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  • 1
    Electronic Resource
    Electronic Resource
    Tricyclic antidepressant plasma levels after augmentation with citalopram: a case study (1993)
    Springer
    European journal of clinical pharmacology 44 (1993), S. 403-405 
    Details
    ISSN: 1432-1041
    Keywords: Citalopram ; Depression ; tricyclic antidepressants ; pharmakokinetic interaction ; plasma level ; case report ; drug interaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary In a depressed patient, the addition of citalopram 40–60 mg per day to treatment with amitriptyline 75 mg per day had no effect on the plasma levels of amitriptyline and nortriptyline, but it led to clinical improvement without the appearance of adverse effects. This and similar findings in four other patients comedicated with citalopram and amitriptyline (2 patients), clomipramine or maprotiline suggest that citalopram differs from other selective serotonin reuptake inhibitors, such as fluvoxamine and fluoxetine, which have been shown to increase tricyclic antidepressant plasma levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00316483
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  • 2
    Electronic Resource
    Electronic Resource
    Der Schlafentzug (1975)
    Springer
    European archives of psychiatry and clinical neuroscience 221 (1975), S. 111-122 
    Details
    ISSN: 1433-8491
    Keywords: Sleep Deprivation ; Depression ; Activation ; Tryptophan ; Tyrosine ; Schlafentzug ; Depression ; Aktivierung ; Tryptophan ; Tyrosin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 30 depressive Patienten wurden vor und nach Schlafentzug klinisch, psychophysiologisch und biochemisch untersucht. Klinisch fand sich bei den meisten Patienten eine Besserung nach Schlafentzug. Daneben fanden wir Zeichen von Aktivierung und Stress, aber ohne Korrelation mit der klinischen Besserung. Ebenso korrelierten auch die biochemischen Veränderungen nicht mit der klinischen Besserung.
    Notes: Summary Clinical ratings, psychophysiological and biochemical messures were taken from 30 depressive patients before and after sleep deprivation of one night. Most patients improved after sleep deprivation. We found signs of activation and stress, without correlation with clinical improvement. The biochemical changes did not correlate with clinical improvement either.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00431048
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  • 3
    Electronic Resource
    Electronic Resource
    The measurement of the release of endogenous GABA from rat brain slices by liquid chromatography with electrochemical detection (1988)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 337 (1988), S. 284-288 
    Details
    ISSN: 1432-1912
    Keywords: GABA release ; HPLC ; Electrochemical detection ; Brain slices ; GABA uptake inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A method for the determination of GABA by derivatization with 2,4,6-trinitrobenzenesulphonic acid and subsequent separation and quantitation by HPLC with electrochemical detection was characterized with respect to specificity, reproducibility and sensitivity. No other amino acid occurring in significant amounts in the brain was found to interfere; however, adequate separation of the derivatives of GABA and tryptophan must be carefully checked in each experiment. The sensitivity of the method is essentially determined by baseline noise, which mainly depends on the quality of the HPLC pump; under our conditions, it was about 2 ng/ml analyte. The coefficients of variation determined at two different concentrations relevant for the subsequent experiments were well below 10%. The method proved useful for the assessment of endogenous release of GABA from superfused rat cortical slices by electrical stimulation, which, in contrast to the basal release, was found to be completely calcium-dependent at stimulation frequencies of 5 and 12 Hz, under our conditions. Both stimulated and basal release of GABA was enhanced 4–5-fold by the inhibitor of GABA uptake, SK&F 89976 (10 μM).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168840
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  • 4
    Electronic Resource
    Electronic Resource
    Potential involvement of a baclofen-sensitive autoreceptor in the modulation of the release of endogenous GABA from rat brain slices in vitro (1988)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 337 (1988), S. 289-295 
    Details
    ISSN: 1432-1912
    Keywords: Baclofen ; GABA release ; Brain slices ; Muscimol ; Bicuculline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the GABAA agonist, muscimol, and of the enantiomers of the GABAB agonist, baclofen, on the release of endogenous GABA from slices of the rat cerebral cortex, striatum and hippocampus were measured by means of a HPLC method with electrochemical detection. Moreover, the effect of the GABAA antagonist, bicuculline, and of the frequency of stimulation were studied in cortical slices. The amount of endogenous GABA released per impulse from cortical slices decreased by about 50% when the frequency was increased from 0.25 Hz to 1 Hz. This might indicate that GABA inhibited its own release. (−)-Baclofen at 1 and 10 μM, but not its (+)-enantiomer, markedly inhibited the release of endogenous GABA, to a similar extent in all 3 areas investigated. The effect of (−)-baclofen was dependent on the frequency of stimulation: at lower frequencies (0.25 and 0.5 Hz) it was more marked than at a higher one (4 Hz). This would be expected from the results showing that the release of endogenous GABA decreases with increasing frequency, which suggests that this amino acid inhibits its own release. Muscimol at 10 μM, on the other hand, was ineffective in all 3 areas at a stimulation frequency of 0.5 Hz. Bicuculline (10 μM) at 4 Hz, at which autosuppression of GABA release is maximal did not enhance the release of endogenous GABA from cortical slices. With cerebellar or nigral slices, no adequate stimulation-induced release of endogenous GABA could be obtained under comparable conditions. These data are compatible with, but do not prove the existence of GABAB-type presynaptic autoreceptors modulating the release of this amino acid. More definite conclusions may possibly be drawn when a GABAB antagonist becomes available, which is expected to enhance GABA release under appropriate conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168841
