PMID- 18059437
OWN - NLM
STAT- MEDLINE
DCOM- 20081222
LR  - 20220309
IS  - 1740-634X (Electronic)
IS  - 0893-133X (Linking)
VI  - 33
IP  - 10
DP  - 2008 Sep
TI  - Postnatal phencyclidine administration selectively reduces adult cortical 
      parvalbumin-containing interneurons.
PG  - 2442-55
AB  - Transient postnatal NMDA receptor blockade by phencyclidine (PCP), ketamine, or 
      MK-801 induces developmental neuroapoptosis and adult behavioral deficits, which 
      resemble abnormal human behaviors typically present in schizophrenia. This study 
      tested the hypothesis that PCP-induced developmental apoptosis causes a specific 
      deficit of GABAergic interneurons containing parvalbumin (PV), calretinin (CR), 
      or calbindin (CB). Young adult (PND56) rats that were given a single dose of PCP 
      (10 mg/kg) on PND7 exhibited no densitometric change of either CR or CB neurons 
      in any brain region studied, but demonstrated a selective deficit of 
      PV-containing neurons in the superficial layers (II-IV) of the primary 
      somatosensory (S1), motor (M), and retrosplenial cortices, but not in the 
      striatum (CPu) or hippocampus. Further, CR and CB neurons, which were expressed 
      at the time of PCP administration, showed no colocalization with cellular markers 
      of apoptosis (terminal dUTP nick-end labeling (TUNEL) of broken DNA or cleaved 
      caspase-3), indicating that CR- and CB-containing neurons were protected from the 
      toxic effect of PCP and survived into adulthood. This suggests that the deletion 
      of PV neurons occurred during development, but cleaved caspase-3 showed no 
      colocalization with BrdU, a specific marker of S-phase proliferation. These data 
      suggest that the loss of PV-containing neurons was not due to an effect of PCP on 
      proliferating neurons, but rather an effect on post-mitotic neurons. The 
      developmental dependence and neuronal specificity of this effect of PCP provides 
      further evidence that this model may be valuable in exploring the pathophysiology 
      of schizophrenia.
FAU - Wang, Cheng Z
AU  - Wang CZ
AD  - Department of Pharmacology and Toxicology, University of Texas Medical Branch, 
      Galveston, TX 77555-1031, USA. czwang@utmb.edu
FAU - Yang, San F
AU  - Yang SF
FAU - Xia, Yan
AU  - Xia Y
FAU - Johnson, Kenneth M
AU  - Johnson KM
LA  - eng
GR  - DA02073/DA/NIDA NIH HHS/United States
GR  - MH63871/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20071205
PL  - England
TA  - Neuropsychopharmacology
JT  - Neuropsychopharmacology : official publication of the American College of 
      Neuropsychopharmacology
JID - 8904907
RN  - 0 (CALB2 protein, human)
RN  - 0 (Calb2 protein, rat)
RN  - 0 (Calbindin 2)
RN  - 0 (Calbindins)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Parvalbumins)
RN  - 0 (S100 Calcium Binding Protein G)
RN  - EC 3.4.22.- (Caspase 3)
RN  - G34N38R2N1 (Bromodeoxyuridine)
RN  - J1DOI7UV76 (Phencyclidine)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis/*drug effects/physiology
MH  - Bromodeoxyuridine
MH  - Calbindin 2
MH  - Calbindins
MH  - Caspase 3/metabolism
MH  - Cell Count
MH  - Cell Proliferation/drug effects
MH  - Cell Survival/drug effects/physiology
MH  - Cerebral Cortex/*drug effects/growth & development/metabolism
MH  - Disease Models, Animal
MH  - Excitatory Amino Acid Antagonists/toxicity
MH  - Female
MH  - Interneurons/*drug effects/metabolism
MH  - Male
MH  - Parvalbumins/*metabolism
MH  - Phencyclidine/*toxicity
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - S100 Calcium Binding Protein G/metabolism
MH  - Schizophrenia/chemically induced/*metabolism/physiopathology
MH  - Time
EDAT- 2007/12/07 09:00
MHDA- 2008/12/23 09:00
CRDT- 2007/12/07 09:00
PHST- 2007/12/07 09:00 [pubmed]
PHST- 2008/12/23 09:00 [medline]
PHST- 2007/12/07 09:00 [entrez]
AID - 1301647 [pii]
AID - 10.1038/sj.npp.1301647 [doi]
PST - ppublish
SO  - Neuropsychopharmacology. 2008 Sep;33(10):2442-55. doi: 10.1038/sj.npp.1301647. 
      Epub 2007 Dec 5.