bluuebunny/crossref_metadata_2025_split huggingface dataset:
Deafness‐related plasticity in the inferior colliculus: gene expression profiling following removal of peripheral activity
Authors: Holt Avril Genene , Asako Mikiya , Lomax Catherine A. , MacDonald James W. , Tong Ling , Lomax Margaret I. , Altschuler Richard A. 
Published: June 2005

AbstractThe inferior colliculus (IC) is a major center of integration in the ascending as well as descending auditory pathways, where both excitatory and inhibitory amino acid neurotransmitters play a key role. When normal input to the auditory system is decreased, the balance between excitation and inhibition in the IC is disturbed. We examined global changes in gene expression in the rat IC 3 and 21 days following bilateral deafening, using Affymetrix GeneChip arrays and focused our analysis on changes in expression of neurotransmission‐related genes. Over 1400 probe sets in the Affymetrix Rat Genome U34A Array were identified as genes that were differentially expressed. These genes encoded proteins previously reported to change as a consequence of deafness, such as calbindin, as well as proteins not previously reported to be modulated by deafness, such as clathrin. A subset of 19 differentially expressed genes was further examined using quantitative RT–PCR at 3, 21 and 90 days following deafness. These included several GABA, glycine, glutamate receptor and neuropeptide‐related genes. Expression of genes for GABA‐A receptor subunits β2, β3, and γ2, plus ionotropic glutamate receptor subunits AMPA 2, AMPA 3, and kainate 2, increased at all three times. Expression of glycine receptor α1 initially declined and then later increased, while α2 increased sharply at 21 days. Glycine receptor α3 increased between 3 and 21 days, but decreased at 90 days. Of the neuropeptide‐related genes tested with qRT–PCR, tyrosine hydroxylase decreased approximately 50% at all times tested. Serotonin receptor 2C increased at 3, 21, and 90 days. The 5B serotonin receptor decreased at 3 and 21 days and returned to normal by 90 days. Of the genes tested with qRT–PCR, only glycine receptor α2 and serotonin receptor 5B returned to normal levels of expression at 90 days. Changes in GABA receptor β3, GABA receptor γ2, glutamate receptor 2/3, enkephalin, and tyrosine hydroxylase were further confirmed using immunocytochemistry.
Mapping the areas sensitive to long‐term endotoxin tolerance in the rat brain: a c‐fos mRNA study
Authors: Vallès Astrid , Martí Octavi , Armario Antonio 
Published: June 2005

AbstractWe have recently found that a single endotoxin administration to rats reduced the hypothalamic–pituitary–adrenal response to another endotoxin administration 4 weeks later, which may be an example of the well‐known phenomenon of endotoxin tolerance. However, the time elapsed between the two doses of endotoxin was long enough to consider the above results as an example of late tolerance, whose mechanisms are poorly characterized. To know if the brain plays a role in this phenomenon and to characterize the putative areas involved, we compared the c‐fos mRNA response after a final dose of endotoxin in animals given vehicle or endotoxin 4 weeks before. Endotoxin caused a widespread induction of c‐fos mRNA in the brain, similar to that previously reported by other laboratories. Whereas most of the brain areas were not sensitive to the previous experience with endotoxin, a few showed a reduced response in endotoxin‐pretreated rats: the parvocellular and magnocellular regions of the paraventricular hypothalamic nucleus, the central amygdala, the lateral division of the bed nucleus and the locus coeruleus. We hypothesize that late tolerance to endotoxin may involve plastic changes in the brain, likely to be located in the central amygdala. The reduced activation of the central amygdala in rats previously treated with endotoxin may, in turn, reduce the activation of other brain areas, including the hypothalamic paraventicular nucleus.
Occurrence and possible biological role of the endocannabinoid system in the sea squirt Ciona intestinalis
Authors: Matias Isabel , McPartland John M. , Di Marzo Vincenzo 
Published: June 2005

