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  • 1
    Electronic Resource
    Electronic Resource
    Neuronal dependence of extracellular dopamine, acetylcholine, glutamate, aspartate and gamma-aminobutyric acid (GABA) measured simultaneously from rat neostriatum using in vivo microdialysis: reciprocal interactions (1992)
    Springer
    Amino acids 2 (1992), S. 157-179 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Dopamine ; Acetylcholine ; Glutamate ; Aspartate ; Gamma-aminobutyric acid (GABA) ; Striatum ; Microdialysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The neuronal origin of extracellular levels of dopamine (DA), acetylcholine (ACh), glutamate (Glu), aspartate (Asp) and gamma-aminobutyric acid (GABA) simultaneously collected from the neostriatum of halothane anaesthetized rats with in vivo microdialysis was studied. The following criteria were applied (1) sensitivity to K+-depolarization; (2) sensitivity to inhibition of synaptic inactivation mechanisms; (3) sensitivity to extracellular Ca2+; (4) neuroanatomical regionality; sensitivity to selective lesions and (5) sensitivity to chemical stimulation of the characterized pathways. It was found that: (1) Extracellular DA levels found in perfusates collected from the neostriatum fulfills all the above criteria and therefore the changes in extracellular DA levels measured with microdialysis reflect actual release from functionally active nerve terminals, and so reflect ongoing synaptic transmission. (2) Changes in neostriatal ACh levels reflect neuronal activity, provided that a ACh-esterase inhibitor is present in the perfusion medium. (3) Extracellular Glu, Asp and GABA could be measured in different perfusion media in the rat neostriatum and probably reflect metabolic as well as synaptic release. However, (4) the majority of the extracellular GABA levels found in perfusates collected from the neostriatum may reflect neuronal release, since GABA levels were increased, in a Ca2+-dependent manner, by K+-depolarization, and could be selectively decreased by an intrinsic neostriatal lesion. (5) It was not possible to clearly distinguish between the neuronal and the metabolic pools of Glu and Asp, since neostriatal Glu and Asp levels were only slightly increased by K+-depolarization, and no changes were seen after decortication. A blocker of Glu re-uptake, DHKA, had to be included in the perfusion medium in order to monitor the effect of K+-depolarization on Glu and Asp levels. Under this condition, it was found (6) that neostriatal Glu and Asp levels were significantly increased by K+-depolarization, although only increases in the Glu levels were sensitive to Ca2+ in the perfusion medium, suggesting that Glu but not Asp is released from vesicular pools. (7) Evidence is provided that selective stimulations of nigral DA cell bodies may lead to changes in release patterns from DA terminals in the ipsilateral neostriatum, which are in turn followed by discrete changes in extracellular levels of GABA and Glu in the same region. Finally, some methodological considerations are presented to clarify the contribution of neuronal release to extracellular levels of amino acid neurotransmitters in the rat neostriatum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00806086
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  • 2
    Electronic Resource
    Electronic Resource
    Prevention of mortality induced by perinatal asphyxia: Hypothermia or glutamate antagonism? (1993)
    Springer
    Amino acids 5 (1993), S. 413-419 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Asphyxia ; Hypothermia ; Glutamate receptors ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Perinatal asphyxia was induced by keeping pups-containing uterus horns, removed by hysterectomy, in a 37°C or a 30°C water bath. Asphyxia for a period of 21–22 min at 37°C led to a 97% mortality within the first 20 min period following delivery. When the asphyctic period was extended to more than 22 min all the pups died following delivery. When the asphyxia was induced at 30°C, 100% of the delivered pups survived and were accepted by surrogate mothers. The protective effect of hypothermia could be observed even when the pups-containing uterus horns were exposed to a 45–46 min asphyctic period. Pretreatment with dizocilpine (0.2 mg/kg s.c.), or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX) (3–30 mg/kg s.c.), administered to the mothers one hour before hysterectomy, reduced slightly the mortality induced by a 21–22 min asphyctic period at 37°C. An increase in survival following a 22–23 min asphyctic period could only be observed after the highest dose of NBQX.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00806959
