Trauma and injury necessitate the use of various surgical interventions, yet such procedures themselves are invasive and often interrupt synaptic communications in the nervous system. Because anesthesia is required during surgery, it is important to determine whether long-term exposure of injured nervous tissue to anesthetics is detrimental to regeneration of neuronal processes and synaptic connections. In this study, utilising identified molluscan neurons we provide direct evidence that the anesthetic propofol blocks cholinergic synaptic transmission between soma-soma paired Lymnaea neurons in a dose dependent and reversible manner. These effects do not involve presynaptic secretory machinery but rather postsynaptic acetylcholine receptors were affected by the anesthetic. Moreover, we discovered that long-term (18-24 hours) anesthetic treatment of soma-soma paired neurons blocked synaptogenesis between these cells. However, after several hrs of anesthetic washout, synapses developed between the neurons in a manner similar to that seen in vivo. Long-term anesthetic treatment of the identified neurons VD4 and LPeD1 and the electrically coupled, Pedal A cluster neurons (PeA) did not affect nerve regeneration in cell culture as the neurons continued to exhibit extensive neurite outgrowth. However, these sprouted neurons failed to develop chemical (VD4 and LPeD1) and electrical synapses (PeA) as observed in their control counterparts. Following drug washout, appropriate synapses did reform between the cells, although this synaptogenesis required several days. Taken together, this study provides the first direct evidence that the clinically used anesthetic propofol does not affect nerve regeneration. However, the formation of both chemical and electrical synapses is severely compromised in the presence of this drug. This study emphasises the importance of short-term anesthetic treatment, which may be critical for the restoration of synaptic connections between injured neurons.