Habituation is a form of non-associative learning that appears as a gradual decrease in one or more components of the response to a repeated or prolonged stimulus. The studies that have characterized the genetic and circuit processes underlying habituation, many of which are shared with other forms of learning/memory. The processes by which neuronal activity cause the modification of synapses and plasticity in the central nervous system are not fully understood.

In the field of learning and memory, animal models have been a useful tool to understand the psychological and neurological processes. The disruption of memory greatly impacts behavior and memory receptors, as in post-traumatic stress disorders (PTSD) (Rank et al, 2002). A recent study on the Caenorhabditis elegans shows that heat shock treatments affect cellular processes that are necessary for memory formation without interrupting recovery from habituation (Sugi et al, 2011)

Using the reliable neuroscience model organism, Caenorhabditis elegans (C. elegans), I tested the heat shock on the memory of worms that were specifically trained to respond to tapping stimulation using the own constructed tap apparatus delivering a tap of 2N force, Based on the referenced article, the worms have to learn and show the memory/habituation of the training by showing less backward movement. By utilizing the heat-tolerant (HSF-1) OG532C elegans transgenic strain, the heat shock being the disruptive factor of memory could be found through comparing the controlled heat tolerant C elegans to wild type worms.And by using the Dil dye staining protocol, the impairment of memory could be measured through fluorescence imaging. After the training, the worms were exposed to heat shock via a water bath at 32. Based on the previously referenced article, I predicted that the memory of the worms will be impaired. Evidence of impairment is observable in both the animal's behavior through the distance moved across the grid and in neuronal activity through fluorescence imaging of 5 mechanosensory neurons

Trials were conducted for five groups: Control (unexposed) N2 and HSF-1, Tap Trained N2 worms, Tap Trained and Heat Shocked N2 worms, Tap Trained HSF-1, Tap Trained and Heat Shocked HSF-1 The controlled environment was maintained with NGM agar and bacteria lawn of K12 E. coli All nematodes were age synchronized through dissolving adult worms in 20% Alkaline Hypochlorite to ensure the individuals to be at L1 stage.

To collect the data, worms were first trained with 5 sec ISI Tap Stimuli and 5-sec rest over 1 min and imaged using Toupview. The backward response was analyzed by a distance of the worm moved minus the length of the worm. And worms were tested for the memory after 24h using the same stimuli. The worms were placed on microscope slides in M9 Buffer using the green fluorescence light filter to image worms using Microscope 2.0 on a grayscale. ImageJ was used to analyze for neuron value using the CTAF(Correlated Total Area Florence =Intensity Density -(Area of Neuron =)(mean Background Fluorescence) formula representing the amount of neuron present, Higher values reflected more activation of neurons and the mean of the groups were graphed for statistical comparison.

Using ANOVA, the means of Group I and Group II were significantly different from The Group I was significantly higher than Group Ilwith a p-value << 0.5. The significance of the Group II being lower than the Group Il concludes that heat shock impaired the memory of worms based on the behavior response and the neuron present in the worms, Future studies may further test the long term effect of tap training and the variability of heat shock temperature To determine the possible deeper effects of memory impairment in long-term memory/habituation and to develop a better technique of tracking worms to analyze their behavior and neuron fluorescence to maximize the number of suspects per trial.