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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 65 (1995), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In vivo electrochemical detection with a Nafion-coated carbon fiber working electrode, which provides information on the spatial and temporal dynamics of dopamine overflow, was used to investigate the involvement of nitric oxide (NO) in the dopaminergic transmission in the striatum of urethane-anesthetized Sprague-Dawley rats. A mixture of N-methyl-d-aspartate (NMDA) and nomifensine, a dopamine uptake blocker, was locally pressure-ejected to elicit a transient dopamine overflow from the dopamine-containing nerve terminals in the striatum. Local application of Nω-nitro-l-arginine methyl ester (l-NAME), which blocks endogenous NO formation, increased the magnitude of dopamine release evoked by a subsequent NMDA and nomifensine application but resulted in no significant alteration in the time course. Furthermore, microejection of l-arginine, an NO precursor, or sodium nitroprusside (SNP), an NO generator, did not cause detectable changes in dopamine level in the striatal extracellular space. However, NMDA-induced dopamine release was profoundly inhibited with l-arginine or SNP pretreatment. In addition, NO affects dopamine uptake in rat striatum. Exogenous dopamine applied through a micropipette, reversibly and reproducibly, elicited an electrochemical signal. The time course of these signals was significantly prolonged by l-NAME treatment. These data suggest that NO is diversely involved in regulating dopaminergic transmission in rat striatum.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 78 (2001), S. 1706-1708 
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Ta/NiO/NiFe/Ta multilayers were prepared by rf reactive and dc magnetron sputtering. The exchange coupling field between NiO and NiFe reached 120 Oe. The composition and chemical states at the interface region of NiO/NiFe were studied using the x-ray photoelectron spectroscopy (XPS) and peak decomposition technique. The results show that there are two thermodynamically favorable reactions at NiO/NiFe interface: NiO+Fe=Ni+FeO and 3NiO+2Fe=3Ni+Fe2O3. The thickness of the chemical reaction as estimated by angle-resolved XPS was about 1–1.5 nm. These interface reaction products are magnetic defects, and we believe that the exchange coupling field Hex and the coercivity Hc of NiO/NiFe are affected by these defects. © 2001 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial and engineering chemistry 8 (1969), S. 275-279 
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The inhibitory effects produced by activation of the medial region of caudal medulla on activities of the left and right cardiac sympathetic, vagus and greater splanchnic nerves were studied in chloralose-urethane anaesthetized cats.2. Electrical stimulation of the medial region produced an 80–92% inhibition of the sympathetic nerve activities, and a 45% and 58% inhibition of the left and right cardiac vagal nerve activities, respectively. There were no significant differences between effects elicited in the left and right autonomic nerves. Similar but smaller inhibitory effects were produced by micro-injection of sodium glutamate (0.5 mol/L) or DL-homocysteic acid (50 mmol/L) to the same medullary sites.3. These data suggest that neurons residing in the medial medullary region exert strong inhibitory effects on autonomic nerve activities. Since the vasculature is principally innervated by sympathetic nerves, inhibition of sympathetic nerve activities might be the principal factor responsible for the depressor effects caused by activation of the medial region of caudal medulla. The heart is innervated both by sympathetic and parasympathetic nerves. Thus, their simultaneous inhibition during activation of the medial region elicits only a weak and variable inhibition of the heart.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In chloralose-urethane anaesthetized cats, the dorsal cardiovascular reactive area (DCRA) in the parvocellular reticular nucleus dorsomedial to the facial nucleus, and the ventral cardiovascular reactive area (VCRA) ventromedial to the facial nucleus, were stimulated by microinjections of sodium glutamate (100–200 nmol) or electric current.2. Stimulation of DCRA, with a long latency of 15–20 s, elicited a marked increase of blood flow in the contralateral femoral artery with little change to moderate increase in systemic arterial blood pressure (ABP). In the relatively dorsal portion of DCRA, however, a smaller increase of blood flow in the ipsilateral femoral artery was elicited.3. On the other hand, stimulation of VCRA with a short latency (3–5 s) evoked an increase of blood flow in both femoral arteries which was more prominent on the contralateral side. The responses were accompanied with decreases in the blood flow of other vascular beds with only a slight increase or minimal change in ABP.4. The data suggest that DCRA and VCRA are both viscerotopically organized to alter the resistance of individual vascular beds for redistribution of blood flow.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 10 (1998), S. 0 
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have previously demonstrated that intra-hippocampal injection of corticotrophin-releasing factor improved memory retention of an inhibitory avoidance learning in rats; while the electrophysiological effects corticotrophin-releasing factor produces on hippocampal neurons are largely uncharacterized. In the present study, we found that corticotrophin-releasing factor injected into the dentate gyrus of hippocampus produced a dose-dependent and long-lasting enhancement in synaptic efficacy of these neurons, as measured by an increase in the amplitude and slope of population excitatory postsynaptic potentials, as well as the amplitude of population spike. The onset of corticotrophin-releasing factor-induced potentiation was slow. It was observed approximately 40–60 min after corticotrophin-releasing factor administration and lasted for more than 5 h. This effect of corticotrophin-releasing factor was blocked by pretreatment with the cyclase-adenosine-3,5-monophosphate (cAMP) inhibitor Rp-adenosine-3,5-cyclic monophosphothiolate triethylamine (Rp-cAMPS) and partially blocked by the N-methyl-D-aspartate receptor antagonist MK-801. Further, pretreatment with corticotrophin-releasing factor receptor antagonist dose-dependently diminished tetanization-induced long-term potentiation, and corticotrophin-releasing factor and tetanic stimuli had an additive effect on hippocampal neuron excitation. Moreover, direct injection of corticotrophin-releasing factor increased cAMP level in the dentate gyrus. These results together suggest that corticotrophin-releasing factor-induced potentiation simulates the late phase of tetanization-induced long-term potentiation and cAMP seems to be the messenger mediating this effect. Moreover, corticotrophin-releasing factor-induced potentiation and long-term potentiation may share some similar mechanisms, and corticotrophin-releasing factor is probably involved in the neural circuits underlying long-term potentiation. Thus, corticotrophin-releasing factor may play an important role in modulating synaptic plasticity in the hippocampus.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Cambridge : Cambridge University Press
    The @China quarterly 112 (1987), S. 681-681 
    ISSN: 0305-7410
    Source: Cambridge Journals Digital Archives
    Topics: Linguistics and Literary Studies , History , Political Science , Sociology , Economics
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Cambridge : Cambridge University Press
    The @China quarterly 105 (1986), S. 149-151 
    ISSN: 0305-7410
    Source: Cambridge Journals Digital Archives
    Topics: Linguistics and Literary Studies , History , Political Science , Sociology , Economics
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Cambridge : Cambridge University Press
    The @China quarterly 107 (1986), S. 542-543 
    ISSN: 0305-7410
    Source: Cambridge Journals Digital Archives
    Topics: Linguistics and Literary Studies , History , Political Science , Sociology , Economics
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Chromatography A 549 (1991), S. 410-415 
    ISSN: 0021-9673
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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