The postexcitatory effects of acidic amino acids on spinal neurones

1981 ◽  
Vol 59 (3) ◽  
pp. 239-243 ◽  
Author(s):  
H. McLennan ◽  
Jin-Rong Liu

The excitation of some neurones in the spinal cord of rats by L-glutamate and L-aspartate is followed by a period of reduced excitability. This effect is not observed after excitation by D-glutamate nor, in the case of Renshaw cells, by acetylcholine. The depressions following L-glutamate were reduced by bicuculline and those after aspartate by strychnine, suggesting that they may have been caused through decarboxylation of the excitatory amino acids to yield the inhibitory compounds γ-aminobutyric acid and β-alanine, respectively.

1980 ◽  
Vol 58 (6) ◽  
pp. 692-698 ◽  
Author(s):  
Ante L. Padjen ◽  
Peter A. Smith

The sucrose gap technique was employed to investigate both synaptic and amino acid evoked responses from motoneurones or primary afferents of frog spinal cord. α-D,L-Aminoadipic acid (α-D,L-AAD) selectively antagonized responses to acidic amino acids, especially aspartate. The drug was most effective in antagonizing the polysynaptic components of synaptic potentials evoked by dorsal root or lateral column stimulation but had little effect on their monosynaptic components. The ventral root dorsal root potential which is thought to be mediated by a pathway that does not involve acidic amino acids was insensitive to α-D,L-AAD. These data, which were confirmed by intracellular recording from motoneurones, provided further evidence for the role of acidic amino acids in polysynaptic pathways in frog spinal cord.


1996 ◽  
Vol 13 (12) ◽  
pp. 809-818 ◽  
Author(s):  
GEERT CRAENEN ◽  
SRDIJA JEFTINIJA ◽  
IVETA GRANTS ◽  
JEN HILL LUCAS

1991 ◽  
Vol 547 (2) ◽  
pp. 344-348 ◽  
Author(s):  
Danxia Liu ◽  
Wipawan Thangnipon ◽  
David J. McAdoo

1991 ◽  
Vol 69 (7) ◽  
pp. 1123-1128 ◽  
Author(s):  
David Lodge ◽  
Martyn G. Jones ◽  
Andrew J. Palmer

Although the N-methyl-D-aspartate (NMDA) subtype of L-glutamate receptor is well characterized, the significance of non-NMDA glutamate-sensitive binding sites is not well documented. In this study, a new tricyclic quinoxalinedione (NBQX) and an arthropod toxin (philanthotoxin) were shown to block responses of spinal neurones in vivo to kainate, quisqualate, and AMPA in parallel but had little effect on responses to NMDA. Philanthotoxin appeared to be a use-dependent antagonist consistent with a channel-blocking mode of action. On cortical wedges in vitro, however, NBQX proved to be a more potent antagonist of AMPA and quisqualate than of kainate (pA2 values of 7.1, 7.0, and 5.6, respectively) with no effect at 10 μM on responses to NMDA. These studies provide evidence that on cortical neurones, but not on spinal neurones, AMPA and kainate depolarize by pharmacologically different mechanisms.Key words: glutamate receptors, quinoxalinediones, philanthotoxin, AMPA, kainate.


Sign in / Sign up

Export Citation Format

Share Document