Using in vivo pharmacology in transgenic mouse lines reporting activity in different cell types, we show that parenchymal IOSs are largely independent of neurotransmitter release and neurovascular coupling.
Previous experiments studying an independently made ArKO mouse line reported significant impairment in social recognition (Bakker et al., 2002), which may result from the failure of MeA neurons in ArKO animals to maturate adult patterns of MeA responses.
A chimeric DR4 homozygous transgenic mouse line was reported to spontaneously develop diverse hematological malignancies at a high frequency.
For each of the separate CGG KI mouse lines it was reported that there were very few behavioral phenotypes, and, even when present, the observed effects were rather small.
The single Msh2−/−, Msh6−/− and Msh3−/− mouse lines were generated and reported previously [10], [27], [49].
Generation of the Kirrel3 knockout mouse line was recently reported (Prince et al., 2013).
The ALL-16 xenograft line was established from a patient T-ALL diagnosis sample in the Non-Obese Diabetic/Severe Combined Immunodeficient (NOD/SCID) mouse line as previously reported [ 2].
Genotyping for all other mouse lines was carried out as reported (Buscher et al., 1998; Lu et al., 2002; Schedl et al., 1996 ).
As selective death of specific neuronal subpopulations were reported in mouse lines lacking NT or their receptors, we asked whether the lack of Kidins220 specifically affected one or more of these populations.
Using a selective ARC-deficient POMC mouse line, here we report that former obesity medications augmenting endogenous 5-hydroxytryptamine (5-HT) activity d-fenfluramine and sibutramine require ARC POMC neurons to elicit therapeutic appetite-suppressive effects.
