PMID- 10758147
OWN - NLM
STAT- MEDLINE
DCOM- 20000515
LR  - 20180823
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 83
IP  - 4
DP  - 2000 Apr
TI  - Epileptogenesis up-regulates metabotropic glutamate receptor activation of 
      sodium-calcium exchange current in the amygdala.
PG  - 2458-62
AB  - Postsynaptic metabotropic glutamate (mGlu) receptor-activated inward current 
      mediated by Na(+)-Ca(2+) exchange was compared in basolateral amygdala (BLA) 
      neurons from brain slices of control (naive and sham-operated) and 
      amygdala-kindled rats. In control neurons, the mGlu agonist, quisqualate (QUIS; 
      1-100 microM), evoked an inward current not associated with a significant change 
      in membrane slope conductance, measured from current-voltage relationships 
      between -110 and -60 mV, consistent with activation of the Na(+)-Ca(2+) 
      exchanger. Application of the group I selective mGlu receptor agonist 
      (S)-3,5-dihydroxyphenylglycine [(S)-DHPG; 10-1000 microM] or the endogenous 
      agonist, glutamate (10-1000 microM), elicited the exchange current. QUIS was more 
      potent than either (S)-DHPG or glutamate (apparent EC(50) = 19 microM, 57 microM, 
      and 0.6 mM, respectively) in activating the Na(+)-Ca(2+) exchange current. The 
      selective mGlu5 agonist, (R, S)-2-chloro-5-hydroxyphenylglycine [(R,S)-CHPG; 
      apparent EC(50) = 2. 6 mM] also induced the exchange current. The maximum 
      response to (R, S)-DHPG was about half of that of the other agonists suggesting 
      partial agonist action. Concentration-response relationships of agonist-evoked 
      inward currents were compared in control neurons and in neurons from kindled 
      animals. The maximum value for the concentration-response relationship of the 
      partial agonist (S)-DHPG- (but not the full agonist- [QUIS or (R,S)-CHPG]) 
      induced inward current was shifted upward suggesting enhanced efficacy of this 
      agonist in kindled neurons. Altogether, these data are consistent with a 
      kindling-induced up-regulation of a group I mGlu-, possibly mGlu5-, mediated 
      responses coupled to Na(+)-Ca(2+) exchange in BLA neurons.
FAU - Keele, N B
AU  - Keele NB
AD  - Department of Pharmacology and Toxicology, The University of Texas Medical 
      Branch, Galveston, Texas 77555-1031, USA.
FAU - Zinebi, F
AU  - Zinebi F
FAU - Neugebauer, V
AU  - Neugebauer V
FAU - Shinnick-Gallagher, P
AU  - Shinnick-Gallagher P
LA  - eng
GR  - NS-24643/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (2-chloro-5-hydroxyphenylglycine)
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Phenylacetates)
RN  - 0 (Receptors, Metabotropic Glutamate)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 4368-28-9 (Tetrodotoxin)
RN  - 534-82-7 (Methoxyhydroxyphenylglycol)
RN  - 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione)
RN  - 76726-92-6 (2-Amino-5-phosphonovalerate)
RN  - 8OC22C1B99 (Quisqualic Acid)
RN  - 9NEZ333N27 (Sodium)
RN  - SY7Q814VUP (Calcium)
RN  - TE7660XO1C (Glycine)
RN  - UEH9K539KJ (3,4-dihydroxyphenylglycol)
SB  - IM
MH  - 2-Amino-5-phosphonovalerate/pharmacology
MH  - 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology
MH  - Amygdala/chemistry/*metabolism
MH  - Animals
MH  - Calcium/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Epilepsy/*physiopathology
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Glutamic Acid/pharmacology
MH  - Glycine/analogs & derivatives/pharmacology
MH  - Kindling, Neurologic/physiology
MH  - Male
MH  - Membrane Potentials/drug effects/physiology
MH  - Methoxyhydroxyphenylglycol/analogs & derivatives/pharmacology
MH  - Phenylacetates/pharmacology
MH  - Quisqualic Acid/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Metabotropic Glutamate/*metabolism
MH  - Seizures/physiopathology
MH  - Sodium/*metabolism
MH  - Tetrodotoxin/pharmacology
MH  - Up-Regulation/*physiology
EDAT- 2000/04/12 09:00
MHDA- 2000/05/20 09:00
CRDT- 2000/04/12 09:00
PHST- 2000/04/12 09:00 [pubmed]
PHST- 2000/05/20 09:00 [medline]
PHST- 2000/04/12 09:00 [entrez]
AID - 10.1152/jn.2000.83.4.2458 [doi]
PST - ppublish
SO  - J Neurophysiol. 2000 Apr;83(4):2458-62. doi: 10.1152/jn.2000.83.4.2458.