A multivariate morphometric analysis of hippocampal anatomical variation in C57BL/6 ↔ BALB/c chimeric mice

Crusio, Wim E.; Bar, Isabelle; Schwegler, Herbert; Buselmaier, Werner

doi:10.1016/0006-8993(90)91622-n

Cited by 7 publications

(1 citation statement)

References 12 publications

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“…The disease has been modeled in rodents, especially in mice (Cryan and Slattery, 2007;Pollak et al, 2010;Yan et al, 2010), to either provide a means for improving current therapeutic regimen and screening for putative antidepressant activity, or to foster theories related to the etiology of depression to be explored. Mouse strain differences have been observed in neuroanatomical development (Wainwright and Deeks, 1984;Crusio et al, 1990;Livy and Wahlsten, 1991), electrophysiological traits (Bampton et al, 1999), and pharmacological responses to neurological compounds, especially antidepressants (Seale et al, 1984;Miner and Collins, 1989;Tolliver and Carney, 1994;Miner, 1997;Homanics et al, 1999;Lucki et al, 2001;David et al, 2003;Ripoll et al, 2003;Petit-Demouliere et al, 2005;Sugimoto et al, 2011;Can et al, 2013;O'Neill and Gu, 2013). Mouse strain differences have been observed in neuroanatomical development (Wainwright and Deeks, 1984;Crusio et al, 1990;Livy and Wahlsten, 1991), electrophysiological traits (Bampton et al, 1999), and pharmacological responses to neurological compounds, especially antidepressants (Seale et al, 1984;Miner and Collins, 1989;Tolliver and Carney, 1994;Miner, 1997;Homanics et al, 1999;Lucki et al, 2001;David et al, 2003;Ripoll et al, 2003;Petit-Demouliere et al, 2005;Sugimoto et al, 2011;Can et al, 2013;…”

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confidence: 99%

Immobility responses between mouse strains correlate with distinct hippocampal serotonin transporter protein expression and function

Tang

Meng³

et al. 2014

Int. J. Neuropsychopharm.

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Mouse strain differences in immobility and in sensitivity to antidepressants have been observed in the forced swimming test (FST) and the tail suspension test (TST). However, the neurotransmitter systems and neural substrates that contribute to these differences remain unknown. To investigate the role of the hippocampal serotonin transporter (5-HTT), we measured baseline immobility and the immobility responses to fluoxetine (FLX) in the FST and the TST in male CD-1, C57BL/6, DBA and BALB/c mice. We observed strain differences in baseline immobility time, with CD-1 mice showing the longest and DBA mice showing the shortest. In contrast, DBA and BALB/c mice showed the highest sensitivity to FLX, whereas CD-1 and C57BL/6 mice showed the lowest sensitivity. Also we found strain differences in both the total 5-HTT protein level and the membrane-bound 5-HTT level (estimated by V max) as follows: DBA>BALB/c>CD-1=C57BL/6. The uptake efficiency of the membrane-bound 5-HTT (estimated by 1/K m) was highest in DBA and BALB/c mice and lowest in CD-1 and C57BL/6 mice. A correlation analysis of subregions within the hippocampus revealed that immobility time was negatively correlated with V max and positively correlated with K m in the hippocampus. Therefore a higher uptake capacity of the membrane-bound 5-HTT in the hippocampus was associated with lower baseline immobility and greater sensitivity to FLX. These results suggest that alterations in hippocampal 5-HTT activity may contribute to mouse strain differences in the FST and the TST.

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