Neurons are specialized cells that are responsible for sending electrical signals throughout the body. The action potential is the mechanism in which there is a temporary change in voltage within the resting membrane potential due to sodium influx and potassium efflux. The electrical firings of action potentials from neurons are crucial for neuronal functioning and cell to cell communication. Depolarization is an event in which the voltage of the membrane increases and this allows voltage gated sodium channels to open and allow the flow of sodium into the cell. This event is crucial for the start of an action potential as it is considered dichotomous, or an “all or nothing event”. If the threshold for depolarization is not reached then an action potential will not occur. Lamotrigine (Lamitcal) is an anticonvulsant and prescribed as a mood stabilizer. Lamotrigine is an inhibitory 5-HT receptor antagonist. Through its inhibitory and antagonistic effects on voltage gated sodium channels, its mechanism of action decreases the firing rate of a neuron by inhibiting depolarization from occurring, thus regulating 5-HT levels in the synaptic cleft.  Neurophysiological experiments were conducted on Acheta domesticus (brown crickets) in which extracellular neuronal firings were recorded before and after the administration of Lamotrigine in order to understand the pharmacodynamics of Lamotrigine on neural firing activity.  Lamotragine consistently displayed lower action potential firing rates in comparison to the control trials, thus supporting the hypothesis that Lamotrigine functions as an anticonvulsant and mood stabilizing by impeding the depolarization of the membrane potential and thereby blocking action potentials.