[3H]gamma‐Aminobutyric acid uptake into neuroglial cells of rat superior cervical sympathetic ganglia.

Abstract

KI, 28 /UM), fi-alanine (KI, 55 /LM), y-amino-fl-hydroxybutyric acid (KI, 220 /LM), fl-amino-n-butyric acid (KI, 708 jzm), 3-aminopropanesulphonic acid (KI, 832 /IM) and taurine (KI > 1 mM). Uptake was not depressed by 1 mM-glycine, a-alanine, leucine, serine, methionine or ac-amino-iso-butyric acid.8. Radioactively labelled methionine, leucine, glycine, serine, fi-alanine and taurine (concentrations < 5SUM) were also taken up by ganglia. Of these, only uptake of fl-alanine and taurine were significantly depressed by 1 mm-GABA.9. Autoradiographs confirmed that [3H]GABA and [3H]fl-alanine were taken up predominantly into extraneuronal sites (presumed to be neuroglial cells). Methio-

Differential effect of zinc on the vertebrate GABAA‐receptor complex

“…Larger doses of GABA were now required to observe any response, due to the presence of avid GABA uptake mechanisms in this tissue (Bowery et al, 1979). Zinc (200-500pM) slightly hyperpolarized the cell, similar to the effects observed on foetal cultured neurones, and also increased the resting input resistance.…”

Ganglionic GFAP+ glial Gq-GPCR signaling enhances heart functions in vivo

“…It is possible that SGC Gq-GPCR signaling regulates the excitability of postganglionic neurons via the modulation of these channels and transporters. Sympathetic SGCs also express GABA transporters (76,77), which have been shown to regulate extracellular GABA concentration in a Ca 2+ -dependent manner in astrocytes (78). These endogenous mechanisms can function independently of nicotinic ganglionic transmission, which is not responsible for the cardiovascular phenotypes induced by SGC Gq-GPCR activation in Gfap-hM3Dq mice ( Figure 4E).…”

The EFFECT OF ANAESTHETICS ON THE UPTAKE AND RELEASE OF Γ‐AMINOBUTYRATE AND D‐ASPARTATE IN RAT BRAIN SLICES

“…Similarly, the effect of alphaxalone/alphadolone was weak at anaesthetic concentrations. The bizarre relationship between the (Wheeler & Boyarski, 1968;Schon & Kelly, 1973;Bowery, Brown, White & Yamini, 1979) and can be released from glial cells by elevated extracellular K+ concentrations (Bowery & Brown, 1972;Minchin & Iversen, 1974). However, there is some uncertainty as to whether elevated K+ concentration releases amino acids from nerves (De Feudis, 1971;Weinreich & Hammerschlag, 1975).…”