Supplement ... to the European journal of neuroscience最新文献_第3页

Beta-amyloid peptide potentiates inflammatory responses induced by lipopolysaccharide, interferon -gamma and 'advanced glycation endproducts' in a murine microglia cell line. 在小鼠小胶质细胞系中，β -淀粉样肽增强由脂多糖、干扰素- γ和“晚期糖基化终产物”诱导的炎症反应。

Supplement ... to the European journal of neuroscience Pub Date : 2002-09-01 DOI: 10.1240/SAV_GBM_2002_H_000162

J. Gasic‐Milenkovic, S. Dukic-Stefanovic, W. Deuther-Conrad, U. Gärtner, G. Münch

{"title":"Beta-amyloid peptide potentiates inflammatory responses induced by lipopolysaccharide, interferon -gamma and 'advanced glycation endproducts' in a murine microglia cell line.","authors":"J. Gasic‐Milenkovic, S. Dukic-Stefanovic, W. Deuther-Conrad, U. Gärtner, G. Münch","doi":"10.1240/SAV_GBM_2002_H_000162","DOIUrl":"https://doi.org/10.1240/SAV_GBM_2002_H_000162","url":null,"abstract":"beta-Amyloid (Abeta) plaques are characteristic hallmarks of Alzheimer's disease (AD). In AD, it has been suggested that activation of microglial cells might be the link between Abeta deposition and neuronal degeneration. Activated microglia are associated with senile plaques and produce free radicals and inflammatory cytokines. However, it is still not clear whether Abeta needs a prestimulated environment to exert its proinflammatory potential. Advanced glycation endproducts (AGEs), protein-bound oxidation products of sugars, have been shown to accumulate in senile plaques and could induce a silent but chronic inflammation in the AD brain. We tested whether Abeta acts as an amplifier of a submaximal proinflammatory response initiated by exposure to chicken egg albumin-AGE, lipopolysaccharide or interferon-gamma. Synthetic Abeta was used to produce three different samples (Abeta-fibrilar; Abeta-aggregated; Abeta-AGE), which were characterized for beta-sheeted fibrils by the thioflavin-T test and electron microscopy. As markers of microglial activation, nitric oxide, interleukin-6, macrophage-colony stimulation factor and tumour necrosis factor-alpha production was measured. All three Abeta samples alone could not induce a detectable microglial response. The combination of Abeta preparations, however, with the coinducers provoked a strong microglial response, whereby Abeta-AGE and fibrilar Abeta were more potent inflammatory signals than aggregated Abeta. Thus, Abeta in senile plaques can amplify microglial activation by a coexisting submaximal inflammatory stimulus. Hence, anti-inflammatory therapeutics could either target the primary proinflammatory signal (e.g. by limiting AGE-formation by AGE inhibitors or cross-link breakers) or the amplifyer Abeta (e.g. by limiting Abeta production by beta- or gamma-secretase inhibitors).","PeriodicalId":79424,"journal":{"name":"Supplement ... to the European journal of neuroscience","volume":"66 1","pages":"813-21"},"PeriodicalIF":0.0,"publicationDate":"2002-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76965482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 44

Direction of cross-modal information transfer affects human brain activation: a PET study. 跨模态信息传递方向影响人脑激活:PET研究。

Supplement ... to the European journal of neuroscience Pub Date : 2002-01-01 DOI: 10.1016/S0168-0102(00)81090-1

R. Kawashima, J. Watanabe, Takashi Kato, A. Nakamura, K. Hatano, T. Schormann, Kazunori Sato, H. Fukuda, Kengo Ito, K. Zilles

引用次数: 13

Odour-evoked [Ca2+] transients in mitral cell dendrites of frog olfactory glomeruli. 气味诱发的蛙嗅肾小球二尖瓣细胞树突[Ca2+]瞬变。

Supplement ... to the European journal of neuroscience Pub Date : 2001-05-01 DOI: 10.1046/J.1460-9568.2001.01545.X/PDF