AbstractA cannabinoid receptor orthologue (CiCBR) has been described in the sea squirt Ciona intestinalis. Here we report that CiCBR mRNA expression is highest in cerebral ganglion, branchial pharynx, heart and testis of C. intestinalis, and that this organism also contains cannabinoid receptor ligands and some of the enzymes for ligand biosynthesis and inactivation. Using liquid chromatography–mass spectrometry, the endocannabinoid anandamide was found in all tissues analysed (0.063–5.423 pmol/mg of lipid extract), with the highest concentrations being found in brain and heart. The endocannabinoid 2‐arachidonoylglycerol (2‐AG) was fivefold more abundant than anandamide, and was most abundant in stomach and intestine and least abundant in heart and ovaries (2.677–50.607 pmol/mg of lipid extract). Using phylogenomic analysis, we identified orthologues of several endocannabinoid synthesizing and degrading enzymes. In particular, we identified and partly sequenced a fatty acid amide hydrolase (FAAH) orthologue, showing 44% identity with human FAAH and containing nearly all the amino acids necessary for a functional FAAH enzyme. Ciona intestinalis also contained specific binding sites for cannabinoid receptor ligands, and an amidase enzyme with pH‐dependency and subcellular/tissue distribution similar to mammalian FAAHs. Finally, a typical C. intestinalis behavioural response, siphon reopening after closure induced by mechanical stimulation, was inhibited by the cannabinoid receptor agonist HU‐210, and this effect was significantly attenuated by mammalian cannabinoid receptor antagonists.
GalR1, but not GalR2 or GalR3, levels are regulated by galanin signaling in the locus coeruleus through a cyclic AMP‐dependent mechanism
Authors: Hawes Jessica J. , Brunzell Darlene H. , Wynick David , Zachariou Venetia , Picciotto Marina R. 
Published: June 2005

AbstractThe galanin receptors GalR1, GalR2 and GalR3 are widely expressed throughout the mouse brain and are enriched in catecholaminergic nuclei. Here, we show that GalR1 protein levels are regulated by neuronal activity and changes in cAMP levels. GalR1, but not GalR2 or GalR3, is specifically up‐regulated in the LC‐like Cath.a cell line in a cAMP‐dependent manner. GalR1 protein and mRNA levels are also up‐regulated in the LC of galanin knockout mice, whereas GalR2 and GalR3 are not. Lack of galanin‐maintained cAMP tone in the galanin knockout mouse appears to result in a loss of negative feedback resulting in increased levels of CREB phosphorylation and increased GalR1 expression. These findings suggest that changes in levels of GalR1 may play an important role in modulating signaling events and neuroplasticity underlying physiological functions of the LC.
Nuclear/cytoplasmic shuttling of the transcription factor FoxO1 is regulated by neurotrophic factors
Authors: Gan Lixia , Zheng Wenhua , Chabot Jean‐Guy , Unterman Terry G. , Quirion Remi 
Published: June 2005

AbstractFoxO1, a member of the FoxO subfamily of forkhead transcription factors, is an important target for insulin and growth factor signaling in the regulation of metabolism, cell cycle and proliferation, and survival in peripheral tissues. However, its role in the central nervous system is mostly unknown. In this study, we examined the effect of neurotrophic factors on nuclear/cytoplasmic shuttling of FoxO1. We showed that insulin‐like growth factor‐1 (IGF‐1) and nerve growth factor (NGF) potently induced the nuclear exclusion of FoxO1‐green fluorescent protein (GFP) while neurotrophin (NT)‐3 and NT‐4 were much weaker and brain‐derived neurotrophic factor (BDNF) failed to induce FoxO1 translocation in PC12 cells. FoxO1 translocation was inhibited by LY294002, a well‐established PI3K/Akt kinase inhibitor. Moreover, FoxO1 was phosphorylated at Thr24 and Ser256 residues by the above neurotrophic factors, with the exception of BDNF. Triple mutant FoxO1, in which three Akt/PKB phosphorylation sites (Thr24, Ser256 and Ser319) were mutated to alanine, resulted in the complete nuclear targeting of the expressed FoxO1‐GFP fusion protein in the presence of the above neurotrophic factors in both PC12 cells and cultured hippocampal and cortical neurons. Taken together, these findings demonstrate that neurotrophic factors are able to regulate nuclear/cytoplasmic shuttling of FoxO1 via the PI3K/Akt pathway in neuronal cells.
Molecular and neurochemical evidence for the biosynthesis of dehydroepiandrosterone in the adult rat spinal cord
Authors: Kibaly Cherkaouia , Patte‐Mensah Christine , Mensah‐Nyagan Ayikoe G. 
Published: June 2005

