Open AccessBehavioural phenotyping of sodium‐myo‐inositol cotransporter heterozygous knockout mice with reduced brain inositol
Author(s) -
Shaldubina A.,
Buccafusca R.,
Johanson R. A.,
Agam G.,
Belmaker R. H.,
Berry G. T.,
Bersudsky Y.
Publication year - 2007
Publication title -
genes, brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.315
H-Index - 91
eISSN - 1601-183X
pISSN - 1601-1848
DOI - 10.1111/j.1601-183x.2006.00253.x
Subject(s) - inositol , endocrinology , medicine , knockout mouse , lithium (medication) , apomorphine , inositol trisphosphate , neuroscience , amphetamine , psychology , hippocampus , dopamine , dopaminergic , chemistry , receptor
Inositol plays a key role in dopamine, serotonin, noradrenaline and acetylcholine neurotransmission, and inositol treatment is reported to have beneficial effects in depression and anxiety. Therefore, a reduction in brain intracellular inositol levels could be a cause of some psychiatric disorders, such as depression or anxiety. To determine the behavioural consequences of inositol depletion, we studied the behaviour of sodium‐dependent myo‐inositol cotransporter‐1 heterozygous knockout mice. In heterozygous mice, free inositol levels were reduced by 15% in the frontal cortex and by 25% in the hippocampus, but they did not differ from their wild‐type littermates in cholinergic‐mediated lithium–pilocarpine seizures, in the apomorphine‐induced stereotypic climbing model of dopaminergic system function, in the Porsolt forced‐swimming test model of depression, in amphetamine‐induced hyperactivity, or in the elevated plus‐maze model of anxiety. Reduction of brain inositol by more than 25% may be required to elicit neurobehavioural effects.