New Evidence That L‐glutamate Is a Transmitter at the Squid Giant Synapse

Santis, A. De; Messenger, J. B.

doi:10.1113/expphysiol.1989.sp003259

Cited by 19 publications

(15 citation statements)

References 14 publications

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“…L-Glutamate is the strongest candidate, since transmission at the synapse is reversibly inhibited by several specific blockers of glutamate receptors in other systems (DeSantis & Messenger, 1989). However, attempts to mimic transmission by close postsynaptic iontophoresis or bath application of glutamate or glutamate receptor agonists fail to discharge postsynaptic action potentials and only result in slow, weak depolarizations (Miledi, 1967;DeSantis, Eusebi & Miledi, 1975;Adams & Gillespie, 1988; DeSantis & Messenger, 1989). The giant synapse is a complex structure (Young, 1973) with numerous postsynaptic processes penetrating a tight sheath to make about 15000 functional contacts with the presynaptic fibre (Martin & Miledi, 1986).…”

Section: Introductionmentioning

confidence: 99%

Postsynaptic activation at the squid giant synapse by photolytic release of L‐glutamate from a ‘caged’ L‐glutamate.

Corrie

DeSantis

Katayama

et al. 1993

The Journal of Physiology

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SUMMARY1. Pharmacological evidence suggests L-glutamate is a strong candidate as a transmitter at the giant synapse of the squid. Postsynaptic activation at the giant synapse cannot be effected by conventional application of putative neurotransmitters by iontophoresis or perfusion, apparently because the complex structure of the synapse prevents a sufficiently rapid change in concentration at the postsynaptic membrane. Flash photolytic release of L-glutamate from a pharmacologically inert 'caged' L-glutamate pre-equilibrated in the stellate ganglion of Alloteuthis or Loligo was used to determine whether L-glutamate can produce postsynaptic activation when released rapidly in the synaptic clefts.2. The preparation, reaction mechanism and properties of the caged L-glutamate, iV-i-(2-nitrophenyl)ethoxycarbonyl-L-glutamate, are described. The product quantum yield on photolysis was 065 (±0-05). On flash photolysis glutamate release followed a single exponential timecourse in the pH range 5 5-7 8. The rate constant was proportional to [He] and was 93 s-1 at pH 5 5 and 16 'C in artificial sea water (ionic strength, I = 0-68 M). 3. At pH 7-8 flash photolysis of caged glutamate pre-equilibrated in the synapse caused only a slow depolarization. A second photolytic release of L-glutamate or transynaptic activation produced no further depolarization, suggesting desensitization and inactivation of postsynaptic mechanisms by the initial pulse of Lglutamate.4. Synaptic transmission in the giant synapse was normal at pH 5-5. Flash photolysis at pH 5-5 caused rapid production of L-glutamate within the synaptic cleft and a fast postsynaptic depolarization which generated postsynaptic action potentials.

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Section: Introductionmentioning

confidence: 99%

Postsynaptic activation at the squid giant synapse by photolytic release of L‐glutamate from a ‘caged’ L‐glutamate.

Corrie

DeSantis

Katayama

et al. 1993

The Journal of Physiology

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“…4b) (P = 0.268). The failure of an EC 50 dose of Glu to affect the firing might be due to a marked diffusion barrier across the isolated ganglion and/or to the rapid neurotransmitter removal from the extracellular space (De Santis and Messenger 1989). This result suggests that Glu elicits the bursting activity of RPeD1 under our experimental conditions.…”

Section: Gaba Hyperpolarizes Rped1 By Activating Gaba a Receptorsmentioning

confidence: 51%

“…Therefore, the electrophysiological effects of such agonists on the whole respiratory circuit were investigated and compared with those exerted by Glu. We reasoned that, if any of AMPA-and kainate-sensitive receptors mediated the respiratory discharge, addition of selective agonists to the perfusate could lead to inhibition of firing by receptor desensitization (Adams and Gillespie 1988;De Santis and Messenger 1989;Nesic et al 1996).…”

Section: Gaba Hyperpolarizes Rped1 By Activating Gaba a Receptorsmentioning

confidence: 99%

GABAA- and AMPA-like receptors modulate the activity of an identified neuron within the central pattern generator of the pond snail Lymnaea stagnalis

et al. 2009

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To examine the neurochemistry underlying the firing of the RPeD1 neuron in the respiratory central pattern generator of the pond snail, Lymnaea stagnalis, we examined electrophysiologically and pharmacologically either "active" or "silent" preparations by intracellular recording and pharmacology. GABA inhibited electrical firing by hyperpolarizing RPeD1, while picrotoxin, an antagonist of GABA(A) receptors, excited silent cells and reversed GABA-induced inhibition. Action potential activity was terminated by 1 mM glutamate (Glu) while silent cells were depolarized by the GluR agonists, AMPA, and NMDA. Kainate exerted a complex triphasic effect on membrane potential. However, only bath application of AMPA desensitized the firing. These data indicate that GABA inhibits RPeD1 via activation of GABA(A) receptors, while Glu stimulates the neuron by activating AMPA-sensitive GluRs.

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“…In contrast, in the squid giant synapse, the postsynaptic response is mediated by an ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-like receptor (Fig. 6), but the molecular identification of this receptor is absent (42). Moreover, since some characteristics of invertebrate glutamate receptors, such as chloride conductance (43), are not retained by their vertebrate counterparts, it is probable that the modulation produced by NGF of squid giant synapse involves target(s) not yet identified in vertebrates.…”

Section: Discussionmentioning

confidence: 99%

Nerve growth factor acutely reduces chemical transmission by means of postsynaptic TrkA-like receptors in squid giant synapse

Moreno

Nadal²,

Leznik³

et al. 1998

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

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Tyrosine phosphorylation has been shown to be an important modulator of synaptic transmission in both vertebrates and invertebrates. Such findings hint toward the existence of extracellular ligands capable of activating this widely represented signaling mechanism at or close to the synapse. Examples of such ligands are the peptide growth factors which, on binding, activate receptor tyrosine kinases. To gain insight into the physiological consequences of receptor tyrosine kinase activation in squid giant synapse, a series of growth factors was tested in this preparation. Electrophysiological, pharmacological, and biochemical analysis demonstrated that nerve growth factor (NGF) triggers an acute and specific reduction of the postsynaptic potential amplitude, without affecting the presynaptic spike generation or presynaptic calcium current. The NGF target is localized at a postsynaptic site and involves a new TrkA-like receptor. The squid receptor crossreacts with antibodies generated against mammalian TrkA, is tyrosine phosphorylated in response to NGF stimulation, and is blocked by specific pharmacological inhibitors. The modulation described emphasizes the important role of growth factors on invertebrate synaptic transmission.

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New Evidence That L‐glutamate Is a Transmitter at the Squid Giant Synapse

Cited by 19 publications

References 14 publications

Postsynaptic activation at the squid giant synapse by photolytic release of L‐glutamate from a ‘caged’ L‐glutamate.

Postsynaptic activation at the squid giant synapse by photolytic release of L‐glutamate from a ‘caged’ L‐glutamate.

GABAA- and AMPA-like receptors modulate the activity of an identified neuron within the central pattern generator of the pond snail Lymnaea stagnalis

Nerve growth factor acutely reduces chemical transmission by means of postsynaptic TrkA-like receptors in squid giant synapse

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