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31. |
Predictability of stimulus deviance and the mismatch negativity |
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NeuroReport,
Volume 9,
Issue 18,
1998,
Page 4167-4170
Elyse Sussman,
Walter Ritter,
Herbert Vaughan,
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摘要:
THE purpose of this study was to test the previous report that generation of the mismatch negativity (MMN) component of event-related brain potentials (ERPs) is indifferent to the predictable occurrence of stimulus deviance. A pattern of standards (S) and deviants (D) were delivered in a predictable fashion (SSSSD) at two different speeds (1.3 s and 100 ms). An MMN was obtained to the D position tone at the slow but not the fast pace. These results demonstrate that, unlike the P3 component, the MMN is sensitive to the predictable occurrence of stimulus deviance when the predictability can be detected by the brain within the estimated limits of sensory memory.
ISSN:0959-4965
出版商:OVID
年代:1998
数据来源: OVID
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32. |
A powerful GABABreceptΦ‐mediated inhibition of GABAergic neurons in the arcuate nucleus |
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NeuroReport,
Volume 9,
Issue 18,
1998,
Page 4171-4177
Edward Wagner,
Martha Bosch,
Martin Kelly,
K Rønnekleiv,
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摘要:
WE combined histofluorescence within sit uhybridization to identify GABAergic neurons in the arcuate nucleus (ARC) following electrophysiological recordings, using GAD65as a marker. Intracellular recordings were made in hypothalamic slices prepared from ovariectomized guinea pigs. Over 90% of ARC neurons tested with the GABABreceptor agonist baclofen responded with a membrane hyperpolarization or an outward current. The hyperpolarization was dose-dependent, and the GABABreceptor antagonist CGP 35,348 produced a rightward shift in the agonist dose-response curve. Agonist potency was lower, and the efficacy greater, in GAD-positive neurons. The use of this novel technique for identifying GABAergic neurons thus reveals differences in the pharmacodynamics of GABABreceptor activation GABAergic and non-GABAergic ARC neurons
ISSN:0959-4965
出版商:OVID
年代:1998
数据来源: OVID
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33. |
Representation of nociceptive stimuli in primary sensory cortex |
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NeuroReport,
Volume 9,
Issue 18,
1998,
Page 4179-4187
Howard Berman,
Karl Kim,
Ardesheer Talati,
Joy Hirsch,
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摘要:
USING fMRI, we observed cortical activity associated with nociceptive hot and cold sensations applied to hand and foot that are not spatially restricted to the corresponding regions of the primary somatosensory cortex (SI). Hot (55–57°C) and cold (0–2°C) tactile stimuli were applied separately to the right hand and foot of eight right-handed subjects. Although somatotopic mapping of hand and foot was observed as expected based on the Penfield homunculus, activations associated with hot during both hand and foot stimulation and subsequently, cold, activated regions unique to each thermal modality irrespective of the body part. This distributed system for thermal information is present at both nociceptive and more neutral thermal intensities (i.e. warm and cool sensations) indicating the presence of distributed sensory processing associated with thermal-related sensations in human primary sensorimotor cortex.
ISSN:0959-4965
出版商:OVID
年代:1998
数据来源: OVID
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34. |
Contribution of GABAA‐mediated conductances to anoxia‐induced depolarization |
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NeuroReport,
Volume 9,
Issue 18,
1998,
Page 4189-4192
Margherita D'Antuono,
Hiroto Kawasaki,
Virginia Tancredi,
Massimo Avoli,
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摘要:
CA1 pyramids were studied intracellularly in rat hippocampal slices to establish the contribution of excitatory amino acid (EAA) and GABAAreceptors to the depolarizations induced by brief ± 10 min) anoxic episodes. An increase of the amplitude of the depolarizations evoked by successive anoxic episodes occurred with KCl (n= 4 cells), not with K-acetate-filled (n= 3) recording electrodes. Moreover, with K-acetate-filled electrodes the anoxic depolarization amplitude was reduced, but not abolished by EAA receptor antagonists (n= 14). The residual anoxic depolarizations were blocked by a GABAAreceptor antagonist (n= 5) and decreased by the carbonic anhydrase inhibitor acetazolamide (n= 4). We conclude that the anoxic depolarizations generated by CA1 pyramids are caused by the activation of EAA along with GABAAreceptors leading to an increased membrane conductance to both Cl−and HCO3−.