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of secretogranin II-derived peptides on the release of neurotransmitters monitored in the basal ganglia of the rat with in vivo microdialysis (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 717-724 
    Details
    ISSN: 1432-1912
    Keywords: Key words Basal ganglia ; Neuropeptides ; Monoamines ; Amino acids ; Microdialysis ; Chromogranin C ; Secretogranin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In vivo microdialysis was used to study the effect of secretogranin II-derived peptides on dynorphin B (Dyn B), dopamine, γ-aminobutyric acid (GABA), glutamate and aspartate release in the substantia nigra and neostriatum of halothane-anaesthesized rats. In the substantia nigra, local infusion of secretoneurin (secretogranin II 154–186) (1–50 μM) increased, in a concentration-dependent manner, extracellular aspartate, glutamate, Dyn B, dopamine and GABA levels. The effect was particularly prominent on aspartate and glutamate levels which, following 50 μM of secretoneurin, were increased by 〉20 and 〉10 fold, respectively. However, the effect of secretoneurin on Dyn B release appeared to be more specific, since a significant increase (〉2 fold) was already observed following 1 μM of secretoneurin. In the neostriatum, Dyn B, glutamate, aspartate and GABA levels were also increased by local secretoneurin infusion, but the effect was less prominent than in the substantia nigra. In the substantia nigra, only Dyn B levels were significantly increased following infusion of 10 μM of the secretoneurin-C terminal (secretoneurin-15C), whereas Dyn B and GABA levels were increased by the same concentration of the secretogranin II C terminus (YM). Only glutamate and aspartate levels were increased by local infusion of 10 μM of secretogranin II 133–151 (LF), a peptide adjacent to secretoneurin in the primary amino acid sequence. In the neostriatum, Dyn B and GABA levels were increased by 10 μM of secretoneurin-15C. Dyn B levels were also increased by 10 μM of YM, and glutamate and aspartate levels were increased by 10 μM of both YM and LF. Thus, secretogranin II-derived peptides affect extracellular levels of several putative neurotransmitter systems monitored in the basal ganglia of the rat with in vivo microdialysis. The effect of Dyn B appears to be specific and related to a physiological role of secretoneurin, since (i) it occurs in an area where secretoneurin-immunocytochemistry has been observed, (ii) is exerted at comparatively low concentrations, and (iii) is mimicked by secretoneurin-15C. The increases in excitatory amino acid levels produced by high concentrations of secretoneurin and other secretogranin II-derived peptides reflect, perhaps, a potential neurotoxicity produced by abnormal accumulation of these peptides.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00166897
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of secretogranin II-derived peptides on the release of neurotransmitters monitored in the basal ganglia of the rat with in vivo microdialysis (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 717-724 
    Details
    ISSN: 1432-1912
    Keywords: Basal ganglia ; Neuropeptides ; Monoamines ; Amino acids ; Microdialysis ; Chromogranin C ; Secretogranin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In vivo microdialysis was used to study the effect of secretogranin II-derived peptides on dynorphin B (Dyn B), dopamine, γ-aminobutyric acid (GABA), glutamate and aspartate release in the substantia nigra and neostriatum of halothane-anaesthesized rats. In the substantia nigra, local infusion of secretoneurin (secretogranin II 154–186) (1–50 μM) increased, in a concentration-dependent manner, extracellular aspartate, glutamate, Dyn B, dopamine and GABA levels. The effect was particularly prominent on aspartate and glutamate levels which, following 50 μM of secretoneurin, were increased by 〉20 and 〉10 fold, respectively. However, the effect of secretoneurin on Dyn B release appeared to be more specific, since a significant increase (〉2 fold) was already observed following 1 μM of secretoneurin. In the neostriatum, Dyn B, glutamate, aspartate and GABA levels were also increased by local secretoneurin infusion, but the effect was less prominent than in the substantia nigra. In the substantia nigra, only Dyn B levels were significantly increased following infusion of 10 μM of the secretoneurin-C terminal (secretoneurin-15C), whereas Dyn B and GABA levels were increased by the same concentration of the secretogranin II C terminus (YM). Only glutamate and aspartate levels were increased by local infusion of 10 μM of secretogranin II 133-151 (LF), a peptide adjacent to