Date of Award

Spring 2009

Document Type

Thesis - Restricted

Degree Name

Master of Science (MS)



First Advisor

Buchanan, James T.

Second Advisor

Mynlieff, Michelle

Third Advisor

Wagner, David


Recent research into neuronal networks involved in respiration and neocortical/hippocampal oscillations has implicated gap junctions, a type of intercellular connection composed of two hemichannels that allow the passage of ions and small molecules between connected cells, as playing important roles in generating rhythmic activity. Similarly, in the neonatal rat spinal cord, gap junctions couple motoneurons to fire in synchrony and play a role in locomotor rhythmogenesis. However, the contribution of gap junctions in locomotor networks had not been investigated in the adult vertebrate locomotor system. The current study explored gap junctional involvement in the lamprey locomotqr network using pharmacological gap junction blockers. The four gap junctional blockers used (carbenoxolone, 1-octanol, mefloquine, and 18P-glycerrhetinic.acid) caused a speeding of the lamprey locomotor network to an average of 57% compared to the control. This significant decrease in cycle period indicates that gap junctions do contribute to the function of the lamprey locomotor network. Additionally, each of the blockers significantly lowered phase lag, burst proportion, mean spike frequency and (with the exceptions of mefloquine and 18Pglycerrhetinic acid) quality of rhythmic activity. The blocker carbenoxolone was shown to significantly reduce, although not abolish, the electrical component of mixed synapses. Carbenoxolone did not significantly alter values of resting membrane potential, action potential amplitude or action potential duration, which provided support that the drugs produced the speeding effect on the network by blocking gap junctions rather than through non-specific means. It is uncertain at this time precisely how blocking gap junctions causes a speeding of the locomotor network but it is speculated to be the result of changing electrotonic load between key cells of the lamprey locomotor network.



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