PMID- 18402624
OWN - NLM
STAT- MEDLINE
DCOM- 20080807
LR  - 20161124
IS  - 1399-5618 (Electronic)
IS  - 1398-5647 (Linking)
VI  - 10
IP  - 3
DP  - 2008 May
TI  - Neuroprotective effect of chronic lithium treatment against hypoxia in specific 
      brain regions with upregulation of cAMP response element binding protein and 
      brain-derived neurotrophic factor but not nerve growth factor: comparison with 
      acute lithium treatment.
PG  - 360-8
LID - 10.1111/j.1399-5618.2007.00521.x [doi]
AB  - OBJECTIVES: We evaluated the neuroprotective effect of chronically or acutely 
      administered lithium against hypoxia in several brain regions. Furthermore, we 
      investigated the contribution of brain-derived neurotrophic factor (BDNF), nerve 
      growth factor (NGF), and cAMP response element binding protein (CREB) to the 
      neuroprotective effect of lithium. METHODS: Brain slices were prepared from rats 
      that had been treated chronically or acutely with lithium. The cerebral glucose 
      metabolic rate (CMRglc) before and after hypoxia loading to brain slices was 
      measured using the dynamic positron autoradiography technique with 
      [(18)F]2-fluoro-2-deoxy-D-glucose. The changes of expression of proteins were 
      investigated using Western blot analysis. RESULTS: Before hypoxia loading, the 
      CMRglc did not differ between the lithium-treated and untreated groups. After 
      hypoxia loading, the CMRglc of the untreated group was significantly lower than 
      that before hypoxia loading. However, the CMRglc of the chronic lithium treatment 
      group recovered in the frontal cortex, caudate putamen, hippocampus and 
      cerebellum, but not in the thalamus. In contrast, the CMRglc of the acute lithium 
      treatment group did not recover in any analyzed brain regions. After chronic 
      lithium treatment, the levels of expression of BDNF and phospho-CREB were higher 
      than those of untreated rats in the frontal cortex, but not in the thalamus. 
      However, the expression of NGF did not change in the frontal cortex and thalamus. 
      CONCLUSIONS: These results demonstrated that lithium was neuroprotective against 
      hypoxia only after chronic treatment and only in specific brain regions, and that 
      CREB and BDNF might contribute to this effect.
FAU - Omata, N
AU  - Omata N
AD  - Department of Neuropsychiatry, University of Fukui, Fukui, Japan.
FAU - Murata, T
AU  - Murata T
FAU - Takamatsu, S
AU  - Takamatsu S
FAU - Maruoka, N
AU  - Maruoka N
FAU - Mitsuya, H
AU  - Mitsuya H
FAU - Yonekura, Y
AU  - Yonekura Y
FAU - Fujibayashi, Y
AU  - Fujibayashi Y
FAU - Wada, Y
AU  - Wada Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Denmark
TA  - Bipolar Disord
JT  - Bipolar disorders
JID - 100883596
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Insulin)
RN  - 0 (Lithium Compounds)
RN  - 0 (Neuroprotective Agents)
RN  - 0Z5B2CJX4D (Fluorodeoxyglucose F18)
SB  - IM
MH  - Animals
MH  - Brain/diagnostic imaging/*drug effects/pathology
MH  - Brain Mapping
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/*metabolism
MH  - Drug Administration Schedule
MH  - Fluorodeoxyglucose F18/metabolism
MH  - *Hypoxia/drug therapy/pathology/physiopathology
MH  - In Vitro Techniques
MH  - Insulin/pharmacology
MH  - Lithium Compounds/pharmacology/*therapeutic use
MH  - Male
MH  - Neuroprotective Agents/pharmacology/*therapeutic use
MH  - Positron-Emission Tomography
MH  - Rats
MH  - Rats, Wistar
MH  - Time Factors
MH  - Up-Regulation/*drug effects
EDAT- 2008/04/12 09:00
MHDA- 2008/08/08 09:00
CRDT- 2008/04/12 09:00
PHST- 2008/04/12 09:00 [pubmed]
PHST- 2008/08/08 09:00 [medline]
PHST- 2008/04/12 09:00 [entrez]
AID - BDI521 [pii]
AID - 10.1111/j.1399-5618.2007.00521.x [doi]
PST - ppublish
SO  - Bipolar Disord. 2008 May;10(3):360-8. doi: 10.1111/j.1399-5618.2007.00521.x.