The release of amino acids from nerve during stimulation

Wheeler, D. D.; Boyarsky, L. L.; Brooks, William H.

doi:10.1002/jcp.1040670116

Cited by 68 publications

(25 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…K+ regulation is necessary for axonal function because of the effects of raised [K*l on the resting membrane potential, action potential amplitude, propagation velocity, and excitability and the safety factor for propagation, especially at branch points (Smith, 1980). This study adds to the literature showing that neurotransmitter can be released by structures other than axon terminals (Defeudis, 1971;Johnson and Pilar, 1980;Weinreich and Hammerschlag, 1975;Wheeler et al, 1966) but, more importantly, indicates that such release can have an important role in communication between axons and their surrounding glial cells. The communication is likely to be an essential way in which the glial cell properties are modified to preserve neuronal excitability properties during periods of increased neural activity.…”

Section: Discussionmentioning

confidence: 67%

Evidence that glutamate mediates Axon‐to‐Schwann cell signaling in the squid

Lieberman¹,

Abbott²,

Hassan³

1989

Glia

View full text Add to dashboard Cite

High-frequency stimulation (100 Hz) of isolated giant axons of the small squid Alloteuthis subulata and the large squid Loligo forbesi caused the periaxonal Schwann cell resting potential (Em = -40 mV) to hyperpolarize up to 11 mV in direct proportion to train duration and action potential amplitude. In both species, the Schwann cell also hyperpolarized up to 17 mV with the application of L-glutamate (10(-9) to 10(-6) M), in a dose-dependent manner. By contrast, in the presence of 10(-8) M d-tubocurarine (d-TC) to block the cholinergic component of the Schwann cell response, Schwann cells depolarized 8-9 mV during electrical stimulation of the axon or application of L-glutamate. In the presence of 10(-5) M 2-amino-4-phosphonobutyrate (2-APB), the hyperpolarization to glutamate and to axon stimulation was blocked, whereas the cholinergic (carbachol-induced) hyperpolarization was unaffected. In experiments with Alloteuthis, L-aspartate (10(-7) M) also caused a Schwann cell hyperpolarization, but this was not blocked by 2-APB. In tests with glutamate receptor agonists and antagonists, quisqualate (10(-5) M) produced a hyperpolarization blocked by 10(-4) M L-glutamic acid diethylester (GDEE), which also blocked the response to axonal stimulation. Kainic acid (10(-4) M) also caused a hyperpolarization, but n-methyl-D-aspartate (NMDA; 10(-4) M), ibotenate (10(-5) M), alpha-amino-3-hydroxy-5-methyl-isoxazole proprionate (AMPA; (10(-4) M), and isethionate (10(-5) M) had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Section: Discussionmentioning

confidence: 67%

Evidence that glutamate mediates Axon‐to‐Schwann cell signaling in the squid

Lieberman¹,

Abbott²,

Hassan³

1989

Glia

View full text Add to dashboard Cite

show abstract

“…A Ca2+-insensitive non-quantal 'leakage' of transmitter -acetylcholine in vertebrates, and glutamate in invertebrates -is known to occur at motor nerve terminals (see Katz & Miledi, 1977;Vyskocil, Nikolsky & Edwards, 1983;Antonov & Magazanik, 1988). Glutamate leakage has also been shown to occur from axons in regions distant from sites of synaptic contact such as in the giant axon of the squid 253 (Lieberman, Abbott & Hassan, 1989), where glutamate is thought to mediate axon to Schwann cell signalling, and also in the peripheral and central nerve trunks of vertebrates (Wheeler, Boyarski & Brooks, 1966;Weinreich & Hammerschlag, 1975) and invertebrates (Evans, 1974). This has led to the suggestion (Usowicz et al 1989) that such receptors may be involved in neuronal glial signalling in white matter.…”

Section: Discussionmentioning

confidence: 99%

Activation of glutamate receptors and glutamate uptake in identified macroglial cells in rat cerebellar cultures.

