The interaction of electric and magnetic fields with biological systems is an area of growing research interest due to both development of novel therapeutic applications as well as increasing awareness of potential environmental hazards. The question which was addressed in this thesis is what is the role of the cyclic AMP signal transductive pathway in the biological effects of low energy, low frequency electromagnetic fields (PEMF) at the cellular level? The model system employed was the Cloudman melanoma cell line which can be induced to differentiate with the peptide hormone, α-melanocyte stimulating hormone (MSH). The data indicate that both MSH and PEMF affect both adenylate cyclase (AC) activity and cAMP-dependent protein kinase (PKA) activity, and the sensitivity to PEMF and MSH is partially modulated through the GTP-binding protein, Gi. The link to Gi was established by inhibition of Gi activity through use of pertussis toxin catalyzed ADP-Ribosylation of Gi. Phosphorylation of proteins including the oncogene proteins, c-fos and c-ras, is altered and this may be a reflection of the effects on AC and PKA. In order to target receptor specificity of the PEMF interaction, homologous and heterologous desensitization with the α-adrenergic receptor agonist, epinephrine (EPI) and the β-adrenergic agonist, isoproterenol (ISO) was performed. Both EPI and ISO pretreatment of melanoma cells decreased the response to PEMF with no effects observed on the MSH response. These results indicate a linkage between adrenergic receptor expression and sensitivity to PEMF;​ and further suggest that PEMF does not work through the MSH receptor pathway. The conclusion from these studies is PEMF can induce differentiation in a melanoma cell line by manifesting certain functional alterations associated with the normal physiological regulator, MSH. PEMF may also be capable of altering the phenotypic expression of the melanoma cell by differential regulation of protein synthesis and phosphorylation. This PEMF-induced differentiation is AC and PKA dependent and the results are consistent with an adrenergic receptor target site for PEMF. The generality of these findings in other model systems remains to be investigated.