PMID- 29355693
OWN - NLM
STAT- MEDLINE
DCOM- 20181109
LR  - 20191008
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Print)
IS  - 0304-3940 (Linking)
VI  - 668
DP  - 2018 Mar 6
TI  - Genetic deletion of NMDA receptors suppresses GABAergic synaptic transmission in 
      two distinct types of central neurons.
PG  - 147-153
LID - S0304-3940(18)30024-7 [pii]
LID - 10.1016/j.neulet.2018.01.024 [doi]
AB  - NMDA-type ionotropic glutamate receptors (NMDARs) play an important role in the 
      regulation of synapse development and function in the brain. Recently we have 
      shown that NMDARs are critical for GABAergic synapse development in developing 
      hippocampal neurons. However, it remains unclear whether NMDARs are important for 
      establishment of GABAergic synaptic transmission in other types of neurons in the 
      brain. Here we report that in both cortical pyramidal neurons and midbrain 
      dopamine neurons in ventral tegmental area (VTA), genetic deletion of the GluN1 
      subunit, which is required for assembly of functional NMDARs, leads to a strong 
      reduction of GABAergic synaptic transmission. These data demonstrate that NMDARs 
      play an important role in the development of GABAergic synaptic transmission in 
      two types of neurons with distinct developmental origins, and suggest that NMDARs 
      are commonly involved in development of GABAergic synaptic transmission in 
      different types of neurons in the brain.
CI  - Published by Elsevier B.V.
FAU - Gu, Xinglong
AU  - Gu X
AD  - Synapse and Neural Circuit Research Unit, National Institute of Neurological 
      Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA.
FAU - Lu, Wei
AU  - Lu W
AD  - Synapse and Neural Circuit Research Unit, National Institute of Neurological 
      Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA. 
      Electronic address: luw4@mail.nih.gov.
LA  - eng
GR  - Z99 NS999999/Intramural NIH HHS/United States
GR  - ZIA NS003136-06/Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
DEP - 20180203
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Gprin1 protein, mouse)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
SB  - IM
MH  - Animals
MH  - Cerebral Cortex/*metabolism
MH  - Dopaminergic Neurons/*metabolism
MH  - Mice
MH  - Nerve Tissue Proteins/deficiency/genetics/*physiology
MH  - Pyramidal Cells/*metabolism
MH  - Receptors, N-Methyl-D-Aspartate/deficiency/genetics/*physiology
MH  - Synaptic Transmission/*physiology
MH  - Ventral Tegmental Area/*metabolism
MH  - gamma-Aminobutyric Acid/*metabolism
PMC - PMC6136253
MID - NIHMS936788
OTO - NOTNLM
OT  - Cortical pyramidal neuron
OT  - Dopamine neuron
OT  - GABAergic synapse
OT  - In utero electroporation
OT  - NMDA receptor
OT  - Synapse development
OT  - mIPSC
COIS- Conflict of Interest None
EDAT- 2018/01/23 06:00
MHDA- 2018/11/10 06:00
PMCR- 2019/03/06
CRDT- 2018/01/23 06:00
PHST- 2017/10/06 00:00 [received]
PHST- 2017/12/23 00:00 [revised]
PHST- 2018/01/12 00:00 [accepted]
PHST- 2018/01/23 06:00 [pubmed]
PHST- 2018/11/10 06:00 [medline]
PHST- 2018/01/23 06:00 [entrez]
PHST- 2019/03/06 00:00 [pmc-release]
AID - S0304-3940(18)30024-7 [pii]
AID - 10.1016/j.neulet.2018.01.024 [doi]
PST - ppublish
SO  - Neurosci Lett. 2018 Mar 6;668:147-153. doi: 10.1016/j.neulet.2018.01.024. Epub 
      2018 Feb 3.