Wyllie

Mathie

Symonds

et al. 1991

The Journal of Physiology

143

View full text Add to dashboard Cite

SUMMARY1. Patch-clamp methods have been used to examine the action of excitatory amino acids on three types of glial cell in cultures of rat cerebellum, namely type-ilike astrocytes, type-2 astrocytes and oligodendrocytes. In addition we have examined glutamate sensitivity of the precursor cell (the O-2A progenitor) that gives rise to type-2 astrocytes and oligodendrocytes.2. Glutamate (30 ftM), quisqualate (3-100 ,tM), (S)-a-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA, 10-30 /SM) and kainate (10-500 ,uM) were applied to cerebellar type-2 astrocytes examined under whole-cell voltage clamp. Each of these agonists induced inward currents in cells held at negative membrane potentials. The currents reversed direction near 0 mV holding potential. N-Methyl-D-aspartate (NMDA, 30-100 /,M) or aspartate (30 ,tM) in the presence of glycine (1 /1M) did not evoke any whole-cell current changes in type-2 astrocytes.3. The distribution of glutamate receptors in type-2 astrocytes was mapped with single-or double-barrelled ionophoretic pipettes containing quisqualate or kainate. Application of these agonists (current pulses 100 ms, 50-100 nA) to cells held at -60 mV evoked inward currents of 20-120 pA in the cell soma and 10-80 pA in the processes. Responses could also be obtained at the extremities of processes (-% 60 ,um from the soma). D. J. A. WYLLIE AND OTHERS type-1-like astrocytes were inhibited when external Na+ was replaced by Li', although Li+ was found to pass through the glutamate channel in type-2 astrocytes.6. Oligodendrocytes in cerebellar cultures did not respond to glutamate, quisqualate or kainate indicating a lack both of a detectable electrogenic glutamate uptake mechanism and of glutamate receptor ion channels in these cells.7. We conclude that, of the various macroglial cells, only the type-2 astrocyte and its progenitor cell possess 'fast' glutamate receptor channels in short-term ( < 4 day) cultures. Detectable uptake currents were confined to type-i-like astrocytes. However, in older cultures (> 7 day) type-I-like astrocytes also developed glutamate receptor channels, in addition to their uptake currents. The possible involvement of glial glutamate receptors and glutamate uptake in neuronal-glial interaction is considered.

show abstract

“…It has been shown that, besides the primary afferent fibers (Wheeler et al, 1966;Roberts, 1974;Takeuchi et al, 1983;Kawagoe et al, 1986), some descending pathways in the dorsal significant. In addition, they found that the release of Glu, but not of Asp, was decreased or abolished in the perfusing medium containing low concentrations of CaZ+ or TTX.…”

Section: Aspmentioning

confidence: 99%

Tachykinins and calcitonin gene-related peptide enhance release of endogenous glutamate and aspartate from the rat spinal dorsal horn slice

1990

View full text Add to dashboard Cite

The effects of dorsal root stimulation and of substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP) on the basal release of 9 endogenous amino acids, including glutamate (Glu) and aspartate (Asp), have been investigated using the rat spinal cord slice-dorsal root ganglion preparation and high-performance liquid chromatography with fluorimetric detection. High-intensity repetitive electrical stimulation of a lumbar dorsal root produced a Ca2(+)- dependent increase in the basal release of Asp, Glu, glycine (Gly), serine (Ser), and threonine (Thr). Low concentrations of SP (2 x 10(-7) M) caused a selective increase in the rate of basal release of Glu, whereas higher concentrations (1–5 x 10(-6) M) produced, in addition, an increase in the basal release of Asp. The SP-induced increase of Glu persisted in the absence of external Ca2+, but the effect was blocked by (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-SP, an SP analog claimed to be an antagonist of the synthetic SP. NKA (5 x 10(-7) - 10(-6) M), a related tachykinin coexpressed with SP in primary sensory neurons, enhanced the basal release of Gly. CGRP (10(-7) M) caused a significant, largely Ca2(+)-independent increase in the basal release of Glu and Asp and a decrease in asparagine. SP and CGRP potentiated the electrically evoked release of Glu and Asp. Neonatal capsaicin treatment did not significantly alter the basal efflux of 9 endogenous amino acids from the spinal slices, but it prevented the dorsal root stimulation-evoked release of Asp, Glu, Gly, and Thr and the SP-induced increase in the basal release of Glu. However, the effect of CGRP was not significantly modified by the capsaicin treatment. These results indicate that tachykinins (SP and NKA) and CGRP are capable of modulating the basal and electrically evoked release of endogenous Glu and Asp, and these actions may provide an important mechanism by which the peptides contribute to the regulation of the primary afferent synaptic transmission. The enhancement of the basal and the dorsal root stimulation-evoked release of Glu and Asp by tachykinins and CGRP may have important physiological implications for strengthening the synaptic connections in the spinal dorsal horn.

show abstract

The release of amino acids from nerve during stimulation

Cited by 68 publications

References 11 publications

Evidence that glutamate mediates Axon‐to‐Schwann cell signaling in the squid

Evidence that glutamate mediates Axon‐to‐Schwann cell signaling in the squid

Activation of glutamate receptors and glutamate uptake in identified macroglial cells in rat cerebellar cultures.

Tachykinins and calcitonin gene-related peptide enhance release of endogenous glutamate and aspartate from the rat spinal dorsal horn slice

Contact Info

Product

Resources

About