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GABAB Receptor Control of Neurotransmitter Release in Mammalian Brain: Modification During Chronic Inflammation

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Part of the book series: NATO ASI Series ((ASIH,volume 100))

Abstract

The evidence for a GABA receptor which was distinct from the classical chloride-dependent ionotropic receptor first emerged in mammalian peripheral tissues (Bowery et al 1981; see Bowery 1989). In a variety of isolated nerve-smooth muscle and atrial muscle preparations, GABA and its analogue, ß-chlorophenyl GABA (baclofen), were shown to depress the contractile response to nerve stimulation. A typical example of this is shown in Figure 1 where increasing concentrations of baclofen produced a decrease in contraction of the twitch response of the rat anoccocygeus muscle. This reduction in contraction was produced by a decrease in transmitter release from the autonomic innervation. No evidence for any effect at the postsynaptic site was observed. Thus, in general, the influence of GABA was restricted to the nerve input and could be construed as acting on the presynaptic release mechanism in peripheral tissues. The characteristics of the receptor mediating this effect showed little resemblance to the established GABA receptor but it seemed unlikely that it had any physiological significance, perhaps with the exception of the enteric nervous system where GABA neurones have been demonstrated (see Kerr & Ong 1995).

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© 1997 Springer-Verlag Berlin Heidelberg

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Bowery, N.G., Malcangio, M., Teoh, H. (1997). GABAB Receptor Control of Neurotransmitter Release in Mammalian Brain: Modification During Chronic Inflammation. In: Pöğün, Ş. (eds) Neutrotransmitter Release and Uptake. NATO ASI Series, vol 100. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60704-2_10

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  • DOI: https://doi.org/10.1007/978-3-642-60704-2_10

  • Publisher Name: Springer, Berlin, Heidelberg

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