Meeting Abstract
20.4 Sunday, Jan. 4 Examining integration of new cells into neural circuits and the evolution of motor control. HALE, M. E. *; FREMONT, R. T.; Univ. Chicago; Albert Einstein College of Medicine mhale@uchicago.edu
One of the fundamental questions in neuroscience is: How does the brain evolve? The brain and its neural circuits, populations of nerve cells that work together to serve specific functions, are thought to be highly conserved. This is, in part, because many neurons play roles in multiple circuits. Due to this overlap, it is possible that changing one type of cell may alter the functions of many circuits. One of the ways the nervous system may change an individual circuit is to add new cells rather than modifying existing ones. However, such an approach has problems. For example, the nervous system has the potentially complicated task of generating many new connections to allow new cells to function appropriately. In addition, there may be fundamental constraints on where and how new cells can be added. We used a simple behavior, the escape response of fishes, to examine how circuits and behaviors can be modified with nerve cell addition. We examined escapes of the larval zebrafish (Danio rerio) for which behavioral, genetic and neurophysiological approaches have been established. We manipulated the large reticulospinal Mauthner cells as well as associated cells in the hindbrain. We found that new, experimentally added, Mauthner cells make most, but not all, of the appropriate connections into the startle circuit. Although they can generate a typical startle behavior, their activity patterns differ from those of the normal Mauthner cells. This case study provides an example of a circuit that can change significantly with the addition of new neurons and remain functional. It demonstrates that there is a degree of tolerance to aberrant nerve cell activity built into the startle circuit and suggests that this tolerance may facilitate the addition of new circuit components. Supported by NSF grant IBN0238464 to MEH.