ISSN:0959-4965
出版商:OVID
年代:1998
数据来源: OVID
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35. |
The putative cognitive enhancer KA‐672. HCl is an uncompetitive voltage‐dependent NMDA receptor antagonist |
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NeuroReport,
Volume 9,
Issue 18,
1998,
Page 4193-4197
Polina Lishko,
Oleksandr Maximyuk,
Shyam Chatterjee,
Michael Nöldner,
Oleg Krishtal,
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摘要:
KA-672.HCl (KA-672) is a new substance demonstrating anti-dementia properties. It shows modulatory effects on several neurotransmitter systems known to be affected in patients with Alzheimer's disease. In this study the action of KA-672 on the NMDA receptors was examined by applying patch clamp techniques to acutely isolated hippocampal neurons. KA-672 antagonizes NMDA responses in a voltage-dependent manner. At a holding potential of 90 mV the IC50value for the blocking action of KA-672 was 20 ± 7 μM. This action of KA-672 is independent on the concentration either of agonist or coagonist of NMDA receptor. Ketamine, which interacts with the PCP center, does not occlude the action of KA-672. Evidently, KA-672.HCl is a weak NMDA receptor-operated channel blocker. This property may account for its pharmacological profile.
ISSN:0959-4965
出版商:OVID
年代:1998
数据来源: OVID
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36. |
Partial lithium‐associated protection against apoptosis induced by C2‐ceramide in cerebellar granule neurons |
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NeuroReport,
Volume 9,
Issue 18,
1998,
Page 4199-4203
Francisco Centeno,
Alfonso Mora,
José Fuentes,
Germà Soler,
Enrique Claro,
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摘要:
PRIMARY cultures of cerebellar granule neurons, maintained in a serum-containing medium, underwent apoptosis when exposed to C2-ceramide, as assessed by mitochondrial reduction of MTT and intranucleosomal DNA fragmentation. After an 8h exposure to 50 μM C2-ceramide, cell viability decreased by 25–40%. Addition of lithium together with C2-ceramide resulted in a partial protection of apoptosis, which was maximal ab mM lithium (37% protection). When lithium was added h before the apoptotic stimulus the neuroprotective effect of the ion was clearly increased (66% protection). This effect was not due to intracellular inositol depletion or inhibition of NMDA receptors. Our data broaden the nature of apoptotic insults being reversed by lithium, stressing the neuroprotective effects of the ion.
ISSN:0959-4965
出版商:OVID
年代:1998
数据来源: OVID
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37. |
State‐dependent impairment in object recognition after hippocampal NOS inhibition |
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NeuroReport,
Volume 9,
Issue 18,
1998,
Page 4205-4208
Arjan Blokland,
Jos Prickaerts,
Wiel Honig,
Jan de Vente,
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摘要:
IN the present study we investigated the consequences of hippocampal nitric oxide synthase (NOS) inhibition on the performance in an object recognition task in rats. In a first study we injected Nω-nitro-L-arginine (LNA) into the hippocampus directly after the first trial. One hour later the discrimination performance of the animals was assessed. It was found that 1 μ g and 3 O°g, but not 3 μg, L-NA impaired the performance of the rats. In a second study in which we injected L-NA 45 min before the first trial no effects of treatment (10 μg and 3 Oμg) were observed. Since treatment with 30 μg has been found to inhibit hippocampal NOS almost completely and lasts longer than 2 h, it was concluded that hippocampal NOS inhibition induced a state-dependent performance deficit. Consequently, studies that examine the effects of NOS inhibition on cognitive functions should take this confounding effect into account.
ISSN:0959-4965
出版商:OVID
年代:1998
数据来源: OVID
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38. |
Modafinil prevents glutamate cytotoxicity in cultured cortical neurons |
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NeuroReport,
Volume 9,
Issue 18,
1998,
Page 4209-4213
Tiziana Antonelli,
Luca Ferraro,
Joelle Hillion,
Maria Tomasini,
Francis Rambert,
Kjell Fuxe,
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摘要:
THE ability of modafinil (Modiodal®) to protect cortical neurons from glutamate-induced degeneration was evaluated by measuring electrically evoked [3H]GABA release and [3H]GABA uptake in primary cerebral cortical cultures In normal cells, electrical stimulation (10 Hz, 2 min) increased [3H]GABA release (FR-NER St1= 0.77 ± 0.14; St2/St1ratio = 0.94 ± 0.02). The exposure of sister cells to glutamate, reduced electrically evoked [3H]GABA release (FR-NER St1= 0.40 ± 0.05; St2/St1ratio = 0.60 ± 0.08). Modafinil (0.3–1 μM) prevented the glutamate-induced reduction of the St2/St1ratio (0.85 ± 0.11; 0.88 ± 0.05, respectively). A similar protective effect was observed for [3H]GABA uptake. These findings suggest that modafinil may be neuroprotective in that it attenuates glutamate-induced excitotoxicity in cortical neurons
ISSN:0959-4965
出版商:OVID
年代:1998
数据来源: OVID
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