PMID- 8103513
OWN - NLM
STAT- MEDLINE
DCOM- 19931001
LR  - 20171213
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 74
IP  - 6
DP  - 1993 Jun
TI  - Retrotrapezoid nucleus glutamate receptors: control of CO2-sensitive phrenic and 
      sympathetic output.
PG  - 2958-68
AB  - In decerebrate cats, we asked whether endogenous glutamate in the region of the 
      retrotrapezoid nucleus (RTN) was involved in the control of CO2-sensitive phrenic 
      and phrenic-related sympathetic output and, if so, which type of glutamate 
      receptor was predominant. We made unilateral 10-nl injections into the RTN of the 
      nonspecific glutamate receptor antagonist kynurenic acid (100 and 250 mM), the 
      N-methyl-D-aspartic acid (NMDA) receptor antagonist 2-amino-5-phosphonopentanoic 
      acid (AP5; 1 and 10 mM), the non-NMDA receptor antagonist 
      6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX; 1 and 10 mM), and the inactive 
      kynurenic acid analogue xanthurenic acid (100 mM). Each antagonist resulted in a 
      significant dose-dependent decrease in the amplitude of the integrated phrenic 
      nerve signal (PNA) over 30 min (CNQX > AP5 > kynurenic acid). The duration of the 
      phrenic cycle was also decreased because of a shortening of expiratory time (CNQX 
      > kynurenic acid > AP5). All three antagonists significantly decreased the 
      initial slope of the PNA response to increased CO2 by 70-80% with no clear 
      distinction in efficacy. The amplitude of the respiratory-related integrated 
      cervical sympathetic nerve signal (SNA) was significantly decreased after 
      kynurenic acid and CNQX but not AP5. In each case, the decrease in 
      respiratory-related SNA accompanied a decrease in PNA and, at high levels of CO2, 
      the decrease in respiratory-related SNA was greater than that of PNA. Endogenous 
      glutaminergic input to neurons in the RTN via both NMDA and non-NMDA receptors is 
      involved in the control of eucapneic PNA and timing, PNA-related SNA, and the 
      response to increased CO2.
FAU - Nattie, E E
AU  - Nattie EE
AD  - Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire 
      03756-0001.
FAU - Gdovin, M
AU  - Gdovin M
FAU - Li, A
AU  - Li A
LA  - eng
GR  - HL-07449/HL/NHLBI NIH HHS/United States
GR  - HL-28066/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Quinoxalines)
RN  - 0 (Receptors, Glutamate)
RN  - 142M471B3J (Carbon Dioxide)
RN  - 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione)
RN  - 76726-92-6 (2-Amino-5-phosphonovalerate)
RN  - H030S2S85J (Kynurenic Acid)
SB  - IM
MH  - 2-Amino-5-phosphonovalerate/pharmacology
MH  - 6-Cyano-7-nitroquinoxaline-2,3-dione
MH  - Animals
MH  - Blood Pressure/drug effects/physiology
MH  - *Carbon Dioxide
MH  - Cats
MH  - Decerebrate State/physiopathology
MH  - Electrophysiology
MH  - Female
MH  - Kynurenic Acid/pharmacology
MH  - Male
MH  - Medulla Oblongata/anatomy & histology/*physiology
MH  - Phrenic Nerve/*physiology
MH  - Quinoxalines/pharmacology
MH  - Receptors, Glutamate/drug effects/*physiology
MH  - Respiration/drug effects/physiology
MH  - Sympathetic Nervous System/physiology
EDAT- 1993/06/01 00:00
MHDA- 1993/06/01 00:01
CRDT- 1993/06/01 00:00
PHST- 1993/06/01 00:00 [pubmed]
PHST- 1993/06/01 00:01 [medline]
PHST- 1993/06/01 00:00 [entrez]
AID - 10.1152/jappl.1993.74.6.2958 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 1993 Jun;74(6):2958-68. doi: 10.1152/jappl.1993.74.6.2958.