Inhibition of γ-aminobutyric acid uptake into astrocytes by pentobarbital

1978 ◽  
Vol 56 (6) ◽  
pp. 1083-1087 ◽  
Author(s):  
L. Hertz ◽  
B. R. Sastry
Keyword(s):  
Uptake Rate ◽  
Primary Cultures ◽  
Pharmacological Action ◽  
Aminobutyric Acid ◽  
Acid Uptake

Pentobarbital (0.5–2 mM), but not phenobarbital, was found to inhibit the uptake of γ-aminobutyric acid into mouse astrocytes in primary cultures by up to 45%. This inhibition was additive to a reduction in uptake rate caused by excess potassium. Its possible role in the pharmacological action of pentobarbital is discussed.

scholarly journals Inhibition of high-affinity gamma-aminobutyric acid uptake in primary astrocyte cultures by phorbol esters and phospholipase C

1991 ◽  
Vol 275 (2) ◽  
pp. 435-439 ◽  
Author(s):  
J Gomeza ◽  
M Casado ◽  
C Gimenez ◽  
C Aragon
Keyword(s):  
Phospholipase C ◽  
Glial Cells ◽  
Kinase Inhibitor ◽  
Primary Cultures ◽  
Aminobutyric Acid ◽  
Gaba Uptake ◽  
Acid Uptake ◽  
Gamma Aminobutyric Acid ◽  
Gaba Transport ◽  
High Affinity

The effects of phorbol 12-myristate 13-acetate (PMA), a potent activator of protein kinase C (PKC), on high-affinity Na(+)-dependent gamma-aminobutyric acid (GABA) uptake were investigated in primary cultures of neurons and glial cells from rat brain cortex. Incubation of glial cells with PMA led to concentration- and time-dependent decreases in the GABA transport in glial cells. This effect could be completely suppressed by addition of the PKC inhibitor H7. The PMA effects could be mimicked by oleoylacetylglycerol, the diacylglycerol kinase inhibitor R59022 and exogenous phospholipase C. Treatment with PMA did not affect GABA transport in neuronal cells.

Systemic CI-966, a new γ-aminobutyric acid uptake blocker, enhances γ-aminobutyric acid action in CA1 pyramidal layer in situ

1990 ◽  
Vol 68 (9) ◽  
pp. 1194-1199 ◽  
Author(s):  
U. Ebert ◽  
K. Krnjević
Keyword(s):  
Aminobutyric Acid ◽  
Gaba Uptake ◽  
Acid Uptake ◽  
Sprague Dawley ◽  
Nipecotic Acid ◽  
Ca1 Region ◽  
Stratum Pyramidale ◽  
Sprague Dawley Rats ◽  
Pyramidal Layer ◽  
Urethane Anaesthesia

A new potent, blood–brain barrier permeable γ-aminobutyric acid (GABA) uptake blocker, 1-[2-[bis[4-(trifluoromethyl)-phenyl]methoxy]ethyl]-1,2,5,6-tetrahydro-3-pyridinecarboxylic acid (CI-966) was administered systemically by i.p. injection (5 mg/kg) in Sprague–Dawley rats under urethane anaesthesia. Twenty to thirty minutes after injection there was a highly variable, but overall significant, enhancement of the inhibition of hippocampal population spikes by GABA applied by microiontophoresis in the CA1 region. Like the effect of nipecotic acid (applied locally by iontophoresis), the potentiation by CI-966 was clearest when GABA was applied in or near the stratum pyramidale where its action normally is weakest and shows the most pronounced fading. This change in GABA potency is most simply explained by a reduction in GABA uptake.Key words: GABA, muscimol, nipecotic acid, GABA-uptake blocker, epilepsy.

Sleep promoting effect of a putative glial γ-aminobutyric acid uptake blocker applied in the thalamus of cats

1991 ◽  
Vol 209 (1-2) ◽  
pp. 131-133 ◽  
Author(s):  
G. Juhász ◽  
K.A. Kékesi ◽  
Zs. Emri ◽  
J. Ujszászi ◽  
P. Krogsgaard-Larsen ◽  
...  
Keyword(s):  
Aminobutyric Acid ◽  
Acid Uptake ◽  
Promoting Effect

Variations in the kinetic pattern of astrocytic γ-aminobutyric acid uptake when inhibited by different barbiturates

1982 ◽  
Vol 31 (16) ◽  
pp. 2694-2696 ◽  
Author(s):  
Orla M. Larsson ◽  
Arne Schousboe ◽  
Povl Krogsgaard-Larsen ◽  
Leif Hertz
Keyword(s):  
Aminobutyric Acid ◽  
Acid Uptake ◽  
Kinetic Pattern

cAMP stimulates fluorescent bile acid uptake into hepatocytes by membrane hyperpolarization

1996 ◽  
Vol 270 (2) ◽  
pp. G339-G346 ◽  
Author(s):  
S. Grune ◽  
X. J. Meng ◽  
S. A. Weinman
Keyword(s):  
Bile Acid ◽  
Voltage Clamp ◽  
Uptake Rate ◽  
Direct Consequence ◽  
Acid Uptake ◽  
Net Charge ◽  
Membrane Hyperpolarization ◽  
Whole Cell ◽  
Bile Acid Uptake ◽  
Stimulation Of

Elevation of intracellular adenosine 3',5'-cyclic monophosphate (cAMP) hyperpolarizes hepatocytes and increases the uptake rate of bile acids. The purpose of this study was to determine to what extent these two phenomena are linked. Fluorescent bile acid analogues (FBA) were used to probe bile acid transport into whole cell patch-clamped hepatocytes. Na(+)-dependent uptake of cholyl-nitrobenz-2-oxa-1,3-diazol-4-yl-lysine (C-NBD-L), an FBA with a net charge of -1, was shown to be electrogenic, whereas uptake of cholylglycylamidofluorescein (CGamF), an FBA with a net charge of -2, was neutral. Incubation of hepatocytes with 8-bromo-cAMP (8-BrcAMP; 100 microM) increased the uptake rate of the electrogenically transported FBA by 25% (P = 0.002), but had no effect on the uptake rate of the electroneutrally transported FBA. Microelectrode impalements revealed that 8-BrcAMP or forskolin hyperpolarized hepatocytes by 6-8 mV. To determine if hyperpolarization is responsible for the cAMP-induced increase in uptake rate, cAMP was directly introduced into hepatocytes during whole cell patch clamp under voltage-clamp conditions. As long as voltage clamp was maintained at -30 mV there was no stimulation of C-NBD-L uptake. However, when voltage clamp was terminated by either pipette removal or current clamp, cAMP increased the uptake rate by 25-34% (P < 0.002). In both of these protocols, cAMP had no effect on uptake of the electroneutrally transported FBA, CGamF. Finally, in voltage-clamped hepatocytes in the absence of cAMP, a 10-mV hyperpolarization increased the uptake rate of C-NBD-L by 23%. We therefore conclude that short-term cAMP-induced stimulation of fluorescent bile acid uptake in hepatocytes is a direct consequence of membrane hyperpolarization.

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