PMID- 22669170
OWN - NLM
STAT- MEDLINE
DCOM- 20130109
LR  - 20211021
IS  - 1740-634X (Electronic)
IS  - 0893-133X (Print)
IS  - 0893-133X (Linking)
VI  - 37
IP  - 10
DP  - 2012 Sep
TI  - Severe cross-modal object recognition deficits in rats treated sub-chronically 
      with NMDA receptor antagonists are reversed by systemic nicotine: implications 
      for abnormal multisensory integration in schizophrenia.
PG  - 2322-31
LID - 10.1038/npp.2012.84 [doi]
AB  - Schizophrenia is a complex and debilitating disorder, characterized by positive, 
      negative, and cognitive symptoms. Among the cognitive deficits observed in 
      patients with schizophrenia, recent work has indicated abnormalities in 
      multisensory integration, a process that is important for the formation of 
      comprehensive environmental percepts and for the appropriate guidance of 
      behavior. Very little is known about the neural bases of such multisensory 
      integration deficits, partly because of the lack of viable behavioral tasks to 
      assess this process in animal models. In this study, we used our recently 
      developed rodent cross-modal object recognition (CMOR) task to investigate 
      multisensory integration functions in rats treated sub-chronically with one of 
      two N-methyl-D-aspartate receptor (NMDAR) antagonists, MK-801, or ketamine; such 
      treatment is known to produce schizophrenia-like symptoms. Rats treated with the 
      NMDAR antagonists were impaired on the standard spontaneous object recognition 
      (SOR) task, unimodal (tactile or visual only) versions of SOR, and the CMOR task 
      with intermediate to long retention delays between acquisition and testing 
      phases, but they displayed a selective CMOR task deficit when mnemonic demand was 
      minimized. This selective impairment in multisensory information processing was 
      dose-dependently reversed by acute systemic administration of nicotine. These 
      findings suggest that persistent NMDAR hypofunction may contribute to the 
      multisensory integration deficits observed in patients with schizophrenia and 
      highlight the valuable potential of the CMOR task to facilitate further 
      systematic investigation of the neural bases of, and potential treatments for, 
      this hitherto overlooked aspect of cognitive dysfunction in schizophrenia.
FAU - Jacklin, Derek L
AU  - Jacklin DL
AD  - Department of Psychology and Collaborative Neuroscience Program, University of 
      Guelph, Guelph, ON, Canada.
FAU - Goel, Amit
AU  - Goel A
FAU - Clementino, Kyle J
AU  - Clementino KJ
FAU - Hall, Alexander W M
AU  - Hall AW
FAU - Talpos, John C
AU  - Talpos JC
FAU - Winters, Boyer D
AU  - Winters BD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120606
PL  - England
TA  - Neuropsychopharmacology
JT  - Neuropsychopharmacology : official publication of the American College of 
      Neuropsychopharmacology
JID - 8904907
RN  - 0 (Nicotinic Agonists)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 690G0D6V8H (Ketamine)
RN  - 6LR8C1B66Q (Dizocilpine Maleate)
RN  - 6M3C89ZY6R (Nicotine)
SB  - IM
MH  - Animals
MH  - Cognition Disorders/drug therapy/etiology
MH  - Disease Models, Animal
MH  - Dizocilpine Maleate
MH  - Ketamine
MH  - Male
MH  - Nicotine/*pharmacology
MH  - Nicotinic Agonists/*pharmacology
MH  - Rats
MH  - Rats, Long-Evans
MH  - Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors
MH  - Recognition, Psychology/*drug effects
MH  - Schizophrenia/complications/*physiopathology
PMC - PMC3422496
EDAT- 2012/06/07 06:00
MHDA- 2013/01/10 06:00
PMCR- 2013/09/01
CRDT- 2012/06/07 06:00
PHST- 2012/06/07 06:00 [entrez]
PHST- 2012/06/07 06:00 [pubmed]
PHST- 2013/01/10 06:00 [medline]
PHST- 2013/09/01 00:00 [pmc-release]
AID - npp201284 [pii]
AID - 10.1038/npp.2012.84 [doi]
PST - ppublish
SO  - Neuropsychopharmacology. 2012 Sep;37(10):2322-31. doi: 10.1038/npp.2012.84. Epub 
      2012 Jun 6.