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  • 1
    Electronic Resource
    Electronic Resource
    PREPARATION OF BORON MONOXIDE AT HIGH TEMPERATURES (1956)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 78 (1956), S. 1509-1510 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja01588a065
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  • 2
    Electronic Resource
    Electronic Resource
    A NEW METHOD FOR THE PREPARATION OF BOROHYDRIDES (1956)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 78 (1956), S. 4176-4176 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja01597a093
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  • 3
    Electronic Resource
    Electronic Resource
    Solid-state structure of a layered hydrogen-bonded salt: guanidinium 5-benzoyl-4-hydroxy-2-methoxybenzenesulfonate methanol solvate (1996)
    Copenhagen : International Union of Crystallography (IUCr)
    Acta crystallographica 52 (1996), S. 209-214 
    Details
    ISSN: 1600-5740
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Notes: Guanidinium 5-benzoyl-4-hydroxy-2-methoxybenzene-sulfonate methanol solvate [C(NH2)3+.(C14H11O3)SO3−.CH3OH] crystallizes into a layered structure containing a two-dimensional hydrogen-bonded network typical of guanidinium alkane- and arenesulfonates. All six guanidinium protons and six sulfonate oxygen lone-pair acceptors participate in hydrogen bonding to form nearly planar pseudohexagonal hydrogen-bonded sheets, which can be viewed as parallel connected hydrogen-bonded ribbons. The 5-benzoyl-4-hydroxy-2-methoxybenzene groups are oriented to the same side of each ribbon, but the orientation of these groups on adjacent ribbons alternates with respect to the hydrogen-bonded sheet. The planar sheets stack with interdigitation of the arene groups, resulting in a structure in which layers of 5-benzoyl-4-hydroxy-2-methoxybenzene groups are separated by ionic hydrogen-bonded sheets. Each methanol molecule forms a hydrogen bond to one of the sulfonate O atoms, resulting in this oxygen forming a total of three hydrogen bonds, and fills void volume between the interdigitated 5-benzoyl-4-hydroxy-2-methoxybenzene groups of neighboring sheets. The benzophenone hydroxyl proton forms an intramolecular hydrogen bond to the carbonyl oxygen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1107/S0108768195009980
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  • 4
    Electronic Resource
    Electronic Resource
    Regional distribution of monoamines in the nucleus accumbens of the rat (1988)
    Springer
    Neurochemical research 13 (1988), S. 937-942 
    Details
    ISSN: 1573-6903
    Keywords: Dopamine ; noradrenaline ; serotonin ; nucleus accumbens ; regional distribution
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Monoamine concentrations were low in the rostral area of the nucleus accumbens. Their distributions were not identical. Differences were observed in the medial area. DA concentrations were high in both medial and caudal areas. Noradrenaline (NA) and serotonin (5-HT) concentrations were considerably lower than the dopamine (DA) concentration. The NA concentration was highest in the caudal area of the nucleus accumbens and the (5-HT) concentration was highest in the ventrocaudal area. There was a rostrocaudal decrease in the 3,4-dihydroxyphenylacetic acid (DOPAC)/DA and 5-hydroxyindole-3-acetic acid (5-HIAA)/5-HT ratios. Uptake of [3H]DA and [14C]choline was lowest in the rostral area. The K+-stimulated release of [14C]acetylcholine (ACh) was also lowest rostrally, but there was no rostrocaudal difference in the K+-stimulated release of [3H]DA. These results provide further evidence of the heterogeneity of the nucleus accumbens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00970765
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  • 5
    Electronic Resource
    Electronic Resource
    Increased dopamine D2 receptor-mediated inhibition of [14C]acetylcholine release in the dorsomedial part of the nucleus accumbens (1989)
    Springer
    Neurochemical research 14 (1989), S. 877-881 
    Details
    ISSN: 1573-6903
