[
International Worm Meeting,
2013]
Employing high-resolution laser surgery techniques, we are studying how the C. elegans mechanosensory reflex circuitry recovers from specific neuronal lesion. We find that in vivo laser severing of the lateral synaptic branch of the posterior lateral microtubule neurons (PLM, the prominent posterior mechanosenory neurons) results in an initial hyperactivation of the downstream circuitry and elevated execution of posterior touch avoidance behaviors (i.e. increased forward movement as well as suppression of both spontaneous and anterior touch induced reversals). Over time the animal recovers and its behavior returns to its original baseline level within 24 h. Interestingly, this effect is seen only in surgeries that eliminate all sensory input from the PLM neurons, as single neuron surgery or severing the axon near the cell body have no effect. In addition, post-surgery hyperactivity is eliminated in glutamate receptor mutants suggesting that the effect maybe the results of neuronal modulation following sensory deprivation. Neuronal damage and sensory deprivation are known to elicit hyper-excitability and neuronal remodeling within the mammalian central nervous system. Prominent examples include phantom pain of amputated limbs, acute seizures and epilepsy resulting from traumatic brain damage and cortical rewiring after spinal cord injury or sensory deprivation. Here we are studying similar effects within a well defined, simple and tractable sensory transduction pathway in C. elegans.