secretoneurin in the primary amino acid sequence. In the neostriatum, Dyn B and GABA levels were increased by 10 μM of secretoneurin-15C. Dyn B levels were also increased by 10 μM of YM, and glutamate and aspartate levels were increased by 10 μM of both YM and LF. Thus, secretogranin 11-derived peptides affect extracellular levels of several putative neurotransmitter systems monitored in the basal ganglia of the rat with in vivo microdialysis. The effect of Dyn B appears to be specific and related to a physiological role of secretoneurin, since (i) it occurs in an area where secretoneurin-immunocytochemistry has been observed, (ii) is exerted at comparatively low concentrations, and (iii) is mimicked by secretoneurin-15C. The increases in excitatory amino acid levels produced by high concentrations of secretoneurin and other secretogranin II-derived peptides reflect, perhaps, a potential neurotoxicity produced by abnormal accumulation of these peptides.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00166897
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  • 5
    Electronic Resource
    Electronic Resource
    Cholecystokinin-8S increases dynorphin B, aspartate and glutamate release in the fronto-parietal cortex of the rat via different receptor subtypes (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1997), S. 576-581 
    Details
    ISSN: 1432-1912
    Keywords: Key words Neocortex ; Cholecystokinin ; Dynorphin ; Amino acids ; Microdialysis ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of sulphated cholecystokinin-8 (CCK-8S) on extracellular dynorphin B, aspartate, glutamate and GABA levels in the rat fronto-parietal cortex was investigated with in vivo microdialysis. The peptide was infused through the microdialysis probe trying to mimic local CCK-8S release. Basal levels of dynorphin B were around 20pM, aspartate 100nM, glutamate 600nM and GABA 30nM. CCK-8S (10μM) induced a ≈3-fold increase in extracellular dynorphin B, aspartate and glutamate levels, while GABA levels were only slightly increased. The effect of CCK-8S was restricted to the stimulated neocortex. Systemic pretreatment with the CCKB antagonist, L-365, 260, but not with the CCKA antagonist, L-364, 718, significantly antagonised the effect of CCK-8S on cortical dynorphin B and aspartate release. However, both CCKA and CCKB antagonists inhibited the increase in cortical glutamate levels. Thus, the present results indicate that cortical CCK release exerts a stimulatory modulation on cortical dynorphin B and aspartate release via the CCKB receptor subtype, and on glutamate release via both CCKA and CCKB receptor subtypes. Considering electrophysiological evidence that CCK increases neuronal firing rates in many brain regions, it may be suggested that CCK represents a stimulatory system modulating the function of the neocortex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004986
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  • 6
    Electronic Resource
    Electronic Resource
    Simultaneous determination of cholecystokinin, dopamine, glutamate and aspartate in cortex and striatum of the rat using in vivo microdialysis (1991)
    Springer
    Amino acids 1 (1991), S. 365-373 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Glutamate ; Aspartate ; Dopamine ; Cholecystokinin ; Microdialysis ; Basal Ganglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular levels of cholecystokinin (CCK), dopamine (DA), glutamate (Glu) and aspartate (Asp) were simultaneously monitored in the frontoparietal cortex and the striatum of halothane-anaesthetized rats using in vivo microdialysis. Under basal conditions, cortical and striatal CCK levels were 3.11 ± 0.39 pM and 2.76 ± 0.15 pM, respectively. Local KCl (10−1 M) and bicuculline (10−4 M) co-application in cortex or striatum increased the CCK levels 18-fold and 26-fold, respectively. The DA level in striatum was 3.78 ± 0.28 nM and the local perfusion with KCl + bicuculline led to a 45-fold increase. The cortical and striatal outputs of Glu were of the order of 2 · 10−6 M and Asp levels were around 6 · 10−7 M. Local stimulation with KCl (10−1 M) and bicuculline (10−4 M) caused a small increase (2 fold) in cortical and striatal levels of Glu and Asp. The addition of KCl (10−1 M) and bicuculline (10−4 M) to the cortical perfusion medium did not modify CCK, DA or Glu concentrations in striatum. These results demonstrate that CCK, DA, Glu and Asp may be simultaneously monitored in vivo and support the idea that their extracellular levels recovered in the microdialysis perfusates could be derived from neuronal pools.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00814005
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