Plasticity in auditory cortex during parenthood.

Most animals display robust parental behaviors that support the survival and well-being of their offspring. The manifestation of parental behaviors is accompanied by physiological and hormonal changes, which affect both the body and the brain for better care giving. Rodents exhibit a behavior called pup retrieval - a stereotyped sequence of perception and action - used to identify and retrieve their newborn pups back to the nest. Pup retrieval consists of a significant auditory component, which depends on plasticity in the auditory cortex (ACx). We review the evidence of neural changes taking place in the ACx of rodents during the transition to parenthood. We discuss how the plastic changes both in and out of the ACx support the encoding of pup vocalizations. Key players in the mechanism of this plasticity are hormones and experience, both of which have a clear dynamic signature during the transition to parenthood. Mothers, co caring females, and fathers have been used as models to understand parental plasticity at disparate levels of organization. Yet, common principles of cortical plasticity and the biological mechanisms underlying its involvement in parental behavior are just beginning to be unpacked.

Spinal lumbar dI2 interneurons contribute to stability of bipedal stepping.

Peripheral and intraspinal feedback is required to shape and update the output of spinal networks that execute motor behavior. We report that lumbar dI2 spinal interneurons in chicks receive synaptic input from afferents and premotor neurons. These interneurons innervate contralateral premotor networks in the lumbar and brachial spinal cord, and their ascending projections innervate the cerebellum. These findings suggest that dI2 neurons function as interneurons in local lumbar circuits, are involved in lumbo-brachial coupling, and that part of them deliver peripheral and intraspinal feedback to the cerebellum. Silencing of dI2 neurons leads to destabilized stepping in posthatching day 8 hatchlings, with occasional collapses, variable step profiles, and a wide-base walking gait, suggesting that dI2 neurons may contribute to the stabilization of the bipedal gait.

Natural loss of function of ephrin-B3 shapes spinal flight circuitry in birds.

Flight in birds evolved through patterning of the wings from forelimbs and transition from alternating gait to synchronous flapping. In mammals, the spinal midline guidance molecule ephrin-B3 instructs the wiring that enables limb alternation, and its deletion leads to synchronous hopping gait. Here, we show that the ephrin-B3 protein in birds lacks several motifs present in other vertebrates, diminishing its affinity for the EphA4 receptor. The avian ephrin-B3 gene lacks an enhancer that drives midline expression and is missing in galliforms. The morphology and wiring at brachial levels of the chicken embryonic spinal cord resemble those of ephrin-B3 null mice. Dorsal midline decussation, evident in the mutant mouse, is apparent at the chick brachial level and is prevented by expression of exogenous ephrin-B3 at the roof plate. Our findings support a role for loss of ephrin-B3 function in shaping the avian brachial spinal cord circuitry and facilitating synchronous wing flapping.