K. Delaney, I. Davison, W. Denk

{"title":"Odour-evoked [Ca2+] transients in mitral cell dendrites of frog olfactory glomeruli.","authors":"K. Delaney, I. Davison, W. Denk","doi":"10.1046/J.1460-9568.2001.01545.X/PDF","DOIUrl":"https://doi.org/10.1046/J.1460-9568.2001.01545.X/PDF","url":null,"abstract":"We measured Ca2+ concentration, [Ca2+], transients in mitral cell distal apical dendritic tufts produced by physiological odour stimulation of the olfactory epithelium and electrical stimulation of the olfactory nerve (ON) using two-photon scanning and conventional wide-field microscopy of Ca2+-Green-1 dextran in an in vitro frog nose-brain preparation. Weak or strong ON shock-evoked fluorescence transients always had short latency with an onset 0-10 ms after the onset of the bulb local field potential, rapidly increasing to a peak of up to 25% fractional fluorescence change (DeltaF/F) in 10-30 ms, were blocked by 10 microM CNQX, decaying with a time constant of about 1 s. With stronger ON shocks that activated many receptor axons, an additional, delayed, sustained AP5-sensitive component (peak at approximately 0.5 s, up to 40% DeltaF/F maximum) could usually be produced. Odour-evoked [Ca2+] transients sometimes displayed a rapid onset phase that peaked within 50 ms but always had a sustained phase that peaked 0.5-1.5 s after onset, regardless of the strength of the odour or the amplitude of the response. These were considerably larger (up to 150% DeltaF/F) than those evoked by ON shock. Odour-evoked [Ca2+] transients were also distinguished from ON shock-evoked transients by tufts in different glomeruli responding with different delays (time to onset differed by up to 1.5 s between different tufts for the same odour). Odour-evoked [Ca2+] transients were increased by AMPA-kainate receptor blockade, but substantially blocked by AP5. Electrical stimulation of the lateral olfactory tract (5-6 stimuli at 10 Hz) that evoked granule cell feedback inhibition, blocked 60-100% of the odour-evoked [Ca2+] transient in tufts when delivered within about 0.5 s of the odour. LOT-mediated inhibition was blocked by 10 microM bicuculline.","PeriodicalId":79424,"journal":{"name":"Supplement ... to the European journal of neuroscience","volume":"14 1","pages":"1658-72"},"PeriodicalIF":0.0,"publicationDate":"2001-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73355870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 23

Neurotrophins BDNF and NT-3 promote axonal re-entry into the distal host spinal cord through Schwann cell-seeded mini-channels. 神经营养因子BDNF和NT-3通过雪旺细胞微通道促进轴突重新进入远端宿主脊髓。

Supplement ... to the European journal of neuroscience Pub Date : 2001-01-01 DOI: 10.1046/J.1460-9568.2001.01387.X

Norman I. Bamber, Huaying Li, Xiaobin Lu, M. Oudega, Patrick Aebischer, Xiao Ming Xu

{"title":"Neurotrophins BDNF and NT-3 promote axonal re-entry into the distal host spinal cord through Schwann cell-seeded mini-channels.","authors":"Norman I. Bamber, Huaying Li, Xiaobin Lu, M. Oudega, Patrick Aebischer, Xiao Ming Xu","doi":"10.1046/J.1460-9568.2001.01387.X","DOIUrl":"https://doi.org/10.1046/J.1460-9568.2001.01387.X","url":null,"abstract":"To promote axonal regeneration in the injured adult spinal cord, a two-phase repair strategy was employed to (i) bridge a spinal cord hemilesion cavity with a grafted Schwann cell (SC)-seeded mini-channel, and (ii) promote axonal re-entry into the distal cord by infusing two neurotrophins, BDNF and/or NT-3, directly into the distal cord parenchyma. Here we report that infusion of two neurotrophins, delivered alone or in combination, effectively promotes axonal outgrowth from SC-seeded mini-channels into the distal host spinal cord. When an anterogradely transported marker, PHA-L or BDA, was injected into the spinal cord 3 mm rostral to the graft, a large number of axons was observed to regenerate from the SC graft into the distal cord in neurotrophin-treated groups. A subpopulation of these axons was found to grow up to 6 mm within the distal spinal cord. These axons, which were confined mainly within the grey matter, arborized and formed structures which resemble terminal boutons. In channels containing no SCs, the infusion of neurotrophins did not promote axonal ingrowth from the proximal cord stump. In cases which received SC grafts but no neurotrophin infusion, axonal re-entry into the distal cord was limited. Thus, the present study demonstrates that regenerating axons not only cross a lesion site when a permissive cellular bridge is provided but also penetrate into the distal host spinal cord and elongate for a distance of several cord segments after the infusion of two neurotrophins. The latter event is prerequisite for establishment of appropriate connections between regenerating axons and target neurons and thus, functional recovery.","PeriodicalId":79424,"journal":{"name":"Supplement ... to the European journal of neuroscience","volume":"78 1","pages":"257-68"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74520912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 205

p35/cdk5 binds and phosphorylates beta-catenin and regulates beta-catenin/presenilin-1 interaction. P35 /cdk5结合和磷酸化-catenin并调节-catenin/早老素-1的相互作用。

