Hachimi‐Idrissi Said , Sarre Sophie , Ebinger Guy , Michotte Yvette 
Published: September 2005

AbstractPreviously, we showed that treatment with resuscitative, post‐ischaemic mild hypothermia (34 °C for 2 h) reduced apoptosis in the penumbra (cortex), but not in the core (striatum) of an endothelin‐1 (Et‐1)‐induced focal cerebral infarct in the anaesthetized rat. Therefore, the purpose of this study was to investigate by which pathways resuscitative mild hypothermia exerts its neuroprotective effect in this model. The amino acids glutamate, serine, glutamine, alanine, taurine, arginine and the NO‐related compound citrulline were sampled from the striatum and cortex of the ischaemic hemisphere using in vivo microdialysis. The in vivo salicylate trapping method was applied for monitoring hydroxyl radical formation via 2,3 dihydroxybenzoic acid (2,3 DHBA) detection. Caspase‐3, neuronal nitric oxide synthase (nNOS) immunoreactivity and the volume of ischaemic damage were determined 24 h after the insult. In both the striatum and the cortex, Et‐1‐induced increases in glutamate, taurine and alanine were refractory to mild hypothermia. However, mild hypothermia significantly attenuated the ischaemia‐induced 2,3 DHBA levels and the nNOS immunoreactivity in the cortex, but not in the striatum. These observations were associated with a decreased caspase‐3 immunoreactivity. These results suggest that mild hypothermia exerts its neuroprotective effect in the penumbra partially by reducing nNOS activity and thereby preventing oxidative stress. Furthermore, we confirm our previous findings that the neuroprotective effect of resuscitative hypothermia is not mediated by changes in ischaemia‐induced amino acid release as they could not be associated with the ischaemia‐induced damage in the Et‐1 rat model.
Physiological hypoxia promotes survival of cultured cortical neurons
Authors: Li Dongdong , Marks Jeremy D. , Schumacker Paul T. , Young Regina M. , Brorson James R. 
Published: September 2005

AbstractPhysiological oxygen (O2) tensions in brain tissues vary widely, from ≈ 5 to 40 Torr (1–6%), encompassing levels of moderate hypoxia that have often been considered neurotoxic in vitro. The effects of such hypoxia were examined in embryonic murine cortical neurons cultured continuously from plating in an atmosphere of 1% O2. Remarkably, cortical neurons thrived in 1% O2, with survival at 7–14 days significantly greater than that of neurons cultured in ambient conditions (20% O2). Immunostaining for microtubule‐associated protein‐2 (MAP‐2) and NeuN confirmed the neuronal identity of surviving cells, and demonstrated robust development of dendritic structures and MAP‐2 expression in hypoxia. Survival of neurons in 20% O2 could be promoted by transfer of medium conditioned by neurons in 1% O2, or by pharmacological induction of hypoxia‐inducible factor‐1α (HIF‐1α), suggesting a possible role for secreted factors under transcriptional regulation by HIF‐1 in the trophic effects of hypoxia. Vascular endothelial growth factor (VEGF), a factor regulated by HIF‐1, was strongly stimulated in neurons cultured in 1% O2. Treatment of neurons with exogenous VEGF partially improved survival in 20% O2, and inhibitors of VEGF action reduced survival of neurons in 1% O2. These data point to the dynamic role played by hypoxia, associated with HIF‐1 up‐regulation, in promoting survival of cortical neurons, in part through stimulation of VEGF expression and release.
Excitability changes in human corticospinal projections to muscles moving hand and fingers while viewing a reaching and grasping action
Authors: Montagna Marcella , Cerri Gabriella , Borroni Paola , Baldissera Fausto 
Published: September 2005

AbstractExcitability of the H‐reflex in the relaxed flexor digitorum superficialis (FDS) muscle was tested in five subjects observing a reaching and grasping action. The amplitude of the FDS H‐reflex was modulated with a peak occurring during the hand‐opening phase of the observed movement. When the H‐reflex was facilitated by subliminal transcranial magnetic stimulation (TMS), the modulation was larger than for an unconditioned reflex of similar size. This suggests that the primary motor cortex excitability is modulated by action viewing and reasonably causes the motoneuronal excitability changes. Moreover, motor evoked potentials (MEPs) were elicited by supraliminal TMS in FDS, flexor carpi radialis (FCR) and first dorsal interosseus (FDI) when observing the same movement. MEP amplitude was modulated in FDS with the same time‐course as the H‐reflex, the peak excitability occurring during hand opening. In FDI, however, the maximal excitability occurred during finger closing while in FCR no correlation was found with the movement phases. Finally the EMG activity of FCR, FDS and FDI was recorded while the subjects were actually performing a grasping movement similar to the one observed. In all subjects and for each muscle there was a clear‐cut correspondence between the time‐course of the excitability modulation of MEPs and the temporal pattern of EMG recruitment. In conclusion, the present study suggests that ‘motor resonance’ subliminally activates the same motor pathways that would be overtly recruited in each observer when actually performing the observed movement, reproducing the personal strategy adopted in the same task.
The anti‐epileptic actions of neuropeptide Y in the hippocampus are mediated by Y2 and not Y5 receptors
Authors: El Bahh Bouchaïb , Balosso Silvia , Hamilton Trevor , Herzog Herbert , Beck‐Sickinger Annette G. , Sperk Günther , Gehlert Donald R. , Vezzani Annamaria , Colmers William F. 
Published: September 2005