AbstractVarious studies have indicated that exogenous dehydroepiandrosterone (DHEA) modulates several mechanisms in the CNS of rodents. As adult rodent glands do not secrete significant amounts of DHEA, its role as endogenous modulator of the CNS remains possible only if DHEA is produced by nerve cells. Therefore, the last decade has been marked by diverse unsuccessful investigations aiming to demonstrate the activity of cytochrome P450c17 (P450c17), the key DHEA‐synthesizing enzyme, in adult rodent CNS. Here, we combined molecular, anatomical, cellular and neurochemical approaches to provide the first demonstration of the existence of P450c17 and bioactivity in adult rat spinal cord (SC). Real‐time RT‐PCR revealed P450c17 gene expression in all SC segments. Western blot analyses allowed identification of a specific P450c17 protein in the SC and immunohistochemical studies localized P450c17 in neurones and glial cells. Pulse‐chase experiments combined with HPLC and radioactive steroid detection showed that SC slices converted [3H]pregnenolone into [3H]DHEA, a conversion markedly reduced by ketoconazole, a P450c17 inhibitor. Kinetics studies revealed accumulation of [3H]DHEA newly synthesized by SC slices in the incubation medium as its amount declined slowly. This first cellular mapping of an active P450c17 in adult rodent SC suggests that endogenous DHEA synthesized in spinal neural networks may control various spinally‐mediated activities.
HIV‐Tat protein induces P‐glycoprotein expression in brain microvascular endothelial cells
Authors: Hayashi Kentaro , Pu Hong , Tian Jing , Andras Ibolya E. , Lee Yong Woo , Hennig Bernhard , Toborek Michal 
Published: June 2005

AbstractAmong the different factors which can contribute to CNS alterations associated with HIV infection, Tat protein is considered to play a critical role. Evidence indicates that Tat can contribute to brain vascular pathology through induction of endothelial cell activation. In the present study, we hypothesized that Tat can affect expression of P‐glycoprotein (P‐gp) in brain microvascular endothelial cells (BMEC). P‐gp is an ATP‐dependent cellular efflux transporter which is involved in the removal of specific non‐polar molecules, including drugs used for highly active antiretroviral therapy (HAART). Treatment of BMEC with Tat1−72 resulted in P‐gp overexpression both at mRNA and protein levels. These alterations were confirmed in vivo in brain vessels of mice injected with Tat1−72 into the hippocampus. Furthermore, pre‐treatment of BMEC with SN50, a specific NF‐κB inhibitor, protected against Tat1−72‐stimulated expression of mdr1a gene, i.e. the gene which encodes for P‐gp in rodents. Tat1−72‐mediated changes in P‐gp expression were correlated with increased rhodamine 123 efflux, indicating the up‐regulation of transporter functions of P‐gp. These results suggest that Tat‐induced overexpression of P‐gp in brain microvessels may have significant implications for the development of resistance to HAART and may be a contributing factor for low efficacy of HAART in the CNS.
Dopaminergic neurons in rat ventral midbrain cultures undergo selective apoptosis and form inclusions, but do not up‐regulate iHSP70, following proteasomal inhibition
Authors: Rideout Hardy J. , Lang‐Rollin Isabelle C. J. , Savalle Magali , Stefanis Leonidas 
Published: June 2005

AbstractDysfunction of the ubiquitin‐dependent protein degradation system, either at the level of the proteasome itself, or at the level of ubiquitination, may play a role in the pathogenesis of Parkinson's disease (PD) and other related neurodegenerative disorders. We have employed a cellular model of this dysfunction in which lactacystin or epoxomicin, selective pharmacological inhibitors of the proteasome, are applied to primary cultures of embryonic rat ventral midbrain. Proteasomal inhibition with either agent led to apoptotic death specifically within phenotypically defined tyrosine hydroxylase (TH)‐positive dopaminergic neurons, with little or no apoptotic death induced in GABAergic neurons. Inhibition of the proteasome also led to the formation of ubiquitin and α‐synuclein‐positive cytoplasmic inclusions in TH‐positive and TH‐negative neurons. Inclusions were observed in viable as well as apoptotic neurons, and required new or ongoing transcription. Tyrosine hydroxylase immunolabeling was often present within the inclusions. Such mislocalization may lead to dysfunction of dopamine biosynthesis. Interestingly, dopaminergic neurons, unlike other neurons within these cultures or cultured cortical neurons, failed to induce the chaperone Hsp70 in response to proteasomal inhibition. This failure may explain in part the increased sensitivity of these neurons to proteasomal inhibitors.
Chronic nicotine differentially affects the function of nicotinic receptor subtypes regulating neurotransmitter release
Authors: Grilli Massimo , Parodi Monica , Raiteri Maurizio , Marchi Mario 
Published: June 2005