Supplement ... to the European journal of neuroscience Pub Date : 2001-01-01 DOI: 10.1046/J.1460-9568.2001.01376.X

S. Kesavapany, K. Lau, D. McLoughlin, J. Brownlees, S. Ackerley, P. Leigh, C. Shaw, C. Miller

{"title":"p35/cdk5 binds and phosphorylates beta-catenin and regulates beta-catenin/presenilin-1 interaction.","authors":"S. Kesavapany, K. Lau, D. McLoughlin, J. Brownlees, S. Ackerley, P. Leigh, C. Shaw, C. Miller","doi":"10.1046/J.1460-9568.2001.01376.X","DOIUrl":"https://doi.org/10.1046/J.1460-9568.2001.01376.X","url":null,"abstract":"The neuronal cyclin-dependent kinase p35/cdk5 comprises a catalytic subunit (cdk5) and an activator subunit (p35). To identify novel p35/cdk5 substrates, we utilized the yeast two-hybrid system to screen for human p35 binding partners. From one such screen, we identified beta-catenin as an interacting protein. Confirmation that p35 binds to beta-catenin was obtained by using glutathione S-transferase (GST)-beta-catenin fusion proteins that interacted with both endogenous and transfected p35, and by showing that beta-catenin was present in p35 immunoprecipitates. p35 and beta-catenin also displayed overlapping subcellular distribution patterns in cells including neurons. Finally, we demonstrated that p35/cdk5 phosphorylates beta-catenin. beta-catenin also binds to presenilin-1 and altered beta-catenin/presenilin-1 interactions may be mechanistic in Alzheimer's disease (AD). Abnormal p35/cdk5 activity has also been suggested to contribute to AD. We therefore investigated how modulation of p35/cdk5 activity influenced beta-catenin/presenilin-1 interactions. Inhibition of p35/cdk5 with roscovitine did not alter the steady state levels of either beta-catenin or presenilin-1 but reduced the amount of presenilin-1 bound to beta-catenin. Thus, p35/cdk5 binds and phosphorylates beta-catenin and regulates its binding to presenilin-1. The findings reported here therefore provide a novel molecular framework to connect p35/cdk5 with beta-catenin and presenilin-1 in AD.","PeriodicalId":79424,"journal":{"name":"Supplement ... to the European journal of neuroscience","volume":"13 1","pages":"241-7"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86372018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 91

Astrocyte-endothelial cell calcium signals conveyed by two signalling pathways. 星形胶质细胞-内皮细胞钙信号通过两条信号通路传递。

Supplement ... to the European journal of neuroscience Pub Date : 2001-01-01 DOI: 10.1046/j.1460-9568.2001.01372.x

K. Braet, K. Paemeleire, K. D’Herde, M. Sanderson, L. Leybaert

{"title":"Astrocyte-endothelial cell calcium signals conveyed by two signalling pathways.","authors":"K. Braet, K. Paemeleire, K. D’Herde, M. Sanderson, L. Leybaert","doi":"10.1046/j.1460-9568.2001.01372.x","DOIUrl":"https://doi.org/10.1046/j.1460-9568.2001.01372.x","url":null,"abstract":"Astrocytes and endothelial cells are in close contact with each other at the blood-brain barrier, where important molecular transports take place. Despite these key morphological and functional properties, little is known regarding the dynamic signalling processes that occur between these two cell types. We investigated astrocyte-endothelial cell calcium signalling mechanisms in a coculture model prepared from primary rat cortical astrocytes and ECV304 cells. We used flash photolysis of caged inositol-trisphosphate (IP3) and gentle mechanical stimulation to trigger astrocyte-endothelial cell calcium signals and to investigate the underlying propagation mechanisms. Photolytically releasing IP3 in a single cell triggered increases in cytoplasmic calcium concentration that propagated between astrocytes and endothelial cells in either direction. These propagating calcium signals did not cross cell-free zones and were not affected by fast superfusion or by the purinergic inhibitors apyrase and suramin, indicating that they are communicated through an intracellular pathway in conjunction with gap junctions. Electrophysiological experiments confirmed a low degree of astrocyte-endothelial cell electrical cell-to-cell coupling. Mechanical stimulation of a single cell also triggered astrocyte-endothelial cell calcium signals but, in contrast to the former triggering mode, these signals crossed cell-free zones and were significantly inhibited by apyrase, thus indicating the involvement of an extracellular and purinergic messenger. Astrocyte-endothelial cell calcium signalling also occurred in cocultures prepared with astrocytes and primary rat brain capillary endothelial cells. We conclude that astrocytes and endothelial cells can exchange fast-acting calcium signals (time scale of seconds) that can be communicated through an intracellular/gap junctional pathway and an extracellular purinergic pathway.","PeriodicalId":79424,"journal":{"name":"Supplement ... to the European journal of neuroscience","volume":"49 1","pages":"79-91"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84861377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 54

