We studied c-Fos staining in adult male rats after 48 h of water deprivation and after 46 h of water deprivation with 2 h of access to water or physiological saline. Controls were allowed ad libitum access to water and physiological saline. For immunocytochemistry, anesthetized rats were perfused with a commercially available antibody for c-Fos. Dehydration significantly increased plasma vasopressin (AVP), osmolality, plasma renin activity (PRA), hematocrit, and sodium concentration and decreased urinary volume. Fos staining was significantly increased in the median preoptic nucleus, organum vasculosum of the lamina terminalis, supraoptic nucleus (SON), and magnocellular and parvocellular paraventricular nucleus (PVN), as well as the area postrema, nucleus of the solitary tract (NTS), and rostral ventrolateral medulla (RVL). Rehydration with water significantly decreased AVP levels and Fos staining in the SON, PVN, and RVL and significantly increased Fos expression in the perinuclear zone of the SON, NTS, and parabrachial nucleus. Rehydration with water was associated with decreased urinary sodium concentration and hypotonicity, and hematocrit and PRA were comparable to levels seen after dehydration. After rehydration with saline, plasma osmolality, hematocrit, and PRA were not different from control, but plasma AVP and urinary sodium concentration were increased. In the SON, Fos staining was significantly increased, with a great percentage of the Fos cells also stained for oxytocin compared with water deprivation. Changes in Fos staining were also observed in the NTS, RVL, parabrachial nucleus, and PVN. Rehydration with water or saline produces differential effects on plasma AVP, Fos staining, and sodium concentration.

We studied cFos and FosB staining in the supraoptic nucleus (SON) the organum vasculosum of the lamina terminalis (OVLT) and the median preoptic nucleus (MnPO) in adult male rats after water deprivation (24 h, n = 11; 48 h, n = 12) and water deprivation with rehydration (22 h + water, n = 11; 46 h + water, n = 10). Control rats (n = 15) had water available ad libitum. Separate sets of serial sections from each brain were processed for immunocytochemistry using primary antibodies against either c-Fos or FosB protein. Plasma osmolality, vasopressin, hematocrit, and plasma proteins were measured in separate groups (n = 6-7). The number of c-Fos-positive cells in the SON was significantly increased after 24 and 48 h of water deprivation. In contrast, rehydrated groups were not different from control. Water deprivation significantly increased c-Fos staining in both the OVLT and the MnPO, but c-Fos staining was not altered by rehydration. FosB staining in the SON was significantly increased only by 48-h water deprivation, and this effect was significantly decreased by rehydration. In the MnPO and OVLT, FosB staining was significantly increased by water deprivation, and, like c-Fos staining, these increases were not affected by rehydration. Water deprivation significantly increased osmolality and hematocrit, as well as plasma protein and vasopressin concentrations. Plasma measurements from rehydrated rats were not different from control. We conclude that water deprivation and rehydration differentially affect c-Fos and FosB staining in a region-dependent manner.

The supraoptic nucleus of the hypothalamus contains a population of neurons that project to the posterior pituitary where they release peptides into systemic circulation. The system has two main secretory products--vasopressin and oxytocin. The main systemic affects of vasopressin are related to body fluid homeostasis while circulating oxytocin is involved in parturition and lactation. The circulating levels of both hormones are, to a large part, determined by the electrical activity of the supraoptic neurons and other neurosecretory cells, which is in turn determined by synaptic inputs. More recent work suggests that there may be other dimensions to the cellular response of supraoptic neurons to these synaptic inputs. For example, it has been demonstrated that supraoptic neurons alter their synthesis of vasopressin and oxytocin in response to prolonged stimulation and that the morphology of cells in the supraoptic nucleus and its number of synaptic inputs change with the physiological conditions of the animal. These responses would appear to require some type of activity-dependent set of cellular signals. Candidates for such signals include members of the AP-1 transcription factor family whose expression in neurons has been linked to synaptic stimulation. This review will describe the effects of cardiovascular-related stimuli on the expression of different members of the AP-1 family in the supraoptic nucleus.

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