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Activity of putative cognition enhancers in kynurenate test performed with human neocortex slices

JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期290卷 423-428页

作者： Pittaluga, A Pattarini, R Andrioli, GC Viola, C Munari, C Raiteri, M Univ Genoa Dept Expt Med Pharmacol & Toxicol Sect I-16148 Genoa Italy Univ Genoa Osped Galliera Div Neurochirurg I-16148 Genoa Italy Univ Genoa Clin Neurochirurg I-16148 Genoa Italy

Some cognition enhancers were previously shown to potently prevent antagonism of the N-methyl-D-aspartate (NMDA)evoked release of norepinephrine (NE) brought about in slices of rat hippocampus by kynurenic acid, an endogenous NMDA receptor blocker. We have examined the impact of putative nootropic agents in the kynurenate test performed with slices of human cerebral cortex from patients undergoing neurosurgery. in slices of human neocortex, local application of NMDA evoked release of [(3)H]NE;the effect of NMDA was antagonized by several NMDA receptor antagonists, including kynurenic acid. The antagonism of the NMDA-evoked [(3)H]NE release produced by 300 mu M kynurenate was potently (EC(50) <10 mu M) prevented by most of the nootropics tested, including aniracetam, oxiracetam, D-cycloserine, and the glutamate analog CR 2249 (but not its enantiomer CR 2361). Nicotine or tacrine (up to 10 mu M) did not show any effect in the kynurenate test. Nicotine (30-100 mu M) itself increased the release of [(3)H]NE;interestingly, the nicotine-evoked overflow was blocked not only by the nicotin receptor antagonist mecamylamine but also by NMDA receptor antagonists, suggesting an indirect mechanism mediated by glutamate/aspartate release. To conclude, the similarities between the data obtained here with human neocortex slices and those previously obtained in the rat indicate that the kynurenate test performed with rat brain slices may represent a useful biochemical assay to study cognition-enhancing drugs.

关键词：兴奋性氨基酸激动剂/药理学兴奋性氨基酸拮抗剂/药理学犬尿烯酸/拮抗剂和抑制剂犬尿烯酸/药理学 N-甲基天冬氨酸/药理学新皮质/药物作用新皮质/代谢脑代谢改善药/药理学去甲肾上腺素/代谢受体 N-甲基-D-天冬氨酸/拮抗剂和抑制剂人类

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Regulation of calcium channel α_1A subunit splice variant mRNAs in kainate-induced temporal lobe epilepsy

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NEUROBIOLOGY OF DISEASE 1999年第4期6卷 288-301页

作者： Vigues, S Gastaldi, M Chabret, C Massacrier, A Cau, P Valmier, J Inst Biol CNRS UPR1142 F-34060 Montpellier France Fac Med Marseille Biol Cellulaire Lab F-13385 Marseille 5 France

P/Q-type voltage-gated Ca2+ channels (VGCC) regulate neurotransmitter release in the hippocampus and molecular alterations of their alpha(1A) pore-forming subunits are involved in various animal and human CNS diseases. We evaluated, using RT-PCR and in situ hybridization, the spatio-temporal activation of two alpha(1A) subunits splice variants (alpha(1A-a) and alpha(1A-b)) in control and kainic acid (KA)-treated rats. Six hours after KA treatment, alpha(1A-a) and alpha(1A-b) mRNAs increased, decreased or remained unchanged with area specific patterns. These changes were evidenced in the hippocampus and the dentatus gyrus and absent in the cerebellum. The alpha(1A) mRNA upregulation lasted for at least 7 days after KA treatment. Altogether, these results indicate that alpha(1A-a) and alpha(1A-b) mRNAs following seizure onset exhibit a complex and specific spatio-temporal pattern. The long-lasting changes in alpha(1A) subunit mRNA contents suggests that VGCC may be involved in the mechanisms generating chronic focal hyperexcitability and/or cellular damage in temporal lobe epilepsy. (C) 1999 Academic Press.

