Catecholaminergic neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia.
Acta Neuropsychiatr
; 28(2): 117-23, 2016 Apr.
Article
in En
| MEDLINE
| ID: mdl-26333915
ABSTRACT
BACKGROUND:
The precise aetiology of schizophrenia remains unclear. The neurodevelopmental hypothesis of schizophrenia has been proposed based on the accumulation of genomic or neuroimaging studies.OBJECTIVE:
In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizophrenia 1 (DISC1) knockout (KO) mice, which are considered to be a useful model of schizophrenia.METHODS:
Six DISC1 homozygous KO mice and six age-matched littermates were used. The animals' brains were cut into 20-µm-thick slices, which were then immunohistochemically stained using an anti-tyrosine hydroxylase (TH) monoclonal antibody.RESULTS:
The TH-immunopositive fibres detected in the orbitofrontal cortices of the DISC1 KO mice were significantly shorter than those seen in the wild-type mice.CONCLUSION:
These neuropathological findings indicate that the hypofrontal symptoms of schizophrenia are associated with higher mental function deficiencies or cognitive dysfunction such as a loss of working memory.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Schizophrenia
/
Tyrosine 3-Monooxygenase
/
Prefrontal Cortex
/
Nerve Tissue Proteins
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
Acta Neuropsychiatr
Year:
2016
Type:
Article
Affiliation country:
Japan