PMID- 22805058
OWN - NLM
STAT- MEDLINE
DCOM- 20121112
LR  - 20211021
IS  - 1460-9568 (Electronic)
IS  - 0953-816X (Print)
IS  - 0953-816X (Linking)
VI  - 36
IP  - 2
DP  - 2012 Jul
TI  - The role of voltage dependence of the NMDA receptor in cellular and network 
      oscillation.
PG  - 2121-36
LID - 10.1111/j.1460-9568.2012.08083.x [doi]
AB  - Unraveling the mechanisms underlying oscillatory behavior is critical for 
      understanding normal and pathological brain processes. Here we used 
      electrophysiology in mouse neocortical slices and principles of nonlinear 
      dynamics to demonstrate how an increase in the N-methyl-d-aspartic acid receptor 
      (NMDAR) conductance can create a nonlinear whole-cell current-voltage (I-V) 
      relationship which leads to changes in cellular stability. We discovered two 
      behaviorally and morphologically distinct pyramidal cell populations. Under 
      control conditions, both cell types responded to depolarizing current injection 
      with regular spiking patterns. However, upon NMDAR activation, an intrinsic 
      oscillatory (IO) cell type (n = 44) showed a nonlinear whole-cell I-V 
      relationship, intrinsic voltage-dependent oscillations plus amplification of 
      alternating input current, and these properties persisted after disabling action 
      potential generation with tetrodotoxin (TTX). The other non-oscillatory (NO) 
      neuronal population (n = 24) demonstrated none of these behaviors. Simultaneous 
      intra- and extracellular recordings demonstrated the NMDAR's capacity to promote 
      low-frequency seizure-like network oscillations via its effects on intrinsic 
      neuronal properties. The two pyramidal cell types demonstrated different 
      relationships with network oscillation--the IO cells were leaders that were 
      activated early in the population activity cycle while the activation of the NO 
      cell type was distributed across network bursts. The properties of IO neurons 
      disappeared in a low-magnesium environment where the voltage dependence of the 
      receptor is abolished; concurrently, the cellular contribution to network 
      oscillation switched to synchronous firing. Thus, depending upon the efficacy of 
      NMDAR in altering the linearity of the whole-cell I-V relationship, the two cell 
      populations played different roles in sustaining network oscillation.
CI  - (c) 2012 The Authors. European Journal of Neuroscience (c) 2012 Federation of 
      European Neuroscience Societies and Blackwell Publishing Ltd.
FAU - Martell, Amber L
AU  - Martell AL
AD  - Department of Pediatrics, The University of Chicago, KCBD 4124, 900 E 57th 
      Street, Chicago, IL 60637, USA.
FAU - Ramirez, Jan-Marino
AU  - Ramirez JM
FAU - Lasky, Robert E
AU  - Lasky RE
FAU - Dwyer, Jennifer E
AU  - Dwyer JE
FAU - Kohrman, Michael
AU  - Kohrman M
FAU - van Drongelen, Wim
AU  - van Drongelen W
LA  - eng
GR  - T32 GM007281/GM/NIGMS NIH HHS/United States
GR  - T32 GM007281-35/GM/NIGMS NIH HHS/United States
GR  - T32 HD007009/HD/NICHD NIH HHS/United States
GR  - T32 HD007009-35/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (Sodium Channel Blockers)
RN  - 0 (Sodium Channels)
RN  - 4368-28-9 (Tetrodotoxin)
RN  - I38ZP9992A (Magnesium)
SB  - IM
MH  - Action Potentials
MH  - Animals
MH  - Magnesium/metabolism
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Models, Neurological
MH  - Neocortex/cytology/physiology
MH  - Nerve Net/physiology
MH  - Periodicity
MH  - Pyramidal Cells/cytology/*physiology
MH  - Receptors, N-Methyl-D-Aspartate/*metabolism
MH  - Sodium Channel Blockers/pharmacology
MH  - Sodium Channels/drug effects
MH  - Tetrodotoxin/pharmacology
PMC - PMC3400125
MID - NIHMS358393
EDAT- 2012/07/19 06:00
MHDA- 2012/11/13 06:00
PMCR- 2013/07/01
CRDT- 2012/07/19 06:00
PHST- 2012/07/19 06:00 [entrez]
PHST- 2012/07/19 06:00 [pubmed]
PHST- 2012/11/13 06:00 [medline]
PHST- 2013/07/01 00:00 [pmc-release]
AID - 10.1111/j.1460-9568.2012.08083.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 2012 Jul;36(2):2121-36. doi: 10.1111/j.1460-9568.2012.08083.x.