PMID- 3034375
OWN - NLM
STAT- MEDLINE
DCOM- 19870714
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 407
IP  - 1
DP  - 1987 Mar 24
TI  - After-hyperpolarizations produced in frog motoneurons by excitatory amino acid 
      analogues.
PG  - 94-101
AB  - After-hyperpolarizations (AHPs) produced in frog motoneurons by applications of 
      the excitatory amino acid analogues quisqualate (QUIS), N-methyl-D-aspartate 
      (NMDA), and kainate (KA) were studied in the isolated hemisected frog spinal cord 
      using sucrose gap techniques. AHPs were present following 98% of QUIS-induced 
      depolarizations, but were seen in only 35% and 15% of NMDA- and KA-evoked 
      responses respectively. AHPs produced by QUIS are produced both by direct effects 
      of QUIS on motoneuron membranes and by indirect effects mediated through a 
      synaptic process involving interneurons. Thus, application of Mg2+, Mn2+, or 
      tetrodotoxin (TTX) in concentrations sufficient to block synaptic transmission 
      and interneuronal firing, reduced, but did not abolish the AHPs produced by QUIS. 
      In contrast, NMDA- and KA-AHPs appear to be entirely mediated by indirect means 
      as block of synaptic transmission and interneuronal firing eliminated AHPs 
      produced by these substances. Exposure of the cord to Mn2+ after addition of TTX 
      did not affect the size of QUIS-AHPs. In the presence of TTX, QUIS-AHPs were 
      reduced or completely blocked by addition of dinitrophenol (DNP) and sodium 
      cyanide, by dihydro-ouabain, by removal of K+ from the superfusate, by cooling, 
      and by replacement of 50% of the external Na+ with Li+. The results suggest that 
      the QUIS-AHPs are largely the result of the direct effect of the excitatory amino 
      acid agonist on motoneuron membranes and is caused by activation of an 
      electrogenic Na+ pump. AHPs following depolarizations evoked by NMDA and KA are 
      presumably the result of indirect actions of these latter analogues on 
      interneurons.
FAU - Hackman, J C
AU  - Hackman JC
FAU - Holohean, A M
AU  - Holohean AM
FAU - Wohlberg, C J
AU  - Wohlberg CJ
FAU - Davidoff, R A
AU  - Davidoff RA
LA  - eng
GR  - NS 17577/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Dinitrophenols)
RN  - 0 (Oxadiazoles)
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - 5ACL011P69 (Ouabain)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - 8OC22C1B99 (Quisqualic Acid)
RN  - 9NEZ333N27 (Sodium)
RN  - Q13SKS21MN (2,4-Dinitrophenol)
RN  - RWP5GA015D (Potassium)
RN  - SIV03811UC (Kainic Acid)
SB  - IM
MH  - 2,4-Dinitrophenol
MH  - Animals
MH  - Aspartic Acid/*analogs & derivatives/pharmacology
MH  - Dinitrophenols/pharmacology
MH  - Kainic Acid/*pharmacology
MH  - Membrane Potentials/drug effects
MH  - Motor Neurons/drug effects/*physiology
MH  - N-Methylaspartate
MH  - Ouabain/pharmacology
MH  - Oxadiazoles/*pharmacology
MH  - Potassium/physiology
MH  - Quisqualic Acid
MH  - Ranidae
MH  - Sodium/physiology
MH  - Synaptic Transmission/drug effects
EDAT- 1987/03/24 00:00
MHDA- 1987/03/24 00:01
CRDT- 1987/03/24 00:00
PHST- 1987/03/24 00:00 [pubmed]
PHST- 1987/03/24 00:01 [medline]
PHST- 1987/03/24 00:00 [entrez]
AID - 0006-8993(87)91222-4 [pii]
AID - 10.1016/0006-8993(87)91222-4 [doi]
PST - ppublish
SO  - Brain Res. 1987 Mar 24;407(1):94-101. doi: 10.1016/0006-8993(87)91222-4.