关键词：选择性剪接脑/代谢钙通道/遗传学钙通道/代谢钙通道 N型小脑/代谢疾病模型动物癫痫颞叶/化学诱导癫痫颞叶/代谢基因表达调控海马/代谢原位杂交红藻氨酸新皮质/代谢神经组织蛋白质类/遗传学神经组织蛋白质类/代谢蛋白质亚型/遗传学 RNA 信使/代谢大鼠 Wistar 逆转录聚合酶链反应增量调节/遗传学动物大鼠

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Regulation of area identity in the mammalian neocortex by Emx2 and Pax6

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SCIENCE 2000年第5464期288卷 344-349页

作者： Bishop, KM Goudreau, G O'Leary, DDM Salk Inst Biol Studies Mol Neurobiol Lab La Jolla CA 92037 USA Max Planck Inst Biophys Chem Dept Mol Cell Biol D-37077 Gottingen Germany

The contribution of extrinsic and genetic mechanisms in determining areas of the mammalian neocortex has been a contested issue. This study analyzes the roles of the regulatory genes Emx2 and Pax6, which are expressed in opposing gradients in the neocortical ventricular zone, in specifying areas. Changes in the patterning of molecular markers and area-specific connections between the colter and thalamus suggest that arealization of the neocortex is disproportionately altered in Emx2 and Pax6 mutant mice in opposing manners predicted from their countergradients of expression: rostral areas expand and caudal areas contract in Emx2 mutants, whereas the opposite effect is seen in Pax6 mutants. These findings suggest that Emx2 and Pax6 cooperate to regulate arealization of the neocortex and to confer area identity to cortical cells.

关键词：脑图钙黏着糖蛋白类/生物合成钙黏着糖蛋白类/遗传学 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/生理学眼蛋白质类基因表达基因表达调控发育期基因同源盒基因调节同源盒结构域蛋白质类/遗传学同源盒结构域蛋白质类/生理学小鼠近交C57BL 小鼠近交DBA 小鼠突变型形态发生新皮质/胚胎学新皮质/代谢神经通路枕叶/胚胎学枕叶/代谢成对盒转录因子类阻遏蛋白质类躯体感觉皮质/胚胎学躯体感觉皮质/代谢丘脑/胚胎学转录因子视皮质/胚胎学视皮质/代谢动物小鼠

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Maturation of layer 5 neocortical pyramidal neurons:: amplifying salient layer 1 and layer 4 inputs by Ca²⁺ action potentials in adult rat tuft dendrites

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第3期526卷 571-587页

作者： Zhu, JJ Max Planck Inst Med Forsch Zellphysiol Abt D-69120 Heidelberg Germany

1. Changes in the arborization and electrical excitability of the apical dendritic tufts of pyramidal cells of cortical layer 5 were examined during the first 2 months (postnatal days (P)2-56) of postnatal development in rats. 2. Rt constructions of biocytin-filled neurons showed that the apical dendritic trunk was continually growing, becoming longer and thicker and that the distance between the tuft. and soma increased more than 5-fold, 3. In P2 animals, both the tuft and soma had a high input, resistance (> 500 M Omega) and the tuft was electrotonically close to the some. In contrast, the apical tuft and soma of P56 neurons had a low input resistance (< 50 M Omega) and they were electrotonically isolated From each other. 4. Depolarizing current pulses injected into the tuft of P2 cells generated mostly Na+-dependent regenerative dendritic potentials of short duration (similar to 15 ms) while in the tuft of P56 animals, complex regenerative potentials were generated which had a longer duration (similar to 55 ms) and were Na+ and Ca2+ dependent. In young and juvenile animals (P14-28) dendritic regenerative potentials could br restricted tu the apical dendritic tuft whereas in adult animals (> P42), the: complex regenerative potentials frequently occurred simultaneously wit ll somatic action potentials. 5. The main developmental change in layer 5 pyramidal neurons, as assayed with square pulse current injections and synaptic stimulations, is the progressive electrotonic isolation of thr: dendritic tuft from the soma. This change is concomitant with that the appearance of complex, mostly Na+- and Ca2+-dependent, regenerative dendritic potentials initiated partly in the tuft and partly in the axon. The coupling of the dendritic tuft and axonal initiation zones for regenerative potentials by active dendritic Na+ and Ca2+ conductances enables mature layer 5 pyramidal neurons to detect selectively the salient distal synaptic inputs and coincident synaptic inputs arriving

