Abstract
The effects of applying 4-aminopyridine (10−2 M), aminooxyacetic acid (AOAA — 10−4–10−3 M), β-alanine (10−3–10−2 M), and bicuculline (10−5, 10−4 M) to the intact frog olfactory bulb were investigated. Having measured inhibition of orthodromic potential postsynaptic components produced either by a puff of air on the olfactory mucosa (OB input inhibition) or by single electrical stimulation of the olfactory nerve (postsynaptic inhibition) or by single electrical stimulation of the olfactory nerve (postsynaptic inhibition), it was found that 4-aminopyridine greatly intensified postsynaptic inhibition but strongly reduced that of OB input; inhibition of the latter was raised by AOAA or bicuculline and decreased by β-alanine. These substances failed to exert any consistent, clear-cut effects on postsynaptic inhibition. Findings would support the hypothesis that OB input inhibition produced by a puff of air on the olfactory mucosa could occur as a result of GABA release from glial cells and subsequent binding of GABA to presynaptic GABAB-receptors in glomeruli.
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M. V. Lomonosov Moscow State University. Translated from Neirofiziologiya, Vol. 19, No. 1, pp. 12–20, January–February, 1987.
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Potapov, A.A. Pharmacological study of inhibited frog olfactory bulb glomerular input produced by a puff of air on the olfactory mucosa. Neurophysiology 19, 8–15 (1987). https://doi.org/10.1007/BF01055989
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DOI: https://doi.org/10.1007/BF01055989