PMID- 8896810
OWN - NLM
STAT- MEDLINE
DCOM- 19970218
LR  - 20170301
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 734
IP  - 1-2
DP  - 1996 Sep 23
TI  - Modulation of glycine-induced chloride current in acutely dissociated rat 
      periaqueductal gray neurons by mu-opioid agonist DAGO.
PG  - 72-8
AB  - Effect of a mu-opioid agonist (D-Ala2,N-MePhe4,Gly5-ol-enkephalin, DAGO), on 
      glycine (Gly)-induced chloride current (IGly) was investigated in the 
      periaqueductal gray (PAG) neurons acutely dissociated 1-2-week-old Wistar rats by 
      the use of nystatin-perforated patch recording configuration under voltage-clamp 
      condition. At a holding potential (VH) of -40 mV, DAGO caused a sustained 
      potentiation of IGly at the low concentrations (10(-6)-10(-5) M) but reduced 
      slightly the Gly response at the high concentration (10(-4) M). The reversal 
      potential of IGly was equal to the Cl- equilibrium potential (ECl) and was not 
      changed in the presence of 10(-6) M DAGO. The 10(-5) M Gly response was inhibited 
      by the simultaneous treatment of forskolin and 3-isobutyl-1-methylxanthine 
      (IBMX). H-89, a protein kinase A (PKA) inhibitor, increased the 10(-5) M Gly 
      response but had little effect on the 10(-4) M Gly response. DAGO increased 
      10(-5) M Gly response in the presence of forskolin and IBMX but, not more than in 
      the absence of forskolin and IBMX. The 10(-5) M Gly response augumented by DAGO 
      was not affected by adding H-89. The present results suggest that the 
      glycine-induced chloride current is cAMP dependent and is inhibited by PKA, and 
      that the potentiation of the glycine response by DAGO is also cAMP dependent and 
      is due to the inhibition of PKA as that of H-89. We conclude that the 
      potentiation of glycine response by DAGO is mediated by an inhibition of 
      cAMP-dependent PKA in the PAG neurons.
FAU - Min, B I
AU  - Min BI
AD  - Department of Physiology, College of Medicine, Kyung Hee University, 
      Tongdaemoon-Gu, Seoul, South Korea.
FAU - Kim, C J
AU  - Kim CJ
FAU - Rhee, J S
AU  - Rhee JS
FAU - Akaike, N
AU  - Akaike N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Chlorides)
RN  - 0 (Enkephalins)
RN  - 0 (Receptors, Opioid, mu)
RN  - 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-)
RN  - TE7660XO1C (Glycine)
SB  - IM
MH  - Animals
MH  - Chlorides/*physiology
MH  - Electric Conductivity
MH  - Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
MH  - Enkephalins/*pharmacology
MH  - Glycine/*pharmacology
MH  - Neurons/drug effects/*physiology
MH  - Periaqueductal Gray/cytology/drug effects/*physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Opioid, mu/*agonists
EDAT- 1996/09/23 00:00
MHDA- 1996/09/23 00:01
CRDT- 1996/09/23 00:00
PHST- 1996/09/23 00:00 [pubmed]
PHST- 1996/09/23 00:01 [medline]
PHST- 1996/09/23 00:00 [entrez]
AID - 0006-8993(96)00614-2 [pii]
PST - ppublish
SO  - Brain Res. 1996 Sep 23;734(1-2):72-8.