关键词：动作电位/药物作用动作电位/生理学衰老/生理学镉/药理学钙/代谢细胞分化/生理学细胞膜/代谢树突/药物作用树突/代谢电刺激兴奋性突触后电位/生理学新皮质/细胞学新皮质/药物作用新皮质/代谢镍/药理学锥体细胞/细胞学锥体细胞/药物作用锥体细胞/代谢大鼠 Wistar 河豚毒素/药理学动物大鼠

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Site independence of EPSP time course is mediated by dendritic I_h in neocortical pyramidal neurons

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JOURNAL OF NEUROPHYSIOLOGY 2000年第5期83卷 3177-3182页

作者： Williams, SR Stuart, GJ Australian Natl Univ John Curtin Sch Med Res Div Neurosci Canberra ACT 0200 Australia

Neocortical layer 5 pyramidal neurons possess long apical dendrites that receive a significant portion of the neurons excitatory synaptic input. Passive neuronal models indicate that the time course of excitatory postsynaptic potentials (EPSPs) generated in the apical dendrite will be prolonged as they propagate toward the soma. EPSP propagation may, however, be influenced by the recruitment of dendritic voltage-activated channels. Here we investigate the properties and distribution of I-h channels in the axon, soma, and apical dendrites of neocortical layer 5 pyramidal neurons, acid their effect on EPSP time course. We find a linear increase (9 pA/100 mu m) in the density of dendritic I-h, channels with distance from soma. This nonuniform distribution of I-h channels generates site independence of EPSP time course, such that the half-width at the soma of distally generated EPSPs (up to 435 mu m from soma) was similar to somatically generated EPSPs. As a corollary, a normalization of temporal summation of EPSPs was observed. The site independence of somatic EPSP time course was found to collapse after pharmacological blockade of I-h channels, revealing pronounced temporal summation of distally generated EPSPs, which could be further enhanced by TTX-sensitive sodium channels. These data indicate that an increasing density of apical dendritic I-h channels mitigates the influence of cable filtering on somatic EPSP time course and temporal summation in neocortical layer 5 pyramidal neurons.

关键词：轴突/代谢心血管药物/药理学环核苷酸门控阳离子通道树突/药物作用树突/代谢电刺激兴奋性突触后电位/药物作用兴奋性突触后电位/生理学离子通道/拮抗剂和抑制剂离子通道/代谢膜电位/药物作用膜电位/生理学新皮质/细胞学新皮质/药物作用新皮质/代谢膜片钳术钾通道锥体细胞/药物作用锥体细胞/代谢嘧啶类/药理学大鼠 Wistar 钠通道阻滞剂河豚毒素/药理学动物大鼠

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Agrin is a major heparan sulfate proteoglycan accumulating in Alzheimer's disease brain

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AMERICAN JOURNAL OF PATHOLOGY 1999年第6期155卷 2115-2125页

作者： Verbeek, MM Otte-Höller, I van den Born, J van den Heuvel, LPWJ David, G Wesseling, P de Waal, RMW Univ Nijmegen Hosp Dept Pathol Lab Pediat & Neurol 319 NL-6500 HB Nijmegen Netherlands Univ Nijmegen Hosp Dept Nephrol NL-6500 HB Nijmegen Netherlands Univ Nijmegen Hosp Dept Pediat NL-6500 HB Nijmegen Netherlands Univ Nijmegen Hosp Dept Neurol NL-6500 HB Nijmegen Netherlands Katholieke Univ Leuven Ctr Human Genet Louvain Belgium Flanders Interuniv Inst Biotechnol Louvain Belgium