Antisense knockdown of the glial glutamate transporter GLT-1 exacerbates hippocampal neuronal damage following traumatic injury to rat brain. 神经胶质谷氨酸转运体GLT-1的反义敲低加重了大鼠脑外伤后海马神经元的损伤。

Supplement ... to the European journal of neuroscience Pub Date : 2001-01-01 DOI: 10.1046/J.1460-9568.2001.01367.X

V. Rao, A. Dogan, K. Bowen, K. Todd, R. Dempsey, R. Dempsey

{"title":"Antisense knockdown of the glial glutamate transporter GLT-1 exacerbates hippocampal neuronal damage following traumatic injury to rat brain.","authors":"V. Rao, A. Dogan, K. Bowen, K. Todd, R. Dempsey, R. Dempsey","doi":"10.1046/J.1460-9568.2001.01367.X","DOIUrl":"https://doi.org/10.1046/J.1460-9568.2001.01367.X","url":null,"abstract":"Traumatic injury to rat brain induced by controlled cortical impact (CCI) results in chronic neuronal death in the hippocampus. In the normal brain, glutamate transporters actively clear the glutamate released synaptically to prevent receptor overactivation and excitotoxicity. Glutamate transporter 1 (GLT-1) is the most abundant and active glutamate transporter, which mediates the bulk of glutamate uptake. CCI injury significantly decreased GLT-1 mRNA (by 49-66%, P < 0.05) and protein (by 29-44%, P < 0.05) levels in the ipsilateral hippocampus, compared with either the respective contralateral hippocampus or the sham-operated control, 24-72 h after the injury. CCI injury in rats infused with GLT-1 antisense oligodeoxynucleotides (ODNs) exacerbated the hippocampal neuronal death and mortality, compared with the GLT-1 sense/random ODN-infused controls. At 7 days after the injury, hippocampal neuronal numbers were significantly lower in the CA1 (reduced by 32%, P < 0.05), CA2 (by 45%, P < 0.01), CA3 (by 68%, P < 0.01) and dentate gyrus (by 31%, P < 0.05) in GLT-1 antisense ODN-infused rats, compared with the GLT-1 sense/random ODN-infused controls. This study suggested a role for GLT-1 dysfunction in promoting the hippocampal neuronal death after traumatic brain injury.","PeriodicalId":79424,"journal":{"name":"Supplement ... to the European journal of neuroscience","volume":"43 1","pages":"119-28"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77445481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 107

Evidence that a single exposure to aversive stimuli triggers long-lasting effects in the hypothalamus-pituitary-adrenal axis that consolidate with time. 有证据表明，单次暴露于厌恶刺激会在下丘脑-垂体-肾上腺轴上引发持久的影响，并随着时间的推移而巩固。

Supplement ... to the European journal of neuroscience Pub Date : 2001-01-01 DOI: 10.1046/J.1460-9568.2001.01355.X

