The bed nucleus of the stria terminalis (BNST) is a limbic structure involved in stress responses and negative affective states such as anxiety and fear. Corticotropin-releasing factor (CRF) is also involved in stress responses. Previously, using a conditioned place aversion (CPA) test, we demonstrated that injection of a CRF receptor antagonist into the dorsolateral BNST (dlBNST) suppressed pain-induced aversion. Furthermore, intra-dlBNST CRF injection induced CPA even in the absence of pain stimulation. In the present study, to address cellular mechanisms of CRF-induced CPA, we investigated the effects of CRF on the neuronal excitability in the dlBNST using a whole-cell patch-clamp technique. dlBNST neurons have been categorized into three distinct types (type I-III). We found that CRF depolarized membrane potential specifically in type II dlBNST neurons. Analyses of I-V relationships demonstrated that there may be at least two classes of type II dlBNST neurons, which we designated as type IIa and type IIb, and that CRF depolarized membrane potential by a decrease in potassium conductance and an increase in non-selective cation conductance in the type IIa and type IIb dlBNST neurons, respectively. Depolarizing effects of CRF in type II neurons were blocked by protein kinase A (PKA) inhibitors. Forskolin increased neuronal excitability in type II dlBNST neurons by either a decrease in potassium conductance or an increase in non-selective cation conductance as observed in the CRF-treated type II neurons. In addition, pretreatment with forskolin occluded the depolarizing effects of CRF. These results suggest that depolarizing effects of CRF in type II dlBNST neurons are mediated by an adenylate cyclase-cAMP-PKA pathway.