Heparan sulfate proteoglycans (HSPGs) have been suggested to play an important role in the formation and persistence of senile plaques and neurofibrillary tangles in dementia of the Alzheimer's type (DAT), We performed a comparative immunohistochemical analysis of the expression of the HSPGs agrin, perlecan, glypican-1, and syndecans 1-3 in the lesions of DAT brain neocortex and hippocampus. Using a panel of specific antibodies directed against the protein backbone of the various HSPG species and against the glycosaminoglycan (GAG) side-chains, we demonstrated the following. The basement membrane-associated HSPG, agrin, is widely expressed in senile plaques, neurofibrillary tangles and cerebral blood vessels, whereas the expression of the other basement membrane-associated HSPG, perlecan, is lacking in senile plaques and neurofibrillary tangles and is restricted to the cerebral vasculature. Glypican and three different syndecans, ail cell membrane-associated HSPG species, are also expressed in senile plaques and neurofibrillary tangles, albeit at a lower frequency than agrin, Heparan sulfate GAG side chains are also associated with both senile plaques and: neurofibrillary tangles. Our results suggest that glycosaminoglycan side chains of the HSPGs agrin, syndecan, and glypican, but not perlecan, may play an important role in the formation of both senile plaques and neurofibrillary tangles. In addition, we speculate that agrin, because it contains nine protease-inhibiting domains, may protect the protein aggregates in senile plaques and neurofibrillary tangles against extracellular proteolytic degradation, leading to the persistence of these deposits.

关键词：聚集蛋白/代谢阿尔茨海默病/代谢阿尔茨海默病/病理学类肝素硫酸蛋白聚糖类/代谢类肝素硫酸盐/代谢海马/代谢海马/病理学免疫组织化学膜糖蛋白类/代谢新皮质/代谢新皮质/病理学蛋白聚糖类/代谢多配体蛋白聚糖类泛素类/代谢 tau蛋白质类/代谢老年人女(雌)性人类男(雄)性

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Staging of cytoskeletal and β-amyloid changes in human isocortex reveals biphasic synaptic protein response during progression of Alzheimer's disease

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AMERICAN JOURNAL OF PATHOLOGY 2000年第2期157卷 623-636页

作者： Mukaetova-Ladinska, EB Garcia-Siera, F Hurt, J Gertz, HJ Xuereb, JH Hills, R Brayne, C Huppert, FA Paykel, ES McGee, M Jakes, R Honer, WG Harrington, CR Wischik, CM Univ Cambridge Dept Psychiat Cambridge England Univ Cambridge Dept Pathol Cambridge Brain Bank Lab Cambridge England IPN CINVESTAV Dept Physiol Biophys & Neurosci Mexico City DF Mexico Univ Leipzig Dept Psychiat D-7010 Leipzig Germany Univ Cambridge Inst Publ Hlth Dept Publ Hlth Cambridge England Univ Cambridge Inst Publ Hlth Dept Primary Care Cambridge England Univ Cambridge Inst Publ Hlth MRC Biostat Unit Cambridge England MRC Ctr Mol Biol Lab Cambridge England Univ Aberdeen Dept Mental Hlth Aberdeen Scotland Univ British Columbia Dept Psychiat Vancouver BC Canada