AbstractIt is known that nicotine can activate several subtypes of release‐regulating presynaptic nicotinic receptors (nAChRs) including those situated on central noradrenergic, dopaminergic, cholinergic and glutamatergic axon terminals. The objective of this study was to investigate the effects of chronic administration of (–)nicotine on the function of the above autoreceptors and heteroreceptors using rat superfused synaptosomes. In hippocampal synaptosomes prelabelled with [3H]noradrenaline (NA) the nicotine‐evoked overflow of [3H]NA was higher in rats treated with nicotine for 10 days (via osmotic mini‐pumps) than in vehicle‐treated rats. In striatal synaptosomes, prelabelled with [3H]dopamine (DA), chronic nicotine did not modify the releasing effect of nicotine. No significant change was observed in experiments with synaptosomes from nucleus accumbens prelabelled with [3H]DA. Exposure of hippocampal synaptosomes prelabelled with [3H]choline to nicotine elicited release of [3H]acetylcholine; this effect was almost abolished in synaptosomes from animals administered nicotine for 10 days, suggesting down‐regulation of nicotinic autoreceptors. In hippocampal synaptosomes prelabelled with [3H]d‐aspartate, the releasing effect of epibatidine following chronic nicotine treatment did not differ from that in controls. The K+‐evoked exocytotic release of the neurotransmitters tested was not modified by long‐term nicotine administration. The results show that chronic nicotine differentially affects the function of release‐regulating nAChR subtypes.
Lactate induces tumour necrosis factor‐α, interleukin‐6 and interleukin‐1β release in microglial‐ and astroglial‐enriched primary cultures
Authors: Andersson Anna K. , Rönnbäck Lars , Hansson Elisabeth 
Published: June 2005

AbstractHyperammonaemia has deleterious effects on the CNS in patients with liver dysfunction. Cellular mechanisms underlying the effects of hyperammonaemia are largely unknown, although astrocytes have been the main target of interest. This study investigated how treatment with NH4Cl and lactate, which increase in the brain as a consequence of hyperammonaemia, affects cells in primary rat cultures enriched in either astrocytes or microglia. Morphological changes were studied over time using light microscopy. Release of the proinflammatory cytokines tumour necrosis factor‐α (TNF‐α), interleukin (IL)‐6 and IL‐1β was measured using ELISA. NH4Cl was found to induce vacuole formation in both culture systems. Lactate treatment altered astrocytic appearance, resulting in increased space between individual cells. Microglia adopted a round morphology with either NH4Cl or lactate treatment. Lactate, but not NH4Cl, induced release of TNF‐α and IL‐6 in both astroglial‐ and microglial‐enriched cultures, while IL‐1β was released only in microglial cultures. Cytokine release was higher in the microglial‐ than in the astroglial‐enriched cultures. Additionally, the astroglial‐enriched cultures containing approximately 10% microglial cells released more cytokines than cultures containing about 5% microglial cells. Taken together, our data suggest that most TNF‐α, IL‐6 and IL‐1β release comes from microglia. Thus, microglia could play an important role in the pathological process of hyperammonaemia.
Metabotropic glutamate receptors and neuroadaptation to antidepressants: imipramine‐induced down‐regulation of β‐adrenergic receptors in mice treated with metabotropic glutamate 2/3 receptor ligands
Authors: Matrisciano F. , Scaccianoce S. , Del Bianco P. , Panaccione I. , Canudas A. M. , Battaglia G. , Riozzi B. , Ngomba R. T. , Molinaro G. , Tatarelli R. , Melchiorri D. , Nicoletti F. 
Published: June 2005

AbstractAntidepressant drugs have a clinical latency that correlates with the development of neuroadaptive changes, including down‐regulation of β‐adrenergic receptors in different brain regions. The identification of drugs that shorten this latency will have a great impact on the treatment of major depressive disorders. We report that the time required for the antidepressant imipramine to reduce the expression of β‐adrenergic receptors in the hippocampus is reduced by a co‐administration with centrally active ligands of type 2/3 metabotropic glutamate (mGlu2/3) receptors. Daily treatment of mice with imipramine alone (10 mg/kg, i.p.) reduced the expression of β‐adrenergic receptors in the hippocampus after 21 days, but not at shorter times, as assessed by western blot analysis of β1‐adrenergic receptors and by the amount of specifically bound [3H]CGP‐12177, a selective β‐adrenergic receptor ligand. Down‐regulation of β‐adrenergic receptors occurred at shorter times (i.e. after 14 days) when imipramine was combined with low doses (0.5 mg/kg, i.p.) of the selective mGlu2/3 receptor agonist LY379268, or with the preferential mGlu2/3 receptor antagonist LY341495 (1 mg/kg, i.p.). Higher doses of LY379268 (2 mg/kg, i.p.) were inactive. This intriguing finding suggests that neuroadaptation to imipramine – at least as assessed by changes in the expression of β1‐adrenergic receptors – is influenced by drugs that interact with mGlu2/3 receptors and stimulates further research aimed at establishing whether any of these drugs can shorten the clinical latency of classical antidepressants.
Being Feminist
Authors: Lister Ruth 
Published: June 2005

