PMID- 29453493
OWN - NLM
STAT- MEDLINE
DCOM- 20191203
LR  - 20200225
IS  - 1433-8491 (Electronic)
IS  - 0940-1334 (Linking)
VI  - 269
IP  - 4
DP  - 2019 Jun
TI  - Altered prepulse inhibition of the acoustic startle response in BDNF-deficient 
      mice in a model of early postnatal hypoxia: implications for schizophrenia.
PG  - 439-447
LID - 10.1007/s00406-018-0882-6 [doi]
AB  - The brain-derived neurotrophic factor (BDNF) is a major proliferative agent in 
      the nervous system. Both BDNF-deficiency and perinatal hypoxia represent 
      genetic/environmental risk factors for schizophrenia. Moreover, a decreased BDNF 
      response to birth hypoxia was associated with the disease. BDNF expression is 
      influenced by neuronal activity and environmental conditions such as hypoxia. 
      Thus, it may partake in neuroprotective and reparative mechanisms in acute or 
      chronic neuronal insults. However, the interaction of hypoxia and BDNF is 
      insufficiently understood and the behavioral outcome unknown. Therefore, we 
      conducted a battery of behavioral tests in a classical model of chronic early 
      postnatal mild hypoxia (10% O(2)), known to significantly impair brain 
      development, in BDNF-deficient mice. We found selective deficits in measures 
      associated with sensorimotor gating, namely enhanced acoustic startle response 
      (ASR) and reduced prepulse inhibition (PPI) of ASR in BDNF-deficient mice. 
      Unexpectedly, the alterations of sensorimotor gating were caused only by 
      BDNF-deficiency alone, whereas hypoxia failed to evoke severe deficits and even 
      leads to a milder phenotype in BDNF-deficient mice. As deficits in sensorimotor 
      gating are present in schizophrenia and animal models of the disease, our results 
      are of relevance regarding the involvement of BDNF in its pathogenesis. On the 
      other hand, they suggest that the effect of perinatal hypoxia on long-term brain 
      abnormalities is complex, ranging from protective to deleterious actions, and may 
      critically depend on the degree of hypoxia. Therefore, future studies may refine 
      existing hypoxia protocols to better understand neurodevelopmental consequences 
      associated with schizophrenia.
FAU - Lima-Ojeda, Juan M
AU  - Lima-Ojeda JM
AD  - RG Animal Models in Psychiatry, Department of Psychiatry and Psychotherapy, 
      Central Institute of Mental Health, Medical Faculty Mannheim, University of 
      Heidelberg, Heidelberg, Germany.
AD  - Department of Psychiatry and Psychotherapy, University of Regensburg, Regensburg, 
      Germany.
FAU - Mallien, Anne S
AU  - Mallien AS
AD  - RG Animal Models in Psychiatry, Department of Psychiatry and Psychotherapy, 
      Central Institute of Mental Health, Medical Faculty Mannheim, University of 
      Heidelberg, Heidelberg, Germany.
FAU - Brandwein, Christiane
AU  - Brandwein C
AD  - RG Animal Models in Psychiatry, Department of Psychiatry and Psychotherapy, 
      Central Institute of Mental Health, Medical Faculty Mannheim, University of 
      Heidelberg, Heidelberg, Germany.
FAU - Lang, Undine E
AU  - Lang UE
AD  - Department of Psychiatry (UPK), University of Basel, Wilhelm Klein-Strasse 27, 
      4012, Basel, Switzerland.
FAU - Hefter, Dimitri
AU  - Hefter D
AD  - RG Animal Models in Psychiatry, Department of Psychiatry and Psychotherapy, 
      Central Institute of Mental Health, Medical Faculty Mannheim, University of 
      Heidelberg, Heidelberg, Germany.
FAU - Inta, Dragos
AU  - Inta D
AD  - RG Animal Models in Psychiatry, Department of Psychiatry and Psychotherapy, 
      Central Institute of Mental Health, Medical Faculty Mannheim, University of 
      Heidelberg, Heidelberg, Germany. dragos.inta@upkbs.ch.
AD  - Department of Psychiatry (UPK), University of Basel, Wilhelm Klein-Strasse 27, 
      4012, Basel, Switzerland. dragos.inta@upkbs.ch.
LA  - eng
GR  - IN168/3-1/Deutsche Forschungsgemeinschaft/
PT  - Journal Article
DEP - 20180216
PL  - Germany
TA  - Eur Arch Psychiatry Clin Neurosci
JT  - European archives of psychiatry and clinical neuroscience
JID - 9103030
RN  - 0 (Bdnf protein, mouse)
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Brain-Derived Neurotrophic Factor/*deficiency
MH  - Disease Models, Animal
MH  - Hypoxia/*physiopathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Prepulse Inhibition/*physiology
MH  - Schizophrenia/*physiopathology
MH  - Sensory Gating/*physiology
OTO - NOTNLM
OT  - BDNF
OT  - Neurodevelopment
OT  - Perinatal hypoxia
OT  - Schizophrenia
OT  - Sensorimotor gating
EDAT- 2018/02/18 06:00
MHDA- 2019/12/04 06:00
CRDT- 2018/02/18 06:00
PHST- 2017/09/05 00:00 [received]
PHST- 2018/02/12 00:00 [accepted]
PHST- 2018/02/18 06:00 [pubmed]
PHST- 2019/12/04 06:00 [medline]
PHST- 2018/02/18 06:00 [entrez]
AID - 10.1007/s00406-018-0882-6 [pii]
AID - 10.1007/s00406-018-0882-6 [doi]
PST - ppublish
SO  - Eur Arch Psychiatry Clin Neurosci. 2019 Jun;269(4):439-447. doi: 
      10.1007/s00406-018-0882-6. Epub 2018 Feb 16.