Reduced pain sensitivity in mice lacking latexin, an inhibitor of metallocarboxypeptidases.

Latexin, the endogenous protein inhibitor of the A/B subfamily of metallocarboxypeptidases, is expressed in small nociceptive neurons in sensory ganglia and in a subset of neurons in the telencephalon. In this study, we generated latexin-deficient mice that exhibited increased tail-flick latency compared to wild-type animals upon noxious heat stimulation. The reduced pain sensitivity in the mutants was rescued by the systemic administration of a plant carboxypeptidase inhibitor that inhibits the A/B subfamily of metallocarboxypeptidases.

Role of the protomap and target-derived signals in the development of intrahemispheric connections.

Mechanisms intrinsic to the early cerebral cortex have been implicated in the establishment of cortical area identity. However, the extent to which the cortical protomap contributes to the formation of highly complex intrahemispheric connections remains obscure. Mechanisms by which postmitotic neurons establish correct corticocortical connections later in corticogenesis also remain to be elucidated.

Organization and development of corticocortical associative neurons expressing the orphan nuclear receptor Nurr1.

The developmental mechanism that contributes to the highly organized axonal connections within the cerebral cortex is not well understood. This is partly due to the lack of molecular markers specifically expressed in corticocortical associative neurons during the period of circuit formation. We have shown previously that latexin, a carboxypeptidase A inhibitor, is expressed in intrahemispheric corticocortical neurons from the second postnatal week in the rat (Arimatsu et al.