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  • 1
    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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    Paper (German National Licenses)
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  • 2
    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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    Paper (German National Licenses)
    Fulltext
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