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Glutamate is a transmitter that mediates inhibition at the rectifying electrical motor giant synapse in the crayfish

Heitler, W.J., Watson, Alan, Falconer, Stuart W.P. and Powell, Brian 2001. Glutamate is a transmitter that mediates inhibition at the rectifying electrical motor giant synapse in the crayfish. Journal of Comparative Neurology 430 (1) , pp. 12-26. 10.1002/1096-9861(20010129)430:1<12::AID-CNE1012>3.0.CO;2-J

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Spike transmission at the electrical synapse between the giant fibres (GFs) and motor giant neurone (MoG) in the crayfish can be blocked by depolarising postsynaptic chemical inhibition, which has previously been shown to be mediated in part by γ‐aminobutyric acid (GABA). The authors show that glutamate applied to the synaptic region of the MoG mimics the depolarisation of the chemical input and can also block spike transmission from the GFs. The glutamate induces an inward current mediated by a conductance increase that is 30–40% of that induced by GABA and that is blocked substantially by picrotoxin. Glutamate has no effect on the presynaptic GF, and the effects in the MoG are maintained in the presence of cadmium, indicating that the glutamate is acting directly on the MoG. Both GABA and glutamate have similar effects on the cell body, where the response reverses 10–20 mV positive to resting potential, is dependent on chloride concentration, and is inhibited by picrotoxin. Joint application of glutamate and GABA induces a nonadditive current under voltage clamp, suggesting that the transmitters can activate the same postsynaptic receptors. Immunocytochemical staining shows that, whereas some synaptic profiles impinging on the MoG contain pleomorphic agranular vesicles and are immunoreactive to GABA and not glutamate (as previously reported), there are at least as many other profiles that contain round, agranular vesicles and that are immunoreactive to glutamate and not to GABA. Thus, the authors conclude that some of the interneurones mediating inhibition of the electrical synapse use glutamate as their neurotransmitter

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Publisher: Wiley
ISSN: 0021-9967
Date of First Compliant Deposit: 30 July 2018
Date of Acceptance: 19 December 2000
Last Modified: 31 Jul 2018 14:30

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