PMID- 21672579
OWN - NLM
STAT- MEDLINE
DCOM- 20111027
LR  - 20181201
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 59
IP  - 1
DP  - 2011 Aug
TI  - Presynaptic kainate and NMDA receptors are implicated in the modulation of GABA 
      release from cortical and hippocampal nerve terminals.
PG  - 81-9
LID - 10.1016/j.neuint.2011.04.017 [doi]
AB  - One of the pathways implicated in a fine-tuning control of synaptic transmission 
      is activation of the receptors located at the presynaptic terminal. Here we 
      investigated the intracellular events in rat brain cortical and hippocampal nerve 
      terminals occurring under the activation of presynaptic glutamate receptors by 
      exogenous glutamate and specific agonists of ionotropic receptors, NMDA and 
      kainate. Involvement of synaptic vesicles in exocytotic process was assessed 
      using [(3)H]GABA and pH-sensitive fluorescent dye acridine orange (AO). Glutamate 
      as well as NMDA and kainate were revealed to induce [(3)H]GABA release that was 
      not blocked by NO-711, a selective blocker of GABA transporters. AO-loaded nerve 
      terminals responded to glutamate application by the development of a two-phase 
      process. The first phase, a fluorescence transient completed in  approximately 1min, was 
      similar to the response to high K(+). It was highly sensitive to extracellular 
      Ca(2+) and was decreased in the presence of the NMDA receptor antagonist, MK-801. 
      The second phase, a long-lasting process, was absolutely dependent on 
      extracellular Na(+) and attenuated in the presence of CNQX, the kainate receptor 
      antagonist. NMDA as well as kainate per se caused a rapid and abrupt 
      neurosecretory process confirming that both glutamate receptors, NMDA and 
      kainate, are involved in the control of neurotransmitter release. It could be 
      suggested that at least two types ionotropic receptor are attributed to 
      glutamate-induced two-phase process, which appears to reflect a rapid synchronous 
      and a more prolonged asynchronous vesicle fusion.
CI  - Copyright (c) 2011 Elsevier B.V. All rights reserved.
FAU - Tarasenko, A
AU  - Tarasenko A
AD  - Department of Neurochemistry, Palladin Institute of Biochemistry, National 
      Academy of Sciences of Ukraine, Leontovich Str. 9, Kyiv 01601, Ukraine.
FAU - Krupko, O
AU  - Krupko O
FAU - Himmelreich, N
AU  - Himmelreich N
LA  - eng
PT  - Journal Article
DEP - 20110606
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Receptors, Kainic Acid)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 10028-17-8 (Tritium)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
SB  - IM
MH  - Animals
MH  - Cerebral Cortex/*metabolism
MH  - Hippocampus/*metabolism
MH  - Male
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Kainic Acid/*physiology
MH  - Receptors, N-Methyl-D-Aspartate/*physiology
MH  - Tritium
MH  - gamma-Aminobutyric Acid/*metabolism
EDAT- 2011/06/16 06:00
MHDA- 2011/10/28 06:00
CRDT- 2011/06/16 06:00
PHST- 2010/12/24 00:00 [received]
PHST- 2011/04/21 00:00 [revised]
PHST- 2011/04/28 00:00 [accepted]
PHST- 2011/06/16 06:00 [entrez]
PHST- 2011/06/16 06:00 [pubmed]
PHST- 2011/10/28 06:00 [medline]
AID - S0197-0186(11)00179-3 [pii]
AID - 10.1016/j.neuint.2011.04.017 [doi]
PST - ppublish
SO  - Neurochem Int. 2011 Aug;59(1):81-9. doi: 10.1016/j.neuint.2011.04.017. Epub 2011 
      Jun 6.