In order to clarify the role of neurokinin B (NKB), the dynamic changes in NKB expression and synthesis following water deprivation were examined in the arginine-vasopressin (AVP) neurons of hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. In intact rats, NKB and AVP showed almost the same high level of immunohistochemical reactivity in the magnocellular neurons of the PVN and SON, as well as in the varicose fibers in the median eminence (ME). In contrast, NKB precursor peptide (NKBp) immunoreactivity in the SON and PVN were relatively weak. Five days after water deprivation, AVP and NKB immunoreactivity decreased drastically, while NKBp-immunoreactivity increased in both the PVN and SON magnocellular neurons. Reverse transcription-polymerase chain reaction analysis of control animals revealed high levels of AVP mRNA and substantial amounts of NKB mRNA in the SON. This was contrast to the relatively low levels of AVP mRNA and undetectable levels of NKB mRNA in the PVN. After five days of water deprivation, AVP mRNA in the PVN and NKB mRNA in both the PVN and the SON increased considerably. These results indicate that synthesis and release of NKB, which colocalizes to AVP neurons, are enhanced by water deprivation in the same manner as AVP in the PVN and SON. Thus, NKB seems to be involved in the central control of body fluid levels. The results also suggest that the production rate of NKB under normal conditions in SON dominant.