O. Martı́, Arantxa García, Astrid Vellès, M. Harbuz, Antonio Armario

{"title":"Evidence that a single exposure to aversive stimuli triggers long-lasting effects in the hypothalamus-pituitary-adrenal axis that consolidate with time.","authors":"O. Martı́, Arantxa García, Astrid Vellès, M. Harbuz, Antonio Armario","doi":"10.1046/J.1460-9568.2001.01355.X","DOIUrl":"https://doi.org/10.1046/J.1460-9568.2001.01355.X","url":null,"abstract":"Because of its use as a negative reinforcer in animal studies and its potential pathological impact (e.g. post-traumatic stress disorder and depression), exposure to aversive stimuli is a relevant model for studying CNS plasticity. We present evidence that a single exposure to two predominantly emotional stressors [restraint in tubes and immobilization on wooden boards (IMO)] can modify the response of the hypothalamo-pituitary-adrenal (HPA) axis to a subsequent exposure to the same stressor days later in that a more rapid return to the baseline was observed in the poststress period. In addition, the effect was greater with IMO, the more severe stressor. Using IMO, we have further demonstrated that the effect of a previous single exposure to the stressor (i) increased with days elapsed between the two exposures; (ii) was specific for the previously experienced stressor; and (iii) was mediated via central-mediated effects [corticotropin-releasing factor (CRF) mRNA in the paraventricular nucleus of the hypothalamus]. These data suggest that animals retain memory about a single experience with stressors, resulting in an acceleration of the poststress recovery of the HPA axis that enhances progressively over a period of weeks. The extent to which the present data are relevant regarding post-traumatic stress disorders is unclear, but the study of the HPA response to severe stressors may be suitable for the study of the neurobiological basis of the progressive consolidation of learning over a long period of time (days to weeks).","PeriodicalId":79424,"journal":{"name":"Supplement ... to the European journal of neuroscience","volume":"1 1","pages":"129-36"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89777447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 123

Differential daily expression of Per1 and Per2 mRNA in the suprachiasmatic nucleus of fetal and early postnatal mice. 胎鼠和产后早期小鼠视交叉上核Per1和Per2 mRNA的日表达差异。

Supplement ... to the European journal of neuroscience Pub Date : 2001-01-01 DOI: 10.1016/s0168-0102(00)81854-4

H. Shimomura, Takahiro Moriya, M. Sudo, H. Wakamatsu, M. Akiyama, Yoshiaki Miyake, Shigenobu Shibata

引用次数: 38

cDNA cloning and expression of a gamma-aminobutyric acid A receptor epsilon-subunit in rat brain. 大鼠脑γ -氨基丁酸a受体epsilon亚基的cDNA克隆及表达。

Supplement ... to the European journal of neuroscience Pub Date : 2000-12-01 DOI: 10.1046/J.1460-9568.2000.01343.X

N. Moragues, P. Ciofi, P. Lafon, M. Odessa, G. Tramu, M. Garret

{"title":"cDNA cloning and expression of a gamma-aminobutyric acid A receptor epsilon-subunit in rat brain.","authors":"N. Moragues, P. Ciofi, P. Lafon, M. Odessa, G. Tramu, M. Garret","doi":"10.1046/J.1460-9568.2000.01343.X","DOIUrl":"https://doi.org/10.1046/J.1460-9568.2000.01343.X","url":null,"abstract":"A cDNA encoding a GABA(A) receptor subunit was isolated from rat brain. The predicted protein is 70% identical to the human epsilon-subunit. It was recently reported [Sinkkonen et al. (2000), J. Neurosci., 20, 3588-3595] that the rodent epsilon-subunit mRNA encoded an additional sequence ( approximately 400 residues). We provide evidence that human and rat epsilon-subunit are similar in size. The distribution of cells expressing the GABA(A) epsilon-subunit was examined in the rat brain. In situ hybridization histochemistry revealed that epsilon-subunit mRNA is expressed by neurons located in septal and preoptic areas, as well as in various hypothalamic nuclei, including paraventricular, arcuate, dorsomedial and medial tuberal nuclei. The mRNA was also detected in major neuronal groups with broad-range influence, such as the cholinergic (basal nucleus), dopaminergic (substantia nigra compacta), serotonergic (raphe nuclei), and noradrenergic (locus coeruleus) systems. Immunohistochemistry using an affinity-purified antiserum directed towards the N-terminal sequence unique to the rat epsilon-subunit revealed the presence of epsilon-subunit immunoreactivity over the somatodendritic domain of neurons with a distribution closely matching that of mRNA-expressing cells. Moreover, using in situ hybridization, alpha3, theta and epsilon GABA(A) subunit mRNAs were all detected with an overlapping distribution in neurons of the dorsal raphe and the locus coeruleus. Our results suggest that novel GABA(A) receptors may regulate, neuroendocrine and modulatory systems in the brain.","PeriodicalId":79424,"journal":{"name":"Supplement ... to the European journal of neuroscience","volume":"5 1","pages":"4318-30"},"PeriodicalIF":0.0,"publicationDate":"2000-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89110660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 40