AbstractNeuropeptide Y (NPY) potently inhibits glutamate release and seizure activity in rodent hippocampus in vitro and in vivo, but the nature of the receptor(s) mediating this action is controversial. In hippocampal slices from rats and several wild‐type mice, a Y2‐preferring agonist mimicked, and the Y2‐specific antagonist BIIE0246 blocked, the NPY‐mediated inhibition both of glutamatergic transmission and of epileptiform discharges in two different slice models of temporal lobe epilepsy, stimulus train‐induced bursting (STIB) and 0‐Mg2+ bursting. Whereas Y5 receptor‐preferring agonists had small but significant effects in vitro, they were blocked by BIIE0246, and a Y5 receptor‐specific antagonist did not affect responses to any agonist tested in any preparation. In slices from mice, NPY was without effect on evoked potentials or in either of the two slice seizure models. In vivo, intrahippocampal injections of Y2‐ or Y5‐preferring agonists inhibited seizures caused by intrahippocampal kainate, but again the Y5 agonist effects were insensitive to a Y5 antagonist. Neither Y2‐ nor Y5‐preferring agonists affected kainate seizures in mice. A Y5‐specific antagonist did not displace the binding of two different NPY ligands in WT or mice, whereas all NPY binding was eliminated in the mouse. Thus, we show that Y2 receptors alone mediate all the anti‐excitatory actions of NPY seen in the hippocampus, whereas our findings do not support a role for Y5 receptors either in vitro or in vivo. The results suggest that agonists targeting the Y2 receptor may be useful anticonvulsants.
Fyn kinase‐mediated phosphorylation of NMDA receptor NR2B subunit at Tyr1472 is essential for maintenance of neuropathic pain
Authors: Abe Tetsuya , Matsumura Shinji , Katano Tayo , Mabuchi Tamaki , Takagi Kunio , Xu Li , Yamamoto Akitsugu , Hattori Kotaro , Yagi Takeshi , Watanabe Masahiko , Nakazawa Takanobu , Yamamoto Tadashi , Mishina Masayoshi , Nakai Yoshihide , Ito Seiji 
Published: September 2005

AbstractDespite abundant evidence implicating the importance of N‐methyl‐d‐aspartate (NMDA) receptors in the spinal cord for pain transmission, the signal transduction coupled to NMDA receptor activation is largely unknown for the neuropathic pain state that lasts over periods of weeks. To address this, we prepared mice with neuropathic pain by transection of spinal nerve L5. Wild‐type, NR2A‐deficient, and NR2D‐deficient mice developed neuropathic pain; in addition, phosphorylation of NR2B subunits of NMDA receptors at Tyr1472 was observed in the superficial dorsal horn of the spinal cord 1 week after nerve injury. Neuropathic pain and NR2B phosphorylation at Tyr1472 were attenuated by the NR2B‐selective antagonist CP‐101,606 and disappeared in mice lacking Fyn kinase, a Src‐family tyrosine kinase. Concomitant with the NR2B phosphorylation, an increase in neuronal nitric oxide synthase activity was visualized in the superficial dorsal horn of neuropathic pain mice by NADPH diaphorase histochemistry. Electron microscopy showed that the phosphorylated NR2B was localized at the postsynaptic density in the spinal cord of mice with neuropathic pain. Indomethacin, an inhibitor of prostaglandin (PG) synthesis, and PGE receptor subtype EP1‐selective antagonist reduced the NR2B phosphorylation in these mice. Conversely, EP1‐selective agonist stimulated Fyn kinase‐dependent nitric oxide formation in the spinal cord. The present study demonstrates that Tyr1472 phosphorylation of NR2B subunits by Fyn kinase may have dual roles in the retention of NMDA receptors in the postsynaptic density and in activation of nitric oxide synthase, and suggests that PGE2 is involved in the maintenance of neuropathic pain via the EP1 subtype.
Biotic resistance to plant invasions? Native herbivores prefer non‐native plants
Authors: Parker John D. , Hay Mark E. 
Published: September 2005

AbstractIn contrast to expectations of the enemy release hypothesis, but consistent with the notion of biotic resistance, we found that native generalist crayfishes preferred exotic over native freshwater plants by a 3 : 1 ratio when plants were paired by taxonomic relatedness. Native crayfishes also preferred exotic over native plants when tested across 57 native and 15 exotic plants found growing sympatrically at 11 sites throughout the southeastern USA. Exotic grass carp that share little evolutionary history with most of these plants exhibited no preference for native vs. exotic species. Analyses of three terrestrial data sets showed similar patterns, with native herbivores generally preferring exotic plants, while exotic herbivores rarely exhibited a preference. Thus, exotic plants may escape their coevolved herbivores only to be preferentially consumed by the native generalist herbivores in their new ranges, suggesting that native herbivores may provide biotic resistance to plant invasions.
Magnitude and variability of process rates in fungal diversity‐litter decomposition relationships
Authors: Dang Christian K. , Chauvet Eric , Gessner Mark O. 
Published: September 2005

AbstractThere is compelling evidence that losses in plant diversity can alter ecosystem functioning, particularly by reducing primary production. However, impacts of biodiversity loss on decomposition, the complementary process in the carbon cycle, are highly uncertain. By manipulating fungal decomposer diversity in stream microcosm experiments we found that rates of litter decomposition and associated fungal spore production are unaffected by changes in decomposer diversity under benign and harsher environmental conditions. This result calls for caution when generalizing outcomes of biodiversity experiments across systems. In contrast to their magnitude, the variability of process rates among communities increased when species numbers were reduced. This was most likely caused by a portfolio effect (i.e. statistical averaging), with the uneven species distribution typical of natural communities tending to weaken that effect. Curbing species extinctions to maintain ecosystem functioning thus can be important even in situations where process rates are unaffected.