We have examined the relationships between dementia, loss of synaptic proteins, changes in the cytoskeleton, and deposition of beta-amyloid plaques in the neocortex in a clinicopathologically staged epidemiological cohort using a combination of biochemical and morphometric techniques. We report that loss of synaptic proteins is a late-stage phenomenon, occurring only at Braak stages 5 and 6, or at moderate to severe clinical grades of dementia, Loss of synaptic proteins was seen only after the emergence of the full spectrum of tau and beta-amyloid pathology in the neocortex at stage 4, but not in the presence of beta-amyloid plaques alone. Contrary to previous studies, we report increases in the levels of synaptophysin, syntaxin, and SNAP-25 at stage 3 and of alpha-synuclein and MAP2 at stage 4, Minimal and mild clinical grades of dementia were associated with either unchanged or elevated levels of synaptic proteins in the neocortex, Progressive aggregation of paired helical filament (PHF)-tau protein could be detected biochemically from stage 2 onwards, and this was earliest change relative to the normal aging background defined by Braak stage 1 that we were able to detect in the neocortex. These results are consistent with the possibility that failure of axonal transport associated with early aggregation of tau protein elicits a transient adaptive synaptic response to partial de-afferentation that may be mediated by trophic factors. This early abnormality in cytoskeletal function may contribute directly to the earliest clinically detectable stages of dementia.

关键词：阿尔茨海默病/代谢阿尔茨海默病/病理学淀粉样β肽类/代谢细胞骨架/代谢疾病恶化膜蛋白质类/代谢微管相关蛋白质类/代谢新皮质/代谢新皮质/病理学神经组织蛋白质类/代谢神经原纤维缠结/病理学磷酰化斑块淀粉样/病理学 Qa-SNARE蛋白质类疾病严重程度指数突触/代谢突触囊泡蛋白/代谢突触体相关蛋白质25 突触核蛋白类 α突触核蛋白 tau蛋白质类/代谢女(雌)性人类男(雄)性

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Expression of zinc-positive cells and terminals in fetal neocortical homografts to adult rat depends on lesion type and rearing conditions

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EXPERIMENTAL NEUROLOGY 2000年第1期164卷 176-183页

作者： Zeng, JS Mattsson, B Schulz, MK Johansson, BB Sorensen, JC Univ Lund Hosp S-22185 Lund Sweden Sun Yat Sen Univ Med Sci Affiliated Hosp 1 Dept Neurol Guanzhou Peoples R China Odense Univ Dept Anat & Neurobiol DK-5000 Odense C Denmark Aarhus Univ Inst Anat Dept Neurobiol DK-8000 Aarhus C Denmark

Zinc-positive neurons and terminals, known to be associated with the glutamatergic projections in the brain, can be demonstrated by the histochemical Timm method and later modifications thereof. The adult rat neocortex contain a uniform lamination of zinc-positive cells with specific projections to, e.g., the striatum. We have previously reported that fetal neocortical grafts implanted in the adult rat neocortex combined with rearing in an enriched environment can improve behavioral functions and reduce the secondary atrophy of thalamus after cortex infarction in adult rats. In order to examine whether the expression of zinc positivity is ontogenetically inherent to neocortical neurons we grafted fetal neocortical tissue to aspiration or ischemic lesions of the frontoparietal neocortex of adult rats, followed by histochemical visualization of the vesicular zinc pool by selenite or sulfide. One further aim of the study was to elucidate to what extent the distribution of zinc-containing neurons and terminals in the grafts depended on rearing under different environmental conditions. The foremost finding of the present study was that the overall density of zinc-containing terminals in fetal cortical transplants placed in brain infarcts of adult spontaneously hypertensive rats is higher when the rats are reared in an enriched environment. Moreover, the presence and expression of zinc-positive neurons and terminals do not seem to be ontogenetically inherent to the cortical neurons as the fetal neocortical grafts placed in aspiration lesions contained no zinc-selenide-positive neurons and few or no zinc-selenide-positive terminals. The presence or expression of zinc-positive cells may thus be induced by ingrowth of fibers and terminals from the host brain as transplants placed in the ischemic lesions expressed both zinc-positive neurons and terminals. (C) 2000 Academic Press.

