The involvement of excitatory amino acids in neocortical epileptogenesis: NMDA and non-NMDA receptors

1991 ◽  
Vol 86 (2) ◽  
Author(s):  
G.G.C. Hwa ◽  
M. Avoli
Keyword(s):  
Amino Acids ◽  
Nmda Receptors ◽  
Excitatory Amino Acids

COMPUTER SIMULATION OF COTRANSMISSION BY EXCITATORY AMINO ACIDS AND ACETYLCHOLINE IN THE ENTERIC NERVOUS SYSTEM

2007 ◽  
Vol 07 (02) ◽  
pp. 229-246
Author(s):  
ROUSTEM MIFTAHOF ◽  
N. R. AKHMADEEV
Keyword(s):  
Amino Acids ◽  
Nervous System ◽  
Nmda Receptors ◽  
Enteric Nervous System ◽  
Ampa Receptors ◽  
Excitatory Amino Acids ◽  
Electrical Response ◽  
Ampa And Nmda Receptors ◽  
Irritable Bowel

The role of cotransmission by α-amino-3-hydroxy-5-methyl-4-isoxalose propionic acid (AMPA), L-aspartate, N-methyl-D-aspartate (NMDA), and acetylcholine (ACh) as well as the coexpression of AMPA, NMDA, and nicotinic ACh (nACh) receptors on the electrophysiological activity of the primary sensory (AH) and motor (S) neurons of the enteric nervous system are numerically assessed. Results of computer simulations showed that AMPA and L-Asp alone can induce fast action potentials of short duration on AH and S neurons. Costimulation of nACh and AMPA receptors on the soma of the S neuron resulted in periodic spiking activity. A characteristic biphasic response was recorded from the AH neuron after coactivation of AMPA and NMDA receptors. Glutamate alone acting on NMDA receptors caused prolonged depolarization of the AH neuron and failed to depolarize the S neuron. Cojoint stimulation of the AMPA or nACh receptors was required to produce the effect of glutamate. The overall electrical response of neurons to the activation of NMDA receptors was long-term depolarization. Acetylcholine, AMPA, and glutamate acting alone or cojointly enhanced phasic contraction of the longitudinal smooth muscle. Treatment of neurons with AMPA, NMDA, and nACh receptor antagonists revealed intricate properties of the AH and S neurons. Application of MK-801, D-AP5, and CPP reduced the excitability of the AH neuron and totally abolished electrical activity in the S neuron. The information gained into the cotransmission by excitatory amino acids and acetylcholine in the enteric nervous system may be beneficial in the development of novel effective therapeutics to treat diseases associated with altered visceral nociception, i.e. irritable bowel syndrome.

Ionic changes induced by excitatory amino acids in the rat cerebral cortex

1987 ◽  
Vol 65 (5) ◽  
pp. 1067-1077 ◽  
Author(s):  
R. Pumain ◽  
I. Kurcewicz ◽  
J. Louvel
Keyword(s):  
Amino Acids ◽  
Motor Cortex ◽  
Nmda Receptors ◽  
Excitatory Amino Acids ◽  
Pyramidal Tract ◽  
Potassium Ions ◽  
Channel Blockers ◽  
Pyramidal Tract Neurons ◽  
Ionic Mechanisms ◽  
Inward Currents

The ionic mechanisms underlying the action of excitatory amino acids were investigated in the rat motor cortex. Ion-selective microelectrodes were attached to micropipettes such that their tips were very close and local changes in extracellular concentration of sodium, calcium, and potassium ions elicited through ionophoretic applications of glutamate (Glu) and of its agonists N-methyl-D-aspartate (NMDA), quisqualate (Quis), and kainate (Ka) were measured. These agents produced moderate increases in [K+]o (up to 13 mM) but, in contrast, substantial tetrodotoxin-insensitive decreases in [Na+]o (maximally of 60 mM). NMDA-induced sodium responses could be blocked by manganese, while the Quis- and Ka-induced responses were not. Quis and Ka produced increases in [Ca2+]o or biphasic responses while NMDA, even with small doses, induced each time drastic decreases in [Ca2+]o (maximally of 1.15 mM), which could be attenuated or blocked by manganese but not by organic calcium channel blockers. NMDA responses could be abolished by reduced doses of 2-amino-phosphonovaierate. The largest Glu- and NMDA-induced calcium responses were observed in the superficial cortical layers, but such maxima disappeared after selective degeneration of pyramidal tract neurons. All amino acids produced sizeable reductions in the extracellular space volume. The following can be concluded. (i) All the excitatory amino acids tested induce an increased permeability to sodium and potassium ions. (ii) In addition, the NMDA-operated channels have specifically a large permeability for calcium, although calcium ions contribute only by less than 10% to the NMDA-induced inward currents, (iii) Glu-induced calcium responses are due to the activation by Glu of NMDA receptors. (iv) In the motor cortex, the largest density of NMDA receptors is found on apical dendrites of pyramidal tract neurons.

The role of excitatory amino acids and NMDA receptors in traumatic brain injury

Science ◽  
1989 ◽  
Vol 244 (4906) ◽  
pp. 798-800 ◽  
Author(s):  
A. Faden ◽  
P Demediuk ◽  
S. Panter ◽  
R Vink
Keyword(s):  
Amino Acids ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nmda Receptors ◽  
Excitatory Amino Acids

The action of some analogues of the excitatory amino acids in the dentate gyrus of the rat

1984 ◽  
Vol 62 (4) ◽  
pp. 424-429 ◽  
Author(s):  
G. L. Collingridge ◽  
S. J. Kehl ◽  
H. McLennan
Keyword(s):  
Amino Acids ◽  
Dentate Gyrus ◽  
Nmda Receptors ◽  
Aspartic Acid ◽  
Excitatory Amino Acids ◽  
Granule Cells ◽  
Nmda Antagonist ◽  
Dentate Granule Cells

We have confirmed that γ-D-glutamylglycine and the L-isomer of 2-amino-4-phosphonobutyric acid, and have shown also that L-2-amino-5-phosphonovaleric (L-APV) acid, are antagonists of synaptic excitations of dentate granule cells induced from both lateral and medial perforant paths. The N-methyl-D-aspartic acid (NMDA) antagonist D-APV is without effect. The synaptic antagonists reduce the presynaptic fibre volley particularly in the lateral path, suggesting that a reduced transmitter output contributes to their action. NMDA receptors exist upon the granule cells, but they are not involved with these synaptic processes.

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