TY - JOUR
T1 - Glutamate is a transmitter that mediates inhibition at the rectifying electrical motor giant synapse in the crayfish.
AU - Heitler, William James
AU - Watson, A H D
AU - Falconer, S W P
AU - Powell, B
PY - 2001/1/29
Y1 - 2001/1/29
N2 - 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 gamma -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 las 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. J. Comp. Neurol. 430:12-26, 2001. (C) 2001 Wiley-Liss, Inc.
AB - 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 gamma -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 las 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. J. Comp. Neurol. 430:12-26, 2001. (C) 2001 Wiley-Liss, Inc.
KW - postsynaptic inhibition
KW - escape response
KW - depolarising inhibition
KW - giant fibre
KW - gamma-aminobutyric acid
KW - DEPOLARIZING INHIBITION
KW - ESCAPE BEHAVIOR
KW - NEURONS
KW - GABA
KW - TRANSMISSION
KW - MOTONEURONS
KW - MECHANISMS
KW - SYSTEM
KW - ACID
KW - LEG
UR - http://www.scopus.com/inward/record.url?scp=0035966677&partnerID=8YFLogxK
U2 - 10.1002/1096-9861(20010129)430:1<12::AID-CNE1012>3.0.CO;2-J
DO - 10.1002/1096-9861(20010129)430:1<12::AID-CNE1012>3.0.CO;2-J
M3 - Article
SN - 0092-7317
VL - 430
SP - 12
EP - 26
JO - Journal of Comparative Neurology
JF - Journal of Comparative Neurology
ER -