While the recent release of the Chinese tree shrew （Tupaia belangeri chinensis） genome has made the tree shrew an increasingly viable experimental animal model for biomedical research, further study of the genome may facilitate new insights into the applicability of this model. For example, though the tree shrew has a rapid rate of speed and strong jumping ability, there are limited studies on its locomotion ability. In this study we used the available Chinese tree shrew genome information and compared the evolutionary pattern of 407 locomotion system related orthologs among five mammals （human, rhesus monkey, mouse, rat and dog） and the Chinese tree shrew. Our analyses identified 29 genes with significantly high co （Ka/Ks ratio） values and 48 amino acid sites in 14 genes showed significant evidence of positive selection in the Chinese tree shrew. Some of these positively selected genes, e.g. HOXA6 （homeobox A6） and AVP （arginine vasopressin）, play important roles in muscle contraction or skeletal morphogenesis. These results provide important clues in understanding the genetic bases of locomotor adaptation in the Chinese tree shrew.
Depression is a devastating psychiatric disorder widely attributed to defi cient monoaminergic signaling in the central nervous system. However,most clinical antidepressants enhance monoaminergic neurotransmission with little delay but require 4-8 weeks to reach therapeutic efficacy,a paradox suggesting that the monoaminergic hypothesis of depression is an oversimplifi cation. In contrast to the antidepressants targeting the monoaminergic system,a single dose of the N-methyl-D-aspartate receptor（NMDAR） antagonist ketamine produces rapid（within 2 h） and sustained（over 7 days） antidepressant effi cacy in treatment-resistant patients. Glutamatergic transmission mediated by NMDARs is critical for experience-dependent synaptic plasticity and learning,processes that can be modifi ed indirectly by the monoaminergic system. To better understand the mechanisms of action of the new antidepressants like ketamine,we review and compare the monoaminergic and glutamatergic antidepressants,with emphasis on neural plasticity. The pathogenesis of depression may involve maladaptive neural plasticity in glutamatergic circuits that may serve as a new class of targets to produce rapid antidepressant effects.
