ENHANCED DRINKING AFTER EXCITOTOXIC LESIONS OF THE PARABRACHIAL NUCLEUS IN THE RAT

Previous reports indicate the lateral parabrachial nucleus (lPBN) is important in the regulation of fluid intake. After electrolytic lesions of the lPBN, rats consume increased amounts of water when challenged with pharmacological stimuli that mimic depletion of the extracellular fluid space. Nonetheless, it is possible that neurons within the lPBN are not responsible for the overingestion of water during extracellular thirst challenges, since electrolytic lesions damage fibers of passage as well as neurons within the lPBN. Thus we used the excitatory neurotoxin ibotenic acid to lesion cell bodies within the lPBN. After recovery from surgery, water consumption by lesioned rats was significantly greater than consumption by vehicle or uninjected control rats when challenged with subcutaneous angiotensin II or isoproterenol to stimulate drinking. However, when injected with subcutaneous hypertonic saline to produce cellular dehydration, or when water deprived for 24 h, the water intake of rats with lesions was not different from the intake of control rats. Anatomical examination of the lesion sites revealed that ibotenic acid injection caused a notable loss of neurons in the lPBN with little or no damage to surrounding structures. Moreover, injection of an anterograde tracer into the dorsomedial medulla resulted in labeling of fibers that traverse the ibotenic acid lesion site. Together, these data suggest neurons within the lPBN are involved in the regulation of fluid intake, particularly challenges that involve depletion of the extracellular fluid space.