关键词：行为动物脑缺血/代谢脑缺血/外科学脑组织移植细胞计数去脑皮质术胆碱能纤维/代谢环境胚胎组织移植移植物存活高血压/代谢梗死大脑中动脉新皮质/细胞学新皮质/代谢新皮质/外科学新皮质/移植神经元/细胞学神经元/代谢神经元/移植突触前末梢/代谢大鼠近交SHR 大鼠近交WKY 硒化合物/分析硒化合物/代谢亚硒酸钠/代谢硫化物/分析硫化物/代谢锌/代谢锌化合物/分析锌化合物/代谢动物男(雄)性大鼠

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A network of electrically coupled interneurons drives synchronized inhibition in neocortex

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NATURE NEUROSCIENCE 2000年第9期3卷 904-910页

作者： Beierlein, M Gibson, JR Connors, BW Brown Univ Dept Neurosci Div Biol & Med Providence RI 02912 USA

The neocortex has at least two different networks of electrically coupled inhibitory interneurons: fast-spiking (FS) and low-threshold-spiking (LTS) cells. Agonists of metabotropic glutamate or acetylcholine receptors induced synchronized spiking and membrane fluctuations, with irregular or rhythmic patterns, in networks of LTS cells. LTS activity was closely correlated with inhibitory postsynaptic potentials in neighboring FS interneurons and excitatory neurons. Synchronized LTS activity required electrical synapses, but not fast chemical synapses. Tetanic stimulation of local circuitry induced effects similar to those of metabotropic agonists. We conclude that an electrically coupled network of LTS interneurons can mediate synchronized inhibition when activated by modulatory neurotransmitters.

关键词：动作电位/药物作用动作电位/生理学皮质同步化/方法导电性中间神经元/细胞学中间神经元/药物作用中间神经元/代谢新皮质/细胞学新皮质/药物作用新皮质/代谢神经网/细胞学神经网/药物作用神经网/生理学神经抑制/药物作用神经抑制/生理学神经递质药/代谢大鼠 Sprague-Dawley 受体亲代谢性谷氨酸盐/药物作用受体亲代谢性谷氨酸盐/代谢突触/药物作用突触/代谢动物大鼠

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Cortical degeneration in the absence of neurotrophin signaling: Dendritic retraction and neuronal loss after removal of the receptor TrkB

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NEURON 2000年第1期26卷 233-245页

作者： Xu, BJ Zang, KL Ruff, NL Zhang, YA McConnell, SK Stryker, MP Reichardt, LF Univ Calif San Francisco Howard Hughes Med Inst San Francisco CA 94143 USA Univ Calif San Francisco Dept Physiol San Francisco CA 94143 USA Stanford Univ Dept Sci Biol Stanford CA 94305 USA

To examine functions of TrkB in the adult CNS, TrkB has been removed from neurons expressing CaMKII, primarily pyramidal neurons, using Cre-mediated recombination. A floxed trkB allele was designed so that neurons lacking TrkB express tau-beta-galactosidase. Following trkB deletion in pyramidal cells, their dendritic arbors are altered, and cortical layers II/III and V are compressed, after which there is an apparent loss of mutant neurons expressing the transcription factor SCIP but not of those expressing Otx-1. Loss of neurons expressing SCIP requires deletion of trkB within affected neurons;reduction of neuronal ER81 expression does not, suggesting both direct and indirect effects of TrkB loss. Thus, TrkB is required for the maintenance of specific populations of cells in the adult neocortex.

关键词：细胞计数 DNA结合蛋白质类/代谢树突/代谢树突/病理学小鼠转基因突变/遗传学新皮质/代谢新皮质/病理学神经生长因子类/代谢神经变性疾病/代谢神经变性疾病/病理学神经元/代谢神经元/病理学锥体细胞/代谢受体 trkB/遗传学受体 trkB/代谢转录因子/代谢 β半乳糖苷酶类/代谢动物小鼠

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