Astra Bryant and Rachel Brady in 2007

Posted March 25th, 2010 at 10:49 am.

Astra Bryant and Rachel Brady

Mentor: Professor Peter Brodfuehrer

It is commonly observed that short duration stimuli can elicit prolonged behaviors that greatly outlast the duration of the stimulus that initiates them.  Such is the case for swimming in the medicinal leech, Hirudo medicinalis, in which brief sensory or higher-order interneuron stimulation can trigger prolonged episodes of swimming. The medicinal leeches’ nervous system is comprised of anterior and posterior brains and 21 ganglia (bundles of nerve cell bodies), each located in a separate body segment and linked by neuronal projections. The swim behavior is characterized by rhythmic and episodic sinusoidal forward movement caused by an alternating contraction of longitudinal muscles on the ventral and dorsal surfaces, which travels down the body length. This contraction is caused by the coordinated activity of central pattern generators located in each segmental ganglion.


Central pattern generators are networks of linked cells that once activated can sustain activity without further input. The leeches’ ganglionic central pattern generators produce an oscillating pattern of activation that controls the alternating muscular contraction that characterizes swimming. Some specific cells involved in the swim central pattern generator are: SE1 (a higher-order interneuron located in the anterior brain), cell 204 (a ganglionic swim gating neuron that links the higher-order interneurons, including SE1, to the central pattern generating neurons), and oscillatory interneurons (the ganglionic cells that comprise the central pattern generator).

Considerable information is known about swim-initiating pathways and their synaptic connections to the segmental swim oscillatory network mentioned above (Kristan et al. 2005).  However, little is known about the cellular mechanisms and neuronal interactions responsible for maintaining swim episodes.  Here, we propose the existence of a positive feedback loop, activated by swim initiation inputs and acting on cell 204 and / or oscillatory interneurons, which is responsible for maintaining swim episodes.  Since excitation to cell 204 and several swim oscillator interneurons is mediated by the binding of glutamate to receptors located on the cell body (referred to as non-NMDA receptors), we are testing whether decreasing the excitatory drive of the positive feedback loop affects the sustainability or length of swim episodes. We will examine how well the application of non-NMDA receptor antagonist DNQX (6,7-Dinitroquinoxaline-2,3-dione) correlates with a decrease in the number of bursts per swim episode in isolated nerve cord preparations, as well as a general decrease in tonic intersegmental connective signaling.  In addition, since the application of the neurotransmitter serotonin is known to increase the likelihood of swim episodes, we are testing whether serotonin affects the electrical properties of cells SE1 and 204 in a manner that correlates with an increase in the length of swim episodes and in a general change in tonic intersegmental connective signaling.

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