AbstractThe article starts by locating both the author and men in relation to feminism as an identity, which cuts across the public–private divide. It then attempts to illuminate the meaning of ‘being feminist’ by addressing three, tightly interwoven, issues. First is the question: what is the ‘woman’ who is the subject of feminism? The second section discusses the nature of feminism in its various guises, focusing mainly on feminism in Britain since the late 1960s. It engages with the notions of ‘post-feminism’, ‘global sisterhood’ and a ‘third wave’. Finally, the article analyses critically feminism's uneasy relationship with identity politics.
Biofeedback, Migraine Headache and New Symptom Formation
Authors: Szajnberg Nathan , Diamond Seymour 
Published: June 2005

SYNOPSISIn this retrospective study of 12 migraine patients successfully treated with biofeedback, we find that 67% experienced some form of symptom substitution. This manifested as classical psychosomatic symptoms, clinical depression, or a quasi‐delusional belief in controlling one's own or others' thoughts or feelings.
Effect of Isometheptene on the Distribution and Shunting of 15μ M Microspheres Throughout the Cephalic Circulation of the Cat
Authors: Spierings Egilius L.H. , Saxena Pramod R. 
Published: June 2005

SYNOPSISWe have studied the effect of isometheptene, an indirectly acting sympathomimetic with a reported anti‐migraine action, on carotid blood flow and the distribution of carotid blood flow throughout the cephalic circulation of the cat, using 15μm‐microspheres. Microspheres measuring 15μm in diameter were used to separate capillary flow from flow through the arteriovenous anastomoses. Apart from decreasing carotid blood flow, isometheptene vigorously reduced the fraction of carotid blood flow shunted through the arteriovenous anastomoses. This mode of action of isometheptene may be relevant to its beneficial effect in migraine.
Cluster Headache: Response to Chlorpromazine
Authors: Caviness Verne S. , O'Brien Patrick 
Published: June 2005

SYNOPSISChlorpromazine (CPZ), in doses ranging from 75–700 mg per day, gave full headache relief in twelve of thirteen (93%) of patients with the cluster headache syndrome. For nine, withdrawal of CPZ within two to three weeks was tolerated without recurrence of symptoms. After a period of extended remission, four of these found CPZ equally effective treatment for subsequent attacks. Three others received sustained relief from headache over six to eight months on maintenance CPZ at 75 mg per day although the cluster was not terminated. The apparent effectiveness of CPZ in this limited series is greater than that of other medications currently employed in the treatment of cluster headaches.
A Replication and Generalization of the “Psychobiological” Model of Headache
Authors: Thompson J. Kevin , Haber Joel D. , Figueroa Jorge Luis , Adams Henry E. 
Published: June 2005

SYNOPSISBakal and Kaganov 1 recently reported data supporting a “psychobiological” approach to the study of headache pain. Their results suggested that individuals delineated by degree of self‐reported headache pain would differ on quantitative rather than qualitative headache characteristics. The present study was an attempt to systematically replicate and generalize the above findings. Seventy‐eight undergraduates and 25 chronic headache patients rated the extent to which common symptoms accompanied their “usual” headache on a five point scale. Subjects were divided into groups on the basis of: subjective ratings of headache problem, headache frequency, and headache type. Results were consistent with the psychobiological model. Individuals rating degree of headache problem as moderate or severe reported a significantly greater incidence of symptoms than non‐problem subjects. Headache frequency was not related to quantitative differences in headache symptomatology. Migraine and chronic muscle contraction (CMC) patients reported similar symptoms that differed significantly on quantitative (frequency) characteristics. The results replicate and generalize Bakal and Kaganov's findings and suggest that the model may help explain etiological factors in headache development. Results are discussed with regard to the need for future research in the area.
The Biochemistry of Migraine
Authors: Bruyn G.W. 
Published: June 2005

SYNOPSISIn the stereotyped, transient and paroxysmal triad of autonomic, vascular and nociceptive dysfunction, precipitated by non‐specific factors, known as the migraine attack certain biochemical mediators appear to occupy key‐positions in the chain of pathomechanic events occurring at the neural and humoral interface.Of these are reviewed: histamine and serotonin (inhibitory at the microvascular level), substance P and the kinins (excitatory at the nociceptive neural level), tyramine as an a‐adrenergic activator, and prostaglandins as humoral agents acting on certain cell‐membranes. Anatomical, clinical and biochemical arguments are marshalled to bring the neurogenic origin of the migraine attack into focus, in particular at hypothalamic level.