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  • 5
    Electronic Resource
    Electronic Resource
    Ca2+-dependent release of endogenous GABA from rat cortical slices from different pools by different stimulation conditions (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 339 (1989), S. 200-207 
    Details
    ISSN: 1432-1912
    Keywords: GABA release ; K+-Stimulation ; Electrical stimulation ; Brain slices ; Glutamate effect ; Baclofen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The previously reported inhibitory effect of (−)-baclofen on the electrically evoked release of endogenous GABA from rat brain slices indicated the possibility of existence of GABAB autoreceptors. In this study, we have tested an alternative explanation, i. e. the possibility that (−)-baclofen reduced an excitatory glutamatergic input to GABAergic neurons by inhibiting glutamate release, by investigating the interaction of 10 mmol/1 l-glutamate with the inhibitory effect of 10 μmol/1(−)-baclofen. l-Glutamate did not affect the electrically evoked release of GABA on its own and did not abolish the effect of (−)-baclofen, suggesting that the latter was not secondary to a reduction of glutamate release. On the other hand, it greatly increased the basal release of GABA and more than doubled the GABA content of the slices at the end of the perfusion, indicating a marked enhancement of GABA synthesis. This additional GABA, apparently formed from exogenous l-glutamate, was not releasable by electrical stimulation at 0.5 or 24 Hz, but at least in part by stimulation with 30 mmol/l K+. The previously reported increase of GABA release at 12 Hz as compared to 4 Hz was studied in more detail. GABA released by electrical stimulation at 8–48 Hz was Ca2+-dependent and tetrodotoxin-sensitive. No evidence was obtained for a decrease of the amount of GABA released per impulse with increasing frequency in this range. Moreover, neither (−)-baclofen nor muscimol at 10 μmol/l altered the release of the amino acid at 24 Hz; the former was also tested at a low Ca2+ concentration (0.3 mmol/l) and found to be inactive under these conditions. Thirty mmol/l K+ released about 30% higher amounts of GABA than electrical stimulation at 24 Hz under comparable conditions, in a Ca2+-dependent manner. K+-induced release was not modified by 10 μmol/l (−)-baclofen or muscimol. Our results suggest the existence of at least 2 different, presumably neuronally located, releasable pools of GABA. One is sensitive to electrical stimulation at 0.25–4 Hz and responds to (−)-baclofen, suggesting control by GABAB-type autoreceptors. The existence of a 2nd pool is indicated by the fact that K+ releases substantially more GABA than electrical stimulation and by the exclusive sensitivity of K+-evoked GABA release to exogenous l-glutamate. GABA released by electrical stimulation at frequencies above 4 Hz may come from a 3rd pool. Both the 2nd and the 3rd pool seem to be insensitive to (−)-baclofen and muscimol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165144
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  • 6
    Electronic Resource
    Electronic Resource
    Release of endogenous GABA from the substantia nigra is not controlled by GABA autoreceptors (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 372-378 
    Details
    ISSN: 1432-1912
    Keywords: GABA release ; Electrical/K+ stimulation ; Substantia nigra slices ; Baclofen ; Muscimol ; Bicuculline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The characteristics of the release of GABA from slices of the rat substantia nigra, elicited by electrical stimulation at frequencies of 0.5–48 Hz and by elevated K+ concentrations ranging from 15–35 mmol/l, was studied. Comparisons were made with cortical slices where the data were not available from previous studies. No GABA release could be evoked from rat nigral slices by electrical stimulation between 0.5 and 4 Hz, in contrast to cortical slices, in which this pool is sensitive towards inhibition by (−)-baclofen. Also, comparatively less GABA release could be evoked from nigral than from cortical slices by K+ concentrations between 15 and 25 mmol/l. While (−)-baclofen at 10 μmol/l inhibited release caused by 15 μmol/l K+ in cortical, it did not in nigral slices. GABA release caused by higher frequencies (8–48 Hz) or 30 mmol/l K+ concentrations was Ca2+-dependent and in the former case also tetrodotoxin-sensitive. It had similar characteristics as in cortical slices and was insensitive towards (−)-baclofen, muscimol and bicuculline. Even more markedly than in the cortex, 30 mmol/l K+ released greater amounts of GABA than electrical stimulation at 24 Hz of a similar duration, suggesting the existence of one or several additional pool(s) of lesser excitability. Since the majority of gabaergic nerve endings in the nigra belong to striato- and pallidonigral projection neurons and those in the cortex probably exclusively to various types of interneurons, it seems that (a) one or several of the latter release GABA at low frequencies in a baclofen-sensitive manner and are absent or rare in the s. nigra, and (b) the striato- and pallidonigral projection neurons are not controlled by presynaptic autoreceptors of the GABAA or GABAB type, because neither GABA release elicited by electrical stimulation nor by 30 mmol/l K+ was affected by agents interfering with these types of receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167037
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