PMID- 17251370
OWN - NLM
STAT- MEDLINE
DCOM- 20070521
LR  - 20141120
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 97
IP  - 3
DP  - 2007 Mar
TI  - Giant spontaneous depolarizing potentials in the developing thalamic reticular 
      nucleus.
PG  - 2364-72
AB  - The thalamic reticular nucleus (nRt) provides a major source of inhibition in the 
      thalamo-cortical circuit and is critically involved in the generation of spindle 
      oscillations. Here we describe the properties of thalamic giant depolarizing 
      potentials (tGDPs) that were observed in nRt during early development. tGDPs 
      persisted in presence of ionotropic glutamate antagonists but were completely 
      abolished by GABA(A)R antagonist SR 35591. tGDPs occurred primarily between p3 
      and p8 (in 30-50% of cells) and occasionally up until p15. tGDPs lasted 0.4-3 s 
      with peak conductances of 2-13 nS and occurred at frequencies between 0.02 and 
      0.06 Hz. We used mice with a benzodiazepine-insensitive alpha3 subunit 
      [alpha3(H126R)] to probe for the identity of the GABA receptors responsible for 
      tGDP generation. Benzodiazepine enhancement of tGDP amplitude and duration 
      persisted in nRt neurons in alpha3(H126R) mice, indicating that the GABA(A)Rs 
      containing alpha3 are not critical for tGDP generation and suggesting that tGDPs 
      are mediated by GABA(A)Rs containing the alpha5 subunit, which is transiently 
      expressed in nRt neurons in early postnatal development. Furthermore we found 
      that exogenous GABA application depolarized nRt neurons younger than p8, 
      indicating elevated [Cl(-)](i) at this developmental stage. Taken together, these 
      data suggest that in immature nRt, long-lasting depolarizing responses mediated 
      by GABA receptors could trigger Ca(2+) entry and play a role in functional 
      development of the spindle-generating circuitry.
FAU - Pangratz-Fuehrer, Susanne
AU  - Pangratz-Fuehrer S
AD  - Department of Neurology and Neurological Sciences, Stanford University School of 
      Medicine, Stanford, CA 94305, USA.
FAU - Rudolph, Uwe
AU  - Rudolph U
FAU - Huguenard, John R
AU  - Huguenard JR
LA  - eng
GR  - NS-06477/NS/NINDS NIH HHS/United States
GR  - NS-34774/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20070124
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Chlorides)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (GABA Agents)
RN  - 0 (Gabra3 protein, mouse)
RN  - 0 (Receptors, GABA-A)
SB  - IM
MH  - Action Potentials/drug effects/*physiology/radiation effects
MH  - Age Factors
MH  - Aging/*physiology
MH  - Animals
MH  - Animals, Newborn
MH  - Chlorides/metabolism
MH  - Drug Interactions
MH  - Electric Stimulation/methods
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Female
MH  - GABA Agents/pharmacology
MH  - In Vitro Techniques
MH  - Inhibitory Postsynaptic Potentials/drug effects/physiology/radiation effects
MH  - Male
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Neurons/physiology
MH  - Patch-Clamp Techniques/methods
MH  - Receptors, GABA-A/genetics
MH  - Thalamic Nuclei/cytology/*physiology
EDAT- 2007/01/26 09:00
MHDA- 2007/05/22 09:00
CRDT- 2007/01/26 09:00
PHST- 2007/01/26 09:00 [pubmed]
PHST- 2007/05/22 09:00 [medline]
PHST- 2007/01/26 09:00 [entrez]
AID - 00646.2006 [pii]
AID - 10.1152/jn.00646.2006 [doi]
PST - ppublish
SO  - J Neurophysiol. 2007 Mar;97(3):2364-72. doi: 10.1152/jn.00646.2006. Epub 2007 Jan 
      24.