The neuropeptide galanin (GAL) has been proposed to be an inhibitory modulator of cholinergic transmission in the hippocampus and may impair memory by directly affecting the activity of basal forebrain (BF) cholinergic neurons. Alternatively, GAL may act indirectly and modulate the activity of other neurotransmitter systems which, in turn, influence cholinergic transmission. We have used double in situ hybridization histochemistry to evaluate the co-expression of the GAL receptor subtype, GALR1, within cholinergic neurons in the medial septum/diagonal band of adult male rats. In alternate brain sections, we assessed the co-expression of GALR1 mRNA within another forebrain cell group implicated in memory functions, the neurons of the bed nucleus of the stria terminalis (BNST) and medial amygdala (AMe) which co-express vasopressin (VP) and GAL and project to septo-hippocampus. Despite the abundance of GALR1 mRNA-expressing neurons in the cholinergic BF, we found no evidence for the co-expression of this receptor subtype within cholinergic neurons in the medial septum/diagonal band. In contrast, we detected an extensive co-expression (95%) of GALR1 mRNA within extrahypothalamic VP/GAL neurons. These results do not support the idea that GAL, acting via the GALR1 receptor, directly impairs BF cholinergic neurons but suggest, instead, that non-cholinergic neurons in the BF may play a role in mediating the inhibitory actions of GAL on cholinergic function. However, our findings provide anatomical evidence that GAL could directly modulate the activity and/or secretion pattern of extrahypothalmic VP/GAL neurons into septo-hippocampal regions.