    Keywords: Dopamine ; D2 receptors ; nucleus accumbens ; acetylcholine ; quinpirole ; sulpiride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Dopamine (DA) D2 receptor-mediated inhibition of the K+-stimulated release of [14C]acetylcholine (ACh) from prelabeled rat dorsomedial nucleus accumbens slices was found to be 1.7 times greater than that observed in dorsorostral and ventromedial slices. This observation is consistent with the 1.9 fold higher DA D2 receptor density found in the dorsomedial area. In contrast, there were no differences in the DA D2 receptor-mediated effects on [3H]DA release in these areas. In addition, DA D2 receptor-mediated effects on [3H]DA and [14C]ACh release could not be demonstrated in the ventrorostral part of the nucleus accumbens consistent with the fact that DA D2 receptors were barely detectable in this area. The results suggest that cholinergic terminals in the dorsomedial part of the nucleus accumbens are under greater inhibitory DA control than in other areas of the nucleus accumbens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00964818
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  • 6
    Electronic Resource
    Electronic Resource
    β2 Mediated inhibition of [3H]dopamine release from nucleus accumbens slices and monoamine levels in a rat model for attention-deficit hyperactivity disorder (1995)
    Springer
    Neurochemical research 20 (1995), S. 427-433 
    Details
    ISSN: 1573-6903
    Keywords: SHR ; ADHD ; reinforcement ; nucleus accumbens ; α2-adrenoceptor ; dopamine release ; monoamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The spontaneously hypertensive rat (SHR) has been proposed as an animal model for attentiondeficit disorder (ADHD). The behavioural problems have been suggested to be secondary to altered reinforcement mechanisms in which nucleus accumbens dopaminergic activity plays an important role. Interaction between the noradrenergic and dopaminergic system in the nucleus accumbens has been implicated in the locomotor hyperactivity and impaire discriminative performance of SHR. The present study therefore investigated whether there was any change in the α2-adrenoceptor mediated inhibition of dopamine release from nucleus accumbens slices of SHR in comparison with their normotensive Wistar-Kyoto (WKY) controls. The electrically stimulated release of [3H]dopamine (DA) from nucleus accumbens slices was decreased to a similar extent by UK14,304, an α2-adrenoceptor agonist, in SHR and WKY. Basal norepinephrine (NE) levels were increased in locus coeruleus (LC) and A2 noradrenergic nuclei, but not in the A1 nucleus of SHR, while basal serotonin (5-HT) levels were increased in all these pons-medulla nuclei. These results suggest that a primarily dysfunctional LC and A2 nucleus does not have a secondary effect on dopaminergic transmission in the nucleus accumbens via α2-adrenoceptor mediated inhibition of DA release. Basal monoamine levels in several brain areas of SHR were significantly different from that of WKY. DA, and 5-HT turnover were decreased in SHR versus WKY suggesting hypofunctional dopaminergic and serotonergic systems in some brain areas of SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00973098
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of δ-aminolaevulinic acid, porphobilinogen and structurally related amino acids on 2-deoxyglucose uptake in cultured neurons (1982)
    Springer
    Neurochemical research 7 (1982), S. 1009-1022 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of δ-aminolaevulinic acid (ALA), porphobilinogen (PBG), γ-aminobutyric acid (GABA), muscimol, glutamic acid and kainic acid on [3H]2-deoxy-d-glucose uptake by cultured neurons were investigated. Exposure of the cultures for 4 days, to ALA at concentrations as low as 10 μM caused a significant, dose-dependent decrease in [3H]2-deoxy-d-glucose uptake. Neither ALA nor PBG appeared to interfere directly with glucose transport into the neuron but 1 mM ALA caused an initial stimulation of [3H]2-deoxy-d-glucose uptake which increased to a maximum after 4 hr and fell to below control values after 19 hr exposure. GABA and muscimol caused similar increases in [3H]2-deoxy-d-glucose uptake but these values remained above control levels after 19 hr exposure. Glutamic acid and kainic acid caused an immediate increase in [3H]2-deoxy-d-glucose uptake which declined to mininum values after 4 hr exposure. The effect of ALA on glucose utilization in neurons may be of particular relevance to patients with acute porphyria where a genetic lesion in neural haem and haemoprotein biosynthesis is postulated to occur. ALA appeared to be more toxic to the neurons than any of the other compounds tested, possibly causing a critical depletion of energy reserves and cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00965140
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  • 8
    Electronic Resource
    Electronic Resource
    Effects of combined administration ofl-tryptophan and tricyclic antidepressants on α2- and β-adrenoceptors and monoamine levels in rat brain (1985)
    Springer
    Neurochemical research 10 (1985), S. 1661-1671 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to test whether co-administration of a serotonin precursor with antidepressant drugs could potentiate the effects of the antidepressants on monoamines or adrenoceptors in rat brain,l-tryptophan (20 mg/kg) was administered to rats daily for 7 or 15 days, either alone or in combination with desipramine (10 mg/ kg) or amitriptyline (10 mg/kg). After treatment withl-tryptophan for 7 days, increases were observed in rat hypothalamic and frontal cortex 5-hydroxy-3-indoleacetic acid levels as well as in hypothalamic dopamine and nucleus accumbens 3,4-dihydroxyphenylacetic acid levels. After 15 days, hippocampal β-adrenoceptor density was found to be decreased. There was no evidence of potentiation of desipramine or amitriptyline action whenl-tryptophan was administered in combination with the antidepressants. On the contrary, the antidepressants appeared to interact withl-tryptophan to reduce its effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00988608
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  • 9
    Electronic Resource
    Electronic Resource
    Lack of effect of chronic desipramine treatment on dopaminergic activity in the nucleus accumbens of the rat (1989)
    Springer
    Neurochemical research 14 (1989), S. 661-665 
    Details
    ISSN: 1573-6903
    Keywords: DA/ACh release ; DA D1/D2-receptors ; nucleus accumbens ; desipramine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The binding of [3H]SCH 23390 to dopamine (DA) D1-receptors was measured in the nucleus accumbens of rats treated chronically with desipramine for 14 days. DA D1 — and D2-receptor binding using [3H]SCH 23390 and [3H]spiperone, respectively as ligands, was determined in rats treated for 28 days. NeitherB max norK d values were influenced by chronic desipramine treatment. In addition, chronic desipramine treatment (28 days) did not influence the dose dependent, quinpirole (10–1000 nM)-mediated inhibition of the electrically stimulated release of [3H]DA and [14C]ACh from nucleus accumbens slices or the dose dependent increase in [3H]DA release and decrease in [14C]ACh release in the presence of 1 and 10 μM nomifensine. Therefore, our results suggest that the effect of chronic antidepressant treatment cannot be attributed to changes in either DA D11-or D2-receptor binding or DA D2-receptor function in the nucleus accumbens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00964876
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  • 10
    Electronic Resource
    Electronic Resource
    Effects of α2- and β-adrenoceptor agonists on growth hormone secretion following lesion of the noradrenergic system of the rat (1992)
    Springer
    Neurochemical research 17 (1992), S. 1255-1260 
    Details
    ISSN: 1573-6903
    Keywords: GH ; DSP4 ; 6-OHDA ; MFB ; lesion ; clonidine ; isoproterenol ; PVN
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present investigation was to lesion the noradrenergic system and to measure the effect on growth hormone (GH) secretion following peripheral administration of α2- and β-adrenoceptor agonists. Direct injection of these agonists into the paraventricular nucleus of the hypothalamus (PVN) and its effect on GH secretion were also investigated. Systemic administration of N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4, 60 mg/kg, injected i.p. 10 days prior to experimentation) significantly decreased the noradrenaline (NA) content of the hippocampus, frontal cortex and hypothalamus but had no effect on the dopamine (DA) or serotonin (5-HT) content of these areas. Bilateral injection of 6-hydroxydopamine (6-OHDA, 10 μg/μl, 14 days prior to experimentation) into the medial forebrain bundle (MFB) caused a greater reduction of NA and also decreased the DA and 5-HT content of the hypothalamus. Analysis of the PVN of the hypothalami of rats following 6-OHDA lesion of the MFB showed significantly decreased NA and 5-HT content. Neither DSP4 treatment nor 6-OHDA lesion of the MFB affected the clonidine (250 μg/kg, i.p.) induced stimulation of GH secretion. Injection of isoproterenol (1 mg/kg, i.p.) had varying effects on GH secretion. It stimulated GH release in control rats but not in DSP4 or MFB lesioned rats. Direct injection of clonidine (0.1 μg/μl) into the PVN significantly stimulated GH secretion, whereas injection of isoproterenol (2.5 μg/μl) into the PVN did not affect GH levels when compared to controls. The results of the present study do not support the hypothesis that hypoactivity of the central noradrenergic system may be the cause of the blunted GH response to clonidine observed in depressed patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00968409
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