Absence of vasopressin expression by galanin neurons in the golden hamster: implications for species differences in extrahypothalamic vasopressin pathways.

In golden hamsters, there is a complete absence of the small diameter vasopressin (VP) neurons in the bed nucleus of the stria terminalis (BST) and medial amygdala (Me) which have been shown to exhibit steroid dependency and sexual dimorphism in many other rodent species. In rats, VP in the BST/Me is always colocalized with the neuropeptide galanin (GAL) and the sex difference in VP cell number appears to result from a sex difference in the number of GAL neurons which coexpress VP. Likewise, we reasoned that the species difference in extrahypothalamic VP pathways present in the golden hamster could result from a reduced coexpression of VP by GAL neurons in these regions. Here, we used in situ hybridization histochemistry to determine whether GAL mRNA expressing neurons are present in the BST and Me of golden hamsters despite the absence of VP expression in these regions. In addition, we have used slice binding and receptor autoradiography to identify specific GAL binding sites in the lateral septum, a probable target region of BST/Me neurons, and in situ hybridization to confirm that some of these binding sites correspond to the GALR1 GAL receptor subtype. Our findings indicate that the absence of VP expression in the BST/Me of golden hamsters results from a failure of extrahypothalamic GAL neurons to express the VP phenotype. Because GAL is expressed in the extended amygdaloid complex and GAL receptors are present in the septum of golden hamsters, GAL may play a role in modulating functions previously attributed to BST/Me pathways.