Proton gradient linkage to active uptake of [3H]acetylcholine by Torpedo electric organ synaptic vesicles

Anderson, D. C.; King, S. Bruce; Parsons, Stanley M.

doi:10.1021/bi00256a001

Cited by 135 publications

(63 citation statements)

References 29 publications

(27 reference statements)

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“…Activation of this system increases intracellular sodium, which might suppress the neuronal activities. As another explanation, the synthesis of acetylcholine in the brain has been reported to be impaired even without decreases in ATP during mild hypoxia (GIBSON and BLASS, 1976), and ATP-supported uptake of acetylcholine by synaptic vesicles was found to be suppressed with pH levels remaining acidic (ANDERSON et al, 1982). The decrease in pH has also been shown to inhibit depolarization-induced Cat + entry in synaptosomes (NACHSHEN and BLAUSTEIN, 1979).…”

Section: Discussionmentioning

confidence: 98%

Effect of cerebral ischemia and hypercapnia on cerebral pH studied with 31P-NMR and electrical activity in rat brain.

Yoshizaki¹,

Takanashi²,

Motonaga³

et al. 1989

Jpn.J.Physiol

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The activity of electroencephalogram (EEG) and cortical somatosensory evoked potential (SEP) was suppressed during cerebral Ischemia in rats subjected to the 4-vessel occlusion. Considerable variations were demonstrated in the decrease of phosphocreatine and ATP concentration during ischemia among the rats measured with 31 P-NMR, accompanied with cerebral acidification. Hypercapnia, induced in the rats studied by the inhalation of a gas mixture of 3O-4O° C02, suppressed the activity of EEG and cortical SEP. The cerebral acidification observed during the ischemia was more severe than that under the hypercapnia, implying that cerebral acidification is one of the possible causes for the decrease in the electrical activity of the brain during Ischemia.Key words : cerebral pH, tial, 31 P-NMR.cerebral Ischemia, hypercapnia, evoked potenCerebral ischemia is well known to depress the activity of the brain as demonstrated by electroencephalogram (EEG). NARUSE et al. (1984) demonstrated clearly that cerebral ischemia reduced ATP and phosphocreatine concentration accompanied with cerebral acidification during Ischemia in rats using 31P-NMR. In this study, we examined the effect of ischemia on the activity of cortex and brainstem, monitoring the somatosensory evoked potentials (SEP) and auditory brainstem responses (ABR) together with energy metabolism in rats with 31P-

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Section: Discussionmentioning

confidence: 98%

Effect of cerebral ischemia and hypercapnia on cerebral pH studied with 31P-NMR and electrical activity in rat brain.

Yoshizaki¹,

Takanashi²,

Motonaga³

et al. 1989

Jpn.J.Physiol

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“…This suggests that the vesicular GABA uptake and glycine uptake are both driven by an electrochemical proton gradient, generated by a proton-pump ATPase in the synaptic vesicle membrane. Thus, the nature of the driving force for the vesicular uptake of the inhibitory amino acid neurotransmitters is likely to be very similar to that involved (i) in the vesicular uptake of glutamate (11,12), (ii) in catecholamine uptake into chromaffin granules (22,23) and brain synaptic vesicles (29), or (iii) in acetylcholine uptake into Torpedo synaptic vesicles (30). In contrast, other amino acids such as phenylalanine, leucine, histidine, and proline showed no ATP-dependent uptake into synaptic vesicles prepared from the cerebrum (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Active transport of gamma-aminobutyric acid and glycine into synaptic vesicles.

Kish

Fischer-Bovenkerk

Ueda

1989

Proc. Natl. Acad. Sci. U.S.A.

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Although y-aminobutyric acid (GABA) and glycine are recognized as major amino acid inhibitory neurotransmitters in the central nervous system, their storage is poorly understood. In this study we have characterized vesicular GABA and glycine uptakes in the cerebrum and spinal cord, respectively. We present evidence that GABA and glycine are each taken up into isolated synaptic vesicles in an ATPdependent manner and that the uptake is driven by an electrochemical proton gradient. Uptake for both amino acids exhibited kinetics with low affinity (Km in the millimolar range) similar to vesicular glutamate uptake. The ATP-dependent GABA uptake was not inhibited by the putative amino acid neurotransmitters glycine, taurine, glutamate, or aspartate or by GABA analogs, agonists, and antagonists. Similarly, ATPdependent glycine uptake was hardly affected by GABA, taurine, glutamate, or aspartate or by glycine analogs or antagonists. The GABA uptake was not affected by chloride, which is in contrast to the uptake of the excitatory neurotransmitter glutamate, whereas the glycine uptake was slightly stimulated by low concentrations of chloride. Tissue distribution studies indicate that the vesicular uptake systems for GABA, glycine, and glutamate are distributed in different proportions in the cerebrum and spinal cord. These results suggest that the vesicular uptake systems for GABA, glycine, and glutamate are distinct from each other. y-Aminobutyric acid (GABA) and glycine are the major inhibitory neurotransmitters in the vertebrate central nervous system (1, 2). Recently, the primary structures of GABAA and glycine receptors have been deduced; the subunits of these receptors have been shown to have substantial sequence homology, particularly in the region thought to be involved in conducting chloride (3). GABA and glycine are released upon membrane depolarization, both in a calcium-dependent manner (4-6) and in a calciumindependent manner (4, 7). Recent evidence indicates that the calcium-dependent release of GABA originates from a noncytoplasmic compartment (8). There are also observations indicating that GABA and glycine are concentrated in distinct nerve terminals (9, 10). However, localization of endogenous amino acids in synaptic vesicles has not been clearly demonstrated, either with intact tissues or isolated vesicle preparations. In addition, there has been little study on the vesicular GABA and glycine uptake processes. We have previously provided evidence that glutamate is taken up into synaptic vesicles by a proton-motive force generated by a proton-pump ATPase in the vesicle (11-13). In this communication, we have studied vesicular GABA and glycine uptake, using a synaptic vesicle preparation different from that previously used for vesicular glutamate uptake. We provide evidence that suggests that GABA and glycine are also accumulated into synaptic vesicles in an ATP-dependent manner and that their uptake is driven by an electrochemical proton gradient. We have characterized these uptake systems with r...

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“…Proton-translocating ATPases have also been described in a number of intracellular organelles (Anderson et al, 1982;Hutton, 1982;Dean et al, 1984;Forgac et al, 1983;Galloway et al, 1983;Glickman et al, 1983). Intracellular vesicles with proton pumps fuse with and form from the plasma membrane, and it has been suggested that H+ pumps may participate in cellular pH regulation (Adelsberg & Al-Awqati, 1986).…”

Section: H+-translocating Atpasesmentioning

confidence: 99%