Antagonism of Insect Muscle Glutamate Receptors — with Particular Reference to Arthropod Toxins

1989 ◽  
pp. 13-31 ◽  
Author(s):  
Peter N. R. Usherwood ◽  
Ian S. Blagbrough
Keyword(s):  
Glutamate Receptors ◽  
Insect Muscle

scholarly journals Single-Channel Studies of the Action of (+)-Tubocurarine on Locust Muscle Glutamate Receptors

1987 ◽  
Vol 127 (1) ◽  
pp. 121-134
Author(s):  
C. J. KERRY ◽  
R. L. RAMSEY ◽  
M. S. P. SANSOM ◽  
P. N. R. USHERWOOD ◽  
H. WASHIO
Keyword(s):  
Glutamate Receptors ◽  
Open Channel ◽  
Single Channel ◽  
Muscle Fibres ◽  
Voltage Sensitivity ◽  
Channel Block ◽  
Patch Clamp Technique ◽  
Insect Muscle ◽  
Locust Muscle ◽  
Selective Channel

The effects of (+)-tubocurarine (TC) on single glutamate-activated channels in voltage-clamped locust muscle fibres have been examined using the patch-clamp technique. Glutamate alone produced a concentration-dependent increase in the probability of the channel being in the open state (po), but an increase in the concentration of glutamate (5×10−5-5×10−3 moll−1) in the presence of 5×10−4 moll−1 TC left po essentially unchanged. TC (5×10−6-5×10−4moll−1) caused a concentration- dependent decrease in the mean open time and in po for channels opened by 10−4 moll−4 glutamate. Correlations between successive openings and successive closings, which are characteristic of the kinetics of the muscle glutamate-receptorgated channel of locust muscle, were weakened in the presence of TC. There was little evidence of voltage sensitivity of TC action over the limited membrane potential (Vm) range −70 to −120 mV. The results are consistent with the idea that TC blocks the cation-selective channel gated by glutamate receptors in insect muscle and that the unblocking rate is low. They suggest also that block is at the level of the open channel, a conclusion supported by the wholly activation-induced depression of the neurally evoked twitch contraction of locust muscle by TC. Based upon a simple model for open channel block, TC is estimated to have a dissociation constant of 1.57 μmoll−1 (Vm = −100mV). The rate of association of blocker with channel is estimated to be 8.74×10−3ms−1(moll−1)−1 (Vm=−100mV). The rate of dissociation, estimated indirectly from the single-channel data, is 1.53×10−2ms−1, which gives a mean channel block time of 65.4 ms.

Concanavalin A blocks desensitisation of glutamate receptors on insect muscle fibres

Nature ◽  
1976 ◽  
Vol 259 (5542) ◽  
pp. 409-411 ◽  
Author(s):  
D. A. MATHERS ◽  
P. N. R. USHERWOOD
Keyword(s):  
Glutamate Receptors ◽  
Concanavalin A ◽  
Muscle Fibres ◽  
Insect Muscle

426: Potential Signal Generation Through Metabotropic Glutamate Receptors by Prostate Specific Membrane Antigen

2004 ◽  
Vol 171 (4S) ◽  
pp. 112-112
Author(s):  
Aaron Milbank ◽  
Mike Aleman ◽  
Kelley Harsch ◽  
Nick Detore ◽  
Eric A. Klein ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Signal Generation ◽  
Prostate Specific Membrane Antigen ◽  
Metabotropic Glutamate ◽  
Potential Signal ◽  
Specific Membrane

Glioblastoma invasion and NMDA receptors: A novel prospect

2019 ◽  
Vol 106 (3) ◽  
pp. 250-260 ◽  
Author(s):  
DN Nandakumar ◽  
P Ramaswamy ◽  
C Prasad ◽  
D Srinivas ◽  
K Goswami
Keyword(s):  
Glutamate Receptors ◽  
Cell Lines ◽  
Intracellular Signaling ◽  
Transcript Level ◽  
Glioblastoma Cells ◽  
Invasion And Migration ◽  
Matrigel Invasion ◽  
Nmdar Activation ◽  
And Migration

Purpose Glioblastoma cells create glutamate-rich tumor microenvironment, which initiates activation of ion channels and modulates downstream intracellular signaling. N-methyl-D-aspartate receptors (NMDARs; a type of glutamate receptors) have a high affinity for glutamate. The role of NMDAR activation on invasion of glioblastoma cells and the crosstalk with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) is yet to be explored. Main methods LN18, U251MG, and patient-derived glioblastoma cells were stimulated with NMDA to activate NMDAR glutamate receptors. The role of NMDAR activation on invasion and migration and its crosstalk with AMPAR were evaluated. Invasion and migration of glioblastoma cells were investigated by in vitro trans-well Matrigel invasion and trans-well migration assays, respectively. Expression of NMDARs and AMPARs at transcript level was evaluated by quantitative real-time polymerase chain reaction. Results We determined that NMDA stimulation leads to enhanced invasion in LN18, U251MG, and patient-derived glioblastoma cells, whereas inhibition of NMDAR using MK-801, a non-competitive antagonist of the NMDAR, significantly decreased the invasive capacity. Concordant with these findings, migration was significantly augmented by NMDAR in both cell lines. Furthermore, NMDA stimulation upregulated the expression of GluN2 and GluA1 subunits at the transcript level. Conclusions This study demonstrated the previously unexplored role of NMDAR in invasion of glioblastoma cells. Furthermore, the expression of the GluN2 subunit of NMDAR and the differential overexpression of the GluA1 subunit of AMPAR in both cell lines provide a plausible rationale of crosstalk between these calcium-permeable subunits in the glutamate-rich microenvironment of glioblastoma.

Sign in / Sign up

Export Citation Format

Share Document