| The lateral hypothalamic area (LHA) has long been implicated in fluid homeostasis and drinking: electrical or neurochemical stimulation of this region will lead to drinking, while lesions of this area disrupt drinking. In rats dehydrated for 1 to 5 days by replacement of drinking water with hypertonic saline, a specific region of the LHA (LHA-crh) responds with increasing levels of the mRNAs encoding corticotropin-releasing hormone (CRH) and neurotensin/neuromedin N. This led to the hypothesis that alterations in neuropeptide function of the LHA may underlie autonomic or behavioral mechanisms of homeostasis which respond threats to fluid balance. Neuroanatomical tracing techniques combined with in situ hybridization identified: (1) direct projections to the LHA-crh from neurons in many limbic and autonomic-associated brain regions, including the bed nuclei of the stria terminalis, the central amygdaloid nucleus, and the septum, (2) direct functional projections from forebrain osmosensitive neurons in the median preoptic nucleus and the subfornical organ to LHA-crh, and (3) efferent projections of lateral-hypothalamic CRH neurons to brainstem nuclei associated with gustation and visceral sensation--the parabrachial nucleus and the dorsal vagal complex. These data suggest that the LHA-crh is unique in that it is in a position to integrate information from the internal milieu regarding fluid balance with external sensory information, relayed via sensory association cortices and limbic structures. The outputs of the LHA-crh may then influence such behavioral mechanisms of fluid homeostasis as alterations in taste preference or the sensation of thirst, and such autonomic mechanisms as cardiovascular, urinary, and salivatory function. |
