**The title, authors, and abstract for this completion report are provided below.  For a copy of the completion report, please contact the GLFC via e-mail or via telephone at 734-662-3209**



An in vitro strategy for understanding the neural mechanisms underlying pheromone-activated movements in the sea lamprey



Barbara Zielinski1, and Rejean Dubuc2,3



1 Department of Biological Sciences, University of Windsor, Windsor, Ontario, N9B 3P4

2 Department de Kinesiologie, University du Quebec a Montreal, Montreal Quebec,

3 Groupe de recherché sur le systeme nerveux cental, Department de Physiologie, Universite de Montreal, Montreal, Quebec



December 2010




This study addressed the neurobiology behind the movement of sea lampreys in response to pheromones, by demonstrating the anatomy and physiology of a specific neural circuit linking olfactory sensory input to neural control centers for locomotion. Specifically, this study identified a subsystem within the CNS, dedicated to producing motor responses to olfactory inputs. Neural output from the medial region of the olfactory bulb induced large excitatory responses in reticulospinal cells, the command neurons for locomotion. Olfactory sensory input to this medial region of the olfactory bulb originated from the main olfactory epithelium and the accessory olfactory organ, and both pheromones and feeding type cues (amino acids) stimulated neural activity in this medial bulbar region. The olfactory input that is relayed through the medial part of the olfactory bulb projects to the posterior tuberculum, the mesencephalic locomotor region, to finally reach reticulospinal cells in the hindbrain; and activation of this olfactory motor pathway generated rhythmic ventral root discharges and swimming movements. There were sites where input from surrounding neurons may affect activity along this olfactory-locomotor neural module. We have found that the inhibitory neurotransmitter gamma aminobutyric acid (GABA) is a potent inhibitor of this activity, and that endogenous GABA does in fact cause very strong inhibition. This completion report includes two research publications (Derjean et al, 2010 PLoS Biology 8:12e1000567; Ren et al. 2009 J. Comp. Neurol. 516:105-116), one manuscript (in